ABSTRACTS ism and AI. APS-2 consists of AI, autoimmune thyroid diseases and/or type 1 diabetes mellitus. Autoimmune thyroid diseases associated to other autoimmune diseases (excluding AI and/or hypoparathyroidism), define APS-3. The different combinations of autoimmune diseases not included in the previous groups are characteristics of APS-4. Conclusion: This case illustrates the importance of making an early diagnosis of AAI in the right context of clinical and laboratory data. In addition, the presence of other endocrine gland insufficiencies should prompt an evaluation for APS. Clinicians should be aware of these particular syndromes to avoid the presence of unrecognized endocrine disorders and their complications. ADRENAL DISORDERS Abstract #100 A CASE OF ACUTE ADRENAL INSUFFICIENCY AND HYPOTHYROIDISM: AUTOIMMUNE POLYGLANDULAR SYNDROME? German Velasco, MD, Andrew Weinberg, DO, and Spyros Mezitis, MD, PhD Objective: To illustrate the acute presentation of adrenal insufficiency (AAI) in a patient with hypothyroidism with an overview of autoimmune polyglandular syndromes (APS). Case presentation: A 29 year-old male with a history of hypothyroidism presented to his PMD complaining of a 3-week history of lower extremity weakness, muscle pain and exertional dyspnea. He had a syncopal episode associated with hypoglycemia (43 mg/dL) and was sent to the ED. His physical examination was significant for hypotension. Laboratory data showed hyponatremia (127 meq/L) and hyperkalemia (7.0 meq/L) with no changes on electrocardiogram. A random cortisol level was 0.1 mcg/dL. A suspected diagnosis of AAI was made and he was treated with intravenous hydration and dexamethasone. A cosyntropin stimulation test (250 mcg) showed a low ACTH response, confirming the diagnosis of AI. Additional data included a TSH of 4.72 micro IU/mL, free-T3 223 pg/dL, T4 5.7 mcg/dL, negative adrenal antibodies, and a CT scan of abdomen/pelvis showing markedly diminutive adrenal glands. He also developed anemia with normal iron studies, negative autoantibodies, and an upper endoscopy significant for mild chronic gastric inflammation. Consequently, he received oral hydrocortisone and, upon stabilization of his vital signs and electrolyte abnormalities, he was discharged without complications. Discussion: AAI can be a challenging diagnosis; however, the presence of autoimmune disease (e.g. hypothyroidism) should prompt a suspicion of the diagnosis in the right clinical context. APS consist of multiple endocrine gland insufficiencies associated to autoimmune disease. Currently 4 types have been described. APS-1 is characterized by presence of chronic candidiasis, hypoparathyroid- Abstract #101 UTILITY OF THE GLUCAGON STIMULATION TEST IN THE EVALUATION OF PATIENTS SUSPECTED TO HAVE PHEOCHROMOCYTOMA: A CASE REPORT Krupa Doshi, MD, Dima L. Diab, MD, Emmanuel Bravo, MD, and Amir H. Hamrahian, MD Objective: To demonstrate the utility of the glucagon stimulation test (GST) in confirming the diagnosis of pheochromocytoma (PC). Case Presentation: A 55 year-old male was found to have a 3.2 cm left adrenal incidentaloma with an attenuation value of 13 HU on non-contrast CT scan during workup of chronic diarrhea. He denied history of hypertension or symptoms of palpitations, diaphoresis, headaches or weight gain. Biochemical data was as follows: plasma free metanephrines (MN) 1.01 nmol/L (normal <0.5), urine total MN 1536 Вµg/24 hr (140-785), serum norepinephrine 265 pg/mL (80-520), serum epinephrine 124 pg/mL (10-200) and urine total catecholamines (CA) 105 Вµg/24 hr (26-121). Multiple BP measurements were consistently below 120/64 mm Hg. He underwent a GST in which epinephrine and norepinephrine values increased from 271 pg/mL (at baseline) to 6236 pg/mL (at 120 seconds) and from 462 pg/mL (at baseline) to 1978 pg/mL (at 120 seconds) respectively. His BP rose from 98/69 mm Hg at baseline to 181/86 mm Hg at 120 seconds. At that time, –– ABSTRACTS – Adrenal Disorders he looked pale and complained of headache and lightheadedness, which lasted for a few minutes. He subsequently underwent a successful adrenalectomy and pathology was consistent with PC. Discussion: The diagnosis of PC is made by measurements of 24 hour urine or serum CA and MN levels. Urine total MN >1800 Вµg/24 hr, serum total CA >2000 pg/mL or plasma free MN exceeding 3-4 times the upper limit of normal in the appropriate clinical setting are diagnostic of PC. When clinical suspicion for PC is high but serum or urine CA and MN levels are non-diagnostic, additional testing is necessary. В Clonidine suppression test (CST) is used in patients with elevated serum CA or MN levels. However, this test may be associated with significant hypotension in normotensive patients. GST may be of value in such circumstances but the literature regarding its usefulness is controversial. Young (Eur J Endocrinol 1997; 136:28) reported no utility with the use of the GST in over 500 patients suspected to have PC who had normal urine CA excretion. Grossman et al. (Hypertension 1991; 17:733) reported positive GST results in 25 of 31 patients with PC, 8 of whom had normal baseline plasma CA levels. The result of the GST in our patient suggests that this test may be useful in confirming the diagnosis of PC in normotensive patients with an equivocal biochemical work-up for PC. Conclusion: GST may be of value in normotensive patients suspected to have PC with a biochemical workup not in the diagnostic range for PC. Appropriate patient selection is an important factor to maximize the utility of this test. pressed by low and high dose dexamethasone, Magnetic Resonance imaging showed an adrenal tumor which was removed surgically and patient became normotensive after surgery with restoration of normal blood glucose, cortisol, ACTH and urinary metanephrines. follow up of the patient showed complete resolution of the hypertension, and hyperglycemia on no medications. Conclusion: Pheochromocytoma is a rare cause of hypertension that should be sought in patients with severe hypertension, and it can produce ACTH in addition to catecholamines Abstract #103 CUSHING`S SYNDROME DUE TO ECTOPIC ACTH-PRODUCING PHEOCHROMOCYTOMA Khalil M Alsoutary, MD, FACE, Riad пїЅпїЅпїЅпїЅпїЅпїЅпїЅпїЅпїЅпїЅпїЅпїЅпїЅпїЅпїЅпїЅпїЅпїЅпїЅпїЅпїЅпїЅпїЅ Sulaimani, MD and Hani Alassad, MD Objective: To report a 31 year female patient who presented with Cushing’ s Syndrome, new onset Diabetes Mellitus and hypertension that proved to be due to ectopic ACTH secretion by a pheochromocytoma. Methods: A 31 year female was admitted to our hospital with polyuria, polydypsia, weight loss of 15 kgs and difficult to control hypertension for last 3 months.В Result: Glucose was 35.8 mmol/l, K 2.9 mmol/l, serum cortisol 2280 nmol/l(normal 138-690), ACTH level 568,, urine metanephrines 35763 nmol/24 hrs (normal 2501200).Biochemical profile showed high metanephrine and normetanephrine, and high morning cortisol level not suppressed by low and high dose dexamethasone, Magnetic Resonance imaging showed an adrenal tumor which was removed surgically and patient became normotensive after surgery with restoration of normal blood glucose, cortisol, ACTH and urinary metanephrines. Case Presentation: A 31 year old Saudi female, presented with polyuria, polydypsia and weight loss of 15 kgs over the last 3 months, associated with blurred vision, severe muscle weakness, palpitation, weakness and shortness of breath, but no nausea or vomiting. She had bilateral loin pain and frothy urine. Her menses were regular till the last six months. She was diagnosed to have diabetes 6 months ago and was started on treatment with Metformin and diet. Her blood sugar readings were all high in the last 3 months.В В В В 2 years before,В she had proteinuria of 2.5 gms in 24 hrs urine collection and kidney biopsy performed which showed mesango-proliferative glomerulonephritis. She was treated with prednisolone 30 mgs tapering to 10 mg daily and mycophenolate 500 mgs bid. She was also receiving simvasatatin for dyslipidemia Abstract #102 CUSHING SYNDROME DUE TO ECTOPIC ACTH PRODUCING ADENOMA Khalil M Alsoutary, MD, FACE, Riad Sulaimani, MD and Hani Alassad, MD Objective: To report a 31 year female patient who presented with Cushing’ s Syndrome, New onset Diabetes mellitus and hypertension that proved to be due to ectopic ACTH secretion by a pheochromocytoma. Methods: A 31 year female was admitted to our hospital with polyuria, polydypsia, weight loss of 15 kgs and difficult to control hypertension for last 3 months. Result: Glucose was 35.8 mmol/l, K 2.9 mmol/l, serum cortisol 2280 nmol/l(normal 138-690), ACTH level 568,, urine metanephrines 35763 nmol/24 hrs (normal 2501200). Biochemical profile showed high mwtanephrine and normetanephrine, and high morning cortisol level not sup–– ABSTRACTS – Adrenal Disorders echolamines. In this patient BP returned to normal and is still normal without medication after adrenalectomy. Physical Examination: Patient was obese BMI 39 kg/m2, Bp 210/130 mm Hg, rounded face with acne, no hirsutism or hyperpigmentation, wide violacious striae over the abdomen, lower limbs showed multiple bruises, Fundoscopy showed grade 1 hypertensive changes( AV narrowing), peripheral pulses intact, jugular venous pulse not raised. Heart sounds normal with an ejection systolic murmer 2/6 over the aortic area. Liver was palpable 4 cm below coastal margin, nontender, and spleen not palpable. Lower limbs showed bilateral pitting edema. Laboratory Investigations:В CBC:В WBC’s 6200 /ml, hemoglobin 13.8 gm/dl, HbA1C 9.2.Urinalysis showed protein 3+, glucose 3+-24 hrs urine protein 8.76 gms, Na 138 meq/l, K 2.8 mmol/l, Cl-94, HCO3 33 mmol/l Urea 5.2 mmol/l, creatinine 56 mmol/l. Arterial blood gases: pH 7.49, pCO2 38.5, pO2 84, O2 sat. 97% on room air, Serum Cortisol 280mmol/l (normal 138-690) at 8.00 AM ACTH 568 pg/ml (normal 9-52 at 08В :00 AM) 24 hrs urine metanephrines 35763 nmol/24hrs (normal 250-1200) Normetanephrines 13751 nmol/24hrs (normal 750-2000) 11 deoxycortisone 120 nmol/l (normal <13.8).Low dose dexamehasone: High dose dexamethasone 8 mgs 1 dose at 12 midnight. Radiological Investigation: CT scan of lungs-Normal MRI of pituitary gland: normal size and enhancement. MR Imaging of the abdomen showed a well-defined, round shaped mass in the paravertebral area, suggestive of an adrenal tumor-fig.1.В Hospital Course: В Her high blood pressure was difficult to control even with 4 medications-Atenolol 100 mg, valsartanВ 160 mg, Amlodipine 10 mg/dl and KCL supplement. After the diagnosis was established with the result of metanephrines and failure of suppression of cortisol on both low and high dose dexamehasone, patient was prepared for surgery with IV fluids and phentolamine, On December 13, 2004 she underwent open Right adrenalectomy.В В Pathology: Grossly showed 7.0X3.5x4.0 cm with a polypoid mass 4.5x5.0 cm-its cut section showed a gray soft appearance. Fig.2 Microscopic section:В Hyperplastic adrenal gland with a general nodular appearance with cortical cells of varying appearance, some of these cells have vaculated cytoplasm.В Sections of the adrenal mass show a tumor of well defined nests separated by well vascularized stroma. Mitotic figures were uncommon. The cytoplasm has a granular appearance. IHC for chromogranin stain and synaptophysin are strongly positive. Findings were suggestive of pheochromocytoma. Patient improved dramatically after adrenalectomy with complete normalization of BP and hyperglycemia without medicationВ Conclusion: Pheochromocytoma is a rare cause of hypertension that should be sought in patients with severe hypertension, and it can produce ACTH in addition to cat- Abstract #104 BRONCHIAL CARCINOID SECRETING ACTH: A CASE OF MISDIAGNOSIS Saba Khayal, MD, and Brandy Panunti, MD Introduction: Cushing’s Syndrome (CS) due to ectopic production of ACTH remains a major diagnostic challenge to the endocrinologist. Case: A 27 y/o male presented to his internist with 40 lb wt. gain in the past year, uncontrolled HTN and darkening stretch marks. Diagnosis of CS was established after an overnight 1 mg dexamethasone suppression test and elevated 24 hour urinary free cortisol. ACTH was194 pg/ml. MRI pituitary was normal. After inferior petrosal venous sampling, he underwent transsphenoidal pituitary resection. Pituitary pathology was normal. After surgery ACTH level was 234 pg/ml and serum cortisol was 50 Вµg/ dl. Patient continued to have s/s of hypercortisolism. He was referred to Endocrinology. Reviewing the results of his petrosal venous sampling: ACTH levels from the peripheral vein, left petrosal sinus and right petrosal sinus were 135, 109 and144 pg/ml respectively before CRH stimulation. ACTH levels post CRH stimulation from the peripheral vein, left petrosal sinus and right petrosal sinus were 130, 146 and 143 pg/ ml respectively. The central to peripheral ratios for ACTH were less than 2:1 baseline and less than 3:1 after CRH stimulation, findings not consistent with pituitary or central CS. Patient underwent CT thorax/abd/pelvis, a bronchial adenoma was seen. An octreotide scan was positive in the same area. Biopsy of the lesion was consistent with neuroendocrine tumor. Patient underwent resection of the adenoma. It stained positive for ACTH secreting cells. After surgery, ACTH levels were undetectable. He improved clinically. Discussion: Ectopic ACTH syndrome comprises 1020% of the cases of CS. The classic description of the ectopic ACTH syndrome was made by Grant Liddle in the early 1960’s and was based on a series of patients who mostly had malignant tumors. More recently, the ectopic ACTH syndrome has been recognized with increasing frequency with benign tumors specifically carcinoids. Benign versus malignant lesions typically present in a more subtle clinical manner. Plasma ACTH levels are strikingly high in ectopic CS, usually greater than 200 pg/ml. Inferior petrosal sinus sampling after CRH stimulationВ is a reliable test to dif–– ABSTRACTS – Adrenal Disorders ferentiate between pituitary ACTH CS and ectopic ACTH CS. A central to peripheral ACTH ratio of В± 2 basal and В± 3 after CRH administration is consistent with pituitary ACTH syndrome(which was not the case in our patient). Once diagnosis is established, the next step is CT thorax/ abd/pelvis. Octreotide scan is another important diagnostic tool for tumor localization. Iodinated or indium -111labeled octreotide scanning has been used more recently. Management includes treatment of the underlying lesion. Conclusion: It is important to differentiate between the various etiologies of CS since the treatment modalities are different. normalization of her blood pressure. A repeat cosyntropin stimulation test performed two months later when the patient was offВ MA and steroids wasВ normal. Discussion/Conclusion: Though adrenal insufficiency has been reported as a side effect of MA, it is not well recognized in clinical practice. Also with the widespread use of MA, adrenal insufficiency may present as subtle and diverse presentations. It is important for the clinician to recognize adrenal insufficiency in patients ofВ MA especially with its widespread use in the geriatric population. Though some authors have recommended that routine steroid replacement at the time of MA commencement may be the safest course of action, we recommend that during periods of illness patients receiving MA should receive empiric therapy with stress doses of corticosteroids. Also, when discontinuing chronic MA therapy, it should be gradually tapered off as well the HPA axis tested to confirm normalization. Abstract #105 MEGESTEROL ACETATE ASSOCIATED ADRENAL INSUFFICIENCY Deepti Bulchandani, MD, Jagdish S Nachnani, MD, Alpesh Amin, MD, and John May, MD Abstract #106 Objective: Megesterol acetate (MA) is a commonly used drug in the malnourished geriatric population to promote weight gain.В Adrenal insufficiency is a well documented adverse effect ofВ Megesterol acetate.В We present a case with megesterol induced severe adrenal insufficiency presenting as mental status change, weakness, and ventilatory respiratory failure.В Given the challenge of clinically recognizing adrenal insufficiency in this patient population it is important for clinicians to be alert for this adverse effect when using or even considering Megesterol therapy. Case Presentation: The patient is an 80 year old female admitted for dyspnea.В Prior to this presentation, she had a general declineВ in physical function associated with some weight loss and anorexia consistent with failure to thrive and was started on MA in an effort to stimulate her appetite. Her portable chest Xray was within normal limits and neurologic examination was consistent with generalized weakness andВ cognitive impairment. The rest of her examination including room air oxygen was within normal limits.В During her hospital stay, she developed worsening delirium and dyspnea with hypotension. The patient was subsequently transferred to theВ ICUВ and electively intubated.В Bronchoscopy did not reveal any signs of infection and she continued to oxygenate well on the ventilator. During her stay she underwent an extensive neurological workup including an EEG and MRI and EMG which failed to reveal a cause. A cosyntropin test showed the presence of adrenal insufficiency. MA was at this time discontinued and steroid replacement with dexamethasone was initiated. В The patient did improve subsequent to this with INABILITY TO CONCEIVE IN NON-CLASSICAL CONGENITAL ADRENAL HYPERPLASIA Ramya Smita Vedula, DO, and Anne Marie VanHoven, MD Objective: To describe fertility treatment failure in women with Non-classical congenital adrenal hyperplasia (NCCAH). Case: A 29 year old female presents seeking to become pregnant. She had menarche at age 14 but noted her periods were never regular. In 1999 she was started on an oral contraceptive which regulated her menstrual cycles until she stopped in August of 2005. She had intermittent periods thereafter but was not able to conceive despite trying for 6 months. A reproductive endocrinologist was consulted in July 2006, who made a diagnosis of polycystic ovarian syndrome and prescribed metformin, without benefit. The patient has gained 20-25 pounds over the past 2 years, reports no significant stress in life, no hirsutism but some facial acne for which she was using topical acne treatments. In addition, there were no headaches, galactorrhea, eating disorders, excessive exercise, or signs and symptoms of hypo or hyperthyroidism. Physical exam showed a 5’4” woman, weight of 154lbs and BMI of 26, well appearing and in no distress. No hirsutism, acne, thyromegaly, acanthosis nigricans, abdominal stria, or bruises. The rest of the exam was within normal limits. Laboratory data obtained included normal levels of insulin, SHBG, DHEA sulfate, TSH, prolactin and glucose. Total testosterone was –– ABSTRACTS – Adrenal Disorders elevated at 70, LH of 11, FSH of 5 and 17-hydroxyprogesterone was 491. An ACTH stimulation test showed a base line 17-hydroxyprogesterone of 178 and a stimulated 17hydroxyprogesterone of 5815. Based on the clinical history, presentation and lab values, a diagnosis of NCCAH was made and the patient was started on dexamethasone to induce ovulation. Despite 3 months of dexamethasone, the patient has not had a menstrual cycle. Fludrocortisone was recently added. Genetics was consulted for preconception counseling. Discussion: Non-classical congenital adrenal hyperplasia (NCCAH) is a mild enzymatic defect of 21-hydroxylase that results in a delay of symptoms until after puberty. It is often diagnosed as polycystic ovarian syndrome (PCOS). In women affected with NCCAH desiring pregnancy, a trial of dexamethasone is initiated to induce ovulation. Since the doses of glucocorticoids needed to suppress ACTH can cause signs and symptoms of glucocorticoid excess during long term treatment, the treatment is often worse than the disease. As a result, dexamethasone is used mostly for fertility. Conclusion: Since NACCH seems to trigger a PCOS like physiology, patients have difficulty with fertility despite glucocorticoid replacement. Concurrent treatment with dexmethasone, fludrocortisone and metformin has been of no benefit, aggressive fertility treatments maybe needed. ADRENAL CARCINOMA PRESENTING AS TYPE 2 DIABETES MELLITUS Chest radiograph showed canon ball shadows suggestive of metastasis. CT Scan abdomen revealed left adrenal mass with metastasis in liver & retroperitoneal lymph nodes. FNAC from lesions of liver was suggestive of metastasis from adrenal carcinoma. She was diagnosed as a case of functioning adrenal carcinoma (Cushing’s syndrome) with multiple metastases. Patient refused for chemotherapy and lost to follow-up after 2 visits. Discussion: Adrenal carcinoma is an uncommon tumor. Most patients present with nonfunctioning tumors and clinical manifestations are related to tumor growth or with an incidentally found adrenal mass detected on radiographic imaging performed for a different reason. Adrenal carcinoma may cause Cushing’s syndrome in 8% of cases. Adults with hormone-secreting adrenal carcinoma usually present with Cushing’s syndrome alone, or a mixed Cushing’s and virilizing syndrome with overproduction of both glucocorticoids and androgens. Fewer than 10% present with virilization alone. This patient had poorly controlled diabetes mellitus since diagnosis that prompted endocrine evaluation for the cause of diabetes mellitus. Conclusion: Adrenal carcinoma is a rare tumor with very poor prognosis. Presentations of Cushing’s syndrome can be varied, and patients can present across a range of disciplines. Early consideration of the diagnosis increases the possibility of successful treatment in cases of persistently uncontrolled diabetes mellitus; a thorough endocrine work-up should be instituted including imaging studies to diagnose early adrenal tumors. The most important and consistently observed determinants of improved survival are localized tumors, complete surgical resection, and tumor grade. Simmi Dube, MD, VK Sharma, and TN Dubey Abstract #108 Abstract #107 Objective: To report a case of adrenal carcinoma who presented as poorly controlled type 2 diabetes mellitus. Case Presentation: 42 years obese female admitted with complaints of type 2 diabetes mellitus for last 2 years and amennorrhoea, proximal muscle weakness, acne and boils since 3 months. She informed that in spite of having diet control, regular exercise and good compliance to anti-diabetic treatment, her diabetes mellitus is poorly controlled. Physical examination revealed hypertension, moon facies, buffalo hump, easy bruising, folliculitis, acne, hirsutism, proximal muscle weakness and tenderness over bones. Complete haemogram and renal function tests were normal. Fasting Blood glucose– 380 mg %, Post meal blood glucose- 415 mg%, Serum sodium – 134 meq/L, Serum Potassium – 3 meq /L, Serum ACTH – 05pg/ml, Serum cortisol – 45ug /dl, Serum DHEA sulphate – 550ug /dl. CUSHING SYNDROME CAUSED BY A NEUROENDOCRINE CORTISOL PRODUCING TUMOR Maria Alejandra Ramos Guifarro, MD, Juan Manuel Rios, Alfredo Reza AlbarrГЎn, Esperanza ValentГn, Edgar AvendaГ±o, Arturo ГЃngeles, Edgardo Reyes, Francisco J GГіmez-PГ©rez, and Juan Rull Objective: To present a case of Cushing’s syndrome caused by a cortisol producing tumor with neuroendocrine histological characteristics. Case Report: A 19 year old female presented for consultation with a 10 month history of weight gain, increased facial hair andВ purple striae in abdomen and legs. Five months earlier she had been diagnosed with Cushing syn–– ABSTRACTS – Adrenal Disorders Clinical Presentation: A 19 year old, G1P0 at 30 weeks gestation, presented with high urine and plasma metanephrines (PM).В She had a family history of MEN2A, and was found to have a RET gene mutation at the time of her sister’s diagnosis (index case).В She underwent prophylactic total thyroidectomy at age 13, and pathology showed medullary thyroid cancer.В Evaluation for pheo prior to surgery was negative.В She was lost to follow up (FU) until 6 years later, when she was next evaluated for pheo.В Exam demonstrated normal BP without orthostasis, a healed necklace scar, non-palpable thyroid and a gravid abdomen. Despite being asymptomatic, both urine and PM were elevated three fold.В Serum calcium, calcitonin and TSH were normal.В An MRI of the abdomen revealed a 2.5 x 3.5 cm lesion in the left adrenal gland, hypointense on T1 and hyperintense on T2 weighted images, consistent with pheo. The patient was started on Phenoxybenzamine 10 mg BID, and referred to high-risk OB.В She did well during the remainder of her pregnancy and underwent an elective Caesarean-section at 39 weeks, with delivery of a healthy infant.В Six weeks later, she underwent an uneventful laparoscopic left elective adrenalectomy (EA).В Pathology revealed pheo with capsular invasion.В She is currently doing well on LT4. Discussion: Pregnancy related pheo is rare, and if unrecognized, is associated with maternal and fetal mortality up to 50%.В В Cardiovascular collapse, uteroplacental insufficiency, fetal hypoxia and death have been reported.В Antenatal recognition significantly reduces these complications, and if diagnosed in late pregnancy, appropriate management becomes crucial. В EA is usually recommended before 3rd trimester, however, specific guidelines for management in late pregnancy are lacking.В Our case was unusual in that the diagnosis was made late in pregnancy precluding elective surgery.В Management with a- adrenergic blockade alone resulted in an uneventful pregnancy.В Hence, a conservative approach with careful monitoring in an asymptomatic patient may be appropriate, if diagnosed in late pregnancy. Conclusion: Once the diagnosis of MEN-2A is confirmed, routine surveillance for pheo is recommended to avoid catastrophic outcomes, including those associated with pregnancy.В FU screening for pheo despite left adrenalectomy is necessary in our patient, as the risk of developing pheo in the contralateral gland is 50% in 10 years.В Finally, in MEN-2A patients, imaging studies in addition to biochemical testing, are appropriate as many of these cases can be clinically silent. drome and an abdominal CT showed a left adrenal adenoma. At diagnosis her urinary cortisol was 1216 mcg/day, with a plasmatic cortisol level of 34.26 mcg/dl; serum ACTH was 19 ng/dl. A laparoscopic left adrenalectomy was performed and pathological report was a neuroendocrine tumor adjacent to a hypotrophic adrenal gland. Her symptoms diminished for a couple of months, but then returned; a new CT scan showed a solid mass located between the rectum and the uterus, 6x6 cm in diameter, with extension to both ovaries and multiple nodules inferior to the spleen. She underwent a laparotomy for tumor removal, but due to tumor burden only biopsy specimens were removed. The pathology report was consistent with neuroendocrine tumor cromogranin+, synaptophysin+, ACTH-.Post-op she received chemotherapy (etoposide, cysplatin ),mitotane 3 mg per dayВ and ketoconazole 600 mg/day. On a follow-up scan 10 months later, only 4 small nodules of less than 2 cm were observed and a new laparotomy was performed to remove all visible tissue; the pathology report was similar. After her last surgery she developed an adrenal crisis, she is now receiving 30 mg a day of cortisone therapy and florinef 0.5 mg a day. Discussion: In this patient, Cushing’s syndrome due to ectopic ACTH secretion was not demonstrated; furthermore, ACTH levels were low and staining for ACTH was negative. Histologically, it was compatible with a cortisol secreting neuroendocrine tumor. There have been reports of adrenocortical carcinomas with positive neuroendocrine staining, although this is extremely unusual; it is even rarer to find a cortisol producing carcinoma with neuroendocrine histology. Conclusion: Adrenocortical and neuroendocrine tumors can overlap in clinical, biochemical, histological and inmunostaining markers. The hypothropic adrenal tissue found adjacent to the neoplastic tissue and the clinical response to medical treatment suggest that the origin of the tumor is neuroendocrine and not adrenal. Abstract #109 MANAGEMENT OF PHEOCHROMOCYTOMA (PHEO) PRESENTING IN LATE PREGNANCY AS PART OF MEN-2A SYNDROME Sonia Gajula, MD, and Lilamani Romayne G Kurukulasuriya Objective: To discuss the outcome of conservative management of pheo diagnosed in late pregnancy. –– ABSTRACTS – Adrenal Disorders Abstract #110 Abstract #111 ADRENOCORTICAL CARCINOMA PRESENTING WITH RESISTANT HYPERTENSION AND HYPOKALEMIA BILATERAL ALDOSTERONE-PRODUCING ADENOMA. THE USEFULNESS OF CONTINUOUS ACTH STIMULATION DURING BILATERAL ADRENAL VENOUS SAMPLING AND 18-HYDROXYCORTICOSTERONE MEASUREMENT Abdullah Hanna-moussa, MD, Khurshid Khan, MD, and Stephen Brietzke, MD Objective: To recognize the different presentations of adrenocortical carcinoma (ACC). Case presentation: 33 year old male presented with uncontrolled hypertension, hyopkalemia, weight loss, and lower extremities edema. Three months prior to his presentation he was diagnosed with DM and his BP was markedly elevated while on multiple medications. A CT scan of the abdomen demonstrated 7.5 cm right adrenal mass, with liver and lung masses. Blood work showed potassium 2.6 mmol/L, CO2 35 mmol/L. His Am cortisol postВ overnight 1 mg dexamethasone was 31.2 mcg/dl, aldosterone, PRA were normal, 24 h urine metanephrine was normal, 24 h urine free cortisol 1221 mcg/d(normal<60mcg/d), DHEA 4.6 ng/mL (1.9 - 7.6 ng/mL), ACTH 3 pg/mL. He under went Laparoscopic right adrenalectomy with, excisional biopsy of liver mass, which showed ACC with and liver metastases. His post surgery course was complicated by refractory hypertension treated with IV medications and ketoconazole 200 mg TID, a subsequent MRI of the brain showed brain metastases. Discussion: ACC presents with excess cotrisol production in approximately 60% of cases, with a median survival of 18 months. Our patient presented with hypertension, weight loss without other common presenting symptoms (weakness, anorexia, nausea, vomiting, and myalgia) with normal DHEAs which when elevated is a clue for ACC. Severe hypokalemia is common and is more likely caused by grossly elevated cortisol secretion, activating the mineralocorticoid receptor. Clinical features of Cushing’s syndrome are often missing because the rapid development of ACC. The role of tumor debulking in the presence of metastatic disease is a matter of debate. Incomplete resection is associated with a poor prognosis, however, tumor debulking may help to control hormone excess. Mitotane is the treatment for inoperable tumors, metastatic disease and after incomplete resection. Chemotherapy is an option in advanced ACC. Conclusion: ACC is a rare malignancy. It can present in different ways and can progress rapidly, high index of suspension can lead to early diagnosis and potentially better outcomes. Farnoosh Farrokhi, MD, Fariha Shad, MD, Javier Clemente, MD, and Luis A. Llerena. MD, FACP, FACE Objective: To present a case of bilateral aldosteroneproducing adenoma (APA) and work up to differentiate it from Idioapthic hyperaldestronism (IHA). Case presentation: 35-year-old female was admitted to the hospital with weakness, severe non-induced hypokalemia, and hypertension (HTN). Routine lab work was unremarkable.В Hyperaldosteronism was suspected due to persistent hypokalemia. Despite of high doses of potassium replacement, her potassium was 2.4 meq/L. Cortisol, ACTH, catecholamines and metanephrines were normal. DHEA-S was upper normal. Plasma aldosterone concentration (PAC) persistently elevated (over 50 ng/dl) (nl. 4.5-35.4), with suppressed plasma renin activity (PRA) (below 0.4 ug/L/hr) (nl. 0.5-1.8). Although PAC did not change significantly from supine to upright position, it was not suppressed after high sodium diet and saline over load test. 1.6 and 1.0 cm nodes were noted on the Ct scan in the left and right adrenal respectively. Bilateral APA was suspected. Adrenal venous sampling during continuous ACTH infusion showed very high levels of aldosterone (A) (10890 ng/dl) and18-oH corticosterone (18-OHC) (23600 ng/dL) in the left adrenal vein. Aldosterone to cortisol ratio (A/C) of 384.8 (nl. Less than 4). In the right side also A and 18-OHC were high (1891 and 6660 ng/dl respectively) with A/C ratio of 25.2. The A in vena cava was only 81 ng/ dl and the A/C ratio 1.08. Patient was started on spironolactone with excellent control of HTN and hypokalemia. She no longer required potassium supplements. Discussion: Bilateral adrenal APA has been reported in only few cases, and it is always a challenge to differentiate from IHA. Adrenal vein sampling obtained during a continuous ACTH infusion has proved to be useful in localization of the tumor. Measurement of 18-oH corticosterone can help in differentiating APA from IHA, as 18-oH corticosterone is not as high inВ IHA. Conclusion: Although we don’t have the pathological confirmation, the secretion of very high levels of aldosterone and 18-oH corticosterone in this patient are highly –– ABSTRACTS – Adrenal Disorders Discussion: We present a case of iatrogenic CS due to the administration of intra-articular triamcinolone.В В Previous reports have focused on frequent and/or larger doses of intra-articular or intralesional glucocorticoids. В Due to slower absorption modest doses of intra-articular doses of triamcinolone acetonide have been regarded as less likely to cause CS than systemic administration of other glucocorticoids.В В Following an administration of a routine dose at a routine interval of triamcinolone our patient developed profound adrenal axis suppression and clinical CS. Conclusion: Intra-articular injections of even modest amounts of high potency steroids can cause iatrogenic CS.В We recommend careful monitoring of the adrenal axis in patients receiving these injections. suggestive that the tumor in both sides of the adrenals are APA not IHA. The good response to spironolactone strongly favors the diagnoses of APA. Unilateral adrenalectomy would not have corrected the problem and bilateral adrenalectomy would have increased morbidity. Abstract #112 IATROGENIC CUSHING’S SYNDROME FROM INTRA-ARTICULAR INJECTION OF TRIAMCINOLONE ACETOMIDE Michael Gardner, MD, Rebecca Kelly, MD, Richard Lugar, MD, David Gardner, MD Objective: To recognize intra-articular injection of high potency steroids as a potential cause of iatrogenic Cushing Syndrome (CS). Case Presentation: A 40 year old female was referred for a rapidly increasing Cushingoid appearance.В She had initially presented for follow up of low back pain about 6 weeks prior to referral and was noted to have thrush which was treated with nystatin.В A month later she had gained 32 pounds with a rounding of her face.В Also, Serum ACTH, 24 hour urine free cortisol, and 8am serum cortisol, were all below the limits of detection.В Upon presentation to our clinic, she was noted to have a round plethoric face, prominent supraclavicular/dorsocervical fat pads, mild proximal muscle weakness, centripetal obesity and purplish abdominal stria.В Repeat labs showed ACTH <2pg/mL (658pg/mL) and 8am cortisol of 0.7mcg/dL (6.7-22.6mcg/ dL).В В TSH, LH, FSH, and prolactin were normal.В A cosyntropin stimulation test (CST) (0.25mg IM) was performed. Baseline (10am) cortisol was 1 mcg/dL, ВЅ hour 5.4 mcg/dL and 1 hour 6.9 mcg/dL.В Iatrogenic and factitious CS were investigated.В Further discussion with the patient revealed injections of 40mg triamcinolone acetonide on two occasions, 7 and 4 weeks prior to referral, into the sacroiliac joints under fluoroscopic guidance.В Direct contact with all of the patient’s physicians confirmed that no other steroids had been administered within the last year.В В Urine spectroscopy for synthetic glucocorticoids (Mayo Medical Laboratory Rochester MN.) was performed 2 months following the last injection and showed the presence of only triamcinolone acetonide at a level of 0.17 mcg/dL with detection of no other synthetic glucocorticoids.В Followup CST 4 months after the last injection, showed normal baseline (7.2 mcg/dL) and stimulated cortisol levels (28.1 mcg/dL at 1 hour). В Baseline ACTH levels had also recovered to 5pg/ml. Abstract #113 FROM HEMATOLOGY TO ENDOCRINOLOGY: CUSHING’S SYNDROME PRESENTING AS PERSISTENT LEUCOCYTOSIS AND ADRENAL MASS Asma Sohail Khan, MD, and Uzma Khan Objective: To recognize the variability in the presentations of Cushing’s syndrome, including its effects on hematologic indices. Case Presentation: A 34 year old female presented to endocrinology service as a referral by the hematology service. One year prior to this she had presented to her PCP for new onset HTN, at which time routine blood work had shown leucocytosis. Her HTN was treated, no infection could be identified as a cause of her high WBC count and she was referred to the hematology service. Hematological workup was negative for any pathology, including JAK-2 mutation for polycythemia vera, BCR-ABL mutation for chronic myelogenous leukemia and a normal erythropoietin level. A CT scan of abdomen was done as part of her evaluation and revealed a 3.2 x 2 cm left adrenal mass with 35 HU on pre contrast phase images. On presentation she gave history of weight gain of 60 pounds in the last 2 years, but accelerated weight gain of 16 pounds in 2 weeks prior to presentation, swelling of legs, fatigue and easy bruising. Exam revealed a BP of 124/90, acne, bruising of skin and skin colored stretch marks. There was no buffalo hump or supraclavicular fat pad. Lab work revealed WBC count of 18.9 thousand/mm3, granulocyte count of 15.6, lymphocyte count of 2.20 and an eosinophil count of 0.90.We suspected Cushing’s syndrome. 24 hour urinary free cortisol (UFC) was 271.8mcg (normal <60), salivary cortisol at 11 pm on two occasions was > 0.55 mcg/dl (normal 0.05-0.17), –– ABSTRACTS – Adrenal Disorders rated very long chain fatty acids in this condition results in cerebral demyelination, peripheral nerve abnormalities, adrenocortical and testicular insufficiency. Our patient had adrenomyeloneuropathy which is the most common phenotype of X-ALD. В He had adrenocortical insufficiency which is a feature seen in В 90% of males with cerebral ALD and 70% of patients with AMN. Virtually all affected men have manifest or subclinical testicular insuffiency. Nonetheless, about 20% of the ALD patients remain free of overt neurologic disability and half of these have “Addison only” phenotype with isolated adrenocortical dysfunction. Several studies have disclosed that a possibly substantial percentage (4-63%) with Addison’s disease in fact may have “Addison only” phenotype of ALD as was seen with the initial presentation of our patient. В The risk for developing future neurological involvement remains high as described above, nonetheless, some of them may escape until much later in life. Conclusion: X- ALD is probably an under diagnosed disease and adrenocortical insufficiency may be the only or the initial manifestation. It is important to be aware of the relatively high incidence in so called idiopathic Addison’s disease and clinical presentation of variants of X -ALD as it is an inherited disease and may result in severe disability or death. ACTH was < 2pg/ml with serum cortisol of 20.7mcg/dl. Cushing’s syndrome of adrenal origin was diagnosed. В Patient underwent laparoscopic removal of the adrenal mass and is currently doing well on hydrocortisoneВ Discussion: Diagnosis of Cushing’s syndrome continues to be challenging. It becomes even more difficult when confronted with an unusual presentation. Exogenous glucocorticoids are known to cause leucocytosis, but very few cases of endogenous Cushing’s syndrome presenting with leucocytosis have been reported in the literature. Conclusion: This case is unique in that the patient’s initial presentation and workup was for leucocytosis. She lacked typical stigmata of Cushing’s syndrome initially. It has been postulated based on the lack of clinical cases, that, leucocytes and lymphocytes are less sensitive to endogenous over production of glucocorticoids. Only one case with high total WBC count in CS due to adrenal mass is reported in the literature. Further studies need to be done to assess whether CS of adrenal origin has a higher incidence of leucocytosis than Cushing’s disease. Abstract #114 ADDISON’S DISEASE ASSOCIATED WITH SPASTIC PARAPLEGIA : AN ADULT VARIANT OF X-LINKED ADRENOLEUKODYSTROPHY Abstract #115 Deepa Taneja, MBBS, Kim Green, Lisa Tannock, Dennis Karounos, and L.R. Reynolds SMALL CELL LUNG CANCER WITH SIADH AND ECTOPIC ACTH PRODUCTION TREATED WITH MITOTANE Objective: X-linked adrenoleukodystrophy (X-ALD) is an inherited disorder of peroxisomal metabolism that is characterized by accumulation of saturated very long chain fatty acids. A more indolent variant with adult onset is called adrenomyeloneuropathy (AMN).В In developed countries, where tuberculosis is not a common cause of adrenal insufficiency, 40% of male patients with Addison’s disease have in fact the biochemical defect of ALD. Case Presentation: A 41 year male was admitted with acute infection requiring high doses of glucocorticoids. He had been diagnosed with adrenal insufficiency at 20 year of age following episodes of lightheadedness, blurry vision and syncope. He also had a tanned skin that was initially attributed to excessive sun exposure. Later, he developed numbness accompanied with slowly progressive sensorimotor weakness in lower limbs. This was followed by sphincter disturbances and sexual dysfunction. He was finally diagnosed with adrenomyeloneuropathy nine years later. Discussion: X-ALD is a rare disease with a prevalence of 1 in 200,000 male births. Accumulation of satu- Tanyanan Tanawuttiwat, MD, Tasma Harindhanavudhi, MD, Raquel Marguerite AГ±el, MD, Tahira Yasmeen, MD, Dan Mihailescu, MD, and Ghassan Zalzaleh, MD Case Presentation: A 46-year-old woman with stage IV small cell lung cancer presented to the office with fatigue and lethargy.В On physical examination, she was hypertensive, cachetic, hyperpigmented, and hirsute.В Laboratory studies showed hypoosmolar hyponatremia with a serum Na of 115 mEq/L (normal, 135-145 mEq/L) and a calculated serum osmolality of 238.6 mOsm/Kg (normal, 275-300 mOsm/Kg).В Her blood urea nitrogen and creatinine were normal.В She was then admitted to the hospital.В A few days later, serum Na was still low at 131 mEq/L, serum osmolality was 274 mOsm/Kg and urine osmolality was high at 328 mOsm/Kg.В Given her euvolemic status, a diagnosis of syndrome of inappropriate antidiuretic hormone secretion (SIADH) was made and fluid restriction was initiated.В Her –– ABSTRACTS – Adrenal Disorders Eight years later patient presents with labs results suggest hyper secretion of the adrenal glands, ( Cushing’sВ Syndrome) also a CT scan of the adrenal glands revealed a plump medial limb of the left adrenal gland,В and an MRI of the pituitary showed a punctuate enhancement within the right aspect of the gland. The Patient also presents pigmented lesions on her left lower lip, lower eyelids, face, palms, back and buttocks. These findings were thought to be suggestive of Carney complex. By Family history patient’s mother had a history of myxomas, patient’s brother was diagnosed with Carney Complex, and patient’s daughter also has Cushing’s syndrome. On April 2007 another stroke like event, patient seeks help on the NIH again were she had bilateral adrenelectomy on June 2007.В Patient was hospitalize at St Luke’s Memorial Hospital in Ponce, Puerto Rico three months ago because of shortness of breath and chest pain, and all cardiac workup were negative. Discussion: Carney’s Syndrome is an autosomal dominant transmitted multisystem tumorous disorder characterized by myxomas (heart, skin, and breast), spotty skin pigmentations, endocrine tumors (adrenal, testicular, thyroid, and pituitary), and peripheral nerves tumors (schwannomas). Approximately 150 affected patients are known worldwide. Conclusion: This patient already had couple of the most prevalent clinical manifestation as spotty skin pigmentation, and Cushing syndrome.В Also her first CVA was caused by one the most serious components of the syndrome cardiac myxoma. serum Na eventually normalized. She had severe hypokalemia with serum potassium of 1.5 mEq/L (normal, 3.5-5 mEq/L).В Further evaluation revealed a markedly elevated morning serum cortisol of 122.5 Ојg/dL (normal, 6-23 Ојg/ dL), 24-hour urine free cortisol of 2703.8 Ојg/dL (normal, <45 Ојg/dL ), and random plasma ACTH level of 543 pg/dL (normal, 9-52 pg/dL).В Renin and aldosterone levels were normal.В She was diagnosed with Cushing’s syndrome from ectopic ACTH production.В She was started on ketoconazole 200 mg thrice daily for her hypercortisolism.В She initially had a good response but her morning serum cortisol increased to 70.7 Ојg/dL despite titration of ketoconazole to 400 mg thrice daily.В Aminoglutethimide was considered but was no longer available in the market.В Medical adrenalectomy was then induced with mitotane 500 mg every 12 hours.В Morning serum cortisol dramatically dropped to 24.9 Ојg/dL.В After a few weeks though, it increased to 118 Ојg/dLВ even after mitotane was increased to the maximum dose of 1000 mg every 12 hours.В Addition of metyrapone was considered but the patient decided to enroll in hospice and died soon after. Discussion: Two of the major endocrine paraneoplastic manifestations of SCLC are SIADH (5-10% of patients) and ectopic ACTH production (3-7%).В The concurrence of both is extremely rare with only six cases reported to date. Ketoconazole is used as medical therapy for Cushing’s syndrome.В It is effective and has a favorable side effect profile.В Mitotane is an adrenocorticolytic drug that is used to achieve medical adrenalectomy.В Conclusion: Our case report illustrates that although rare, concurrent SIADH and ectopic ACTH production from SCLC may happen.В If first-line therapy fails, consideration should be given to combination therapy with a first-line agent and mitotane. Abstract #117 DIRECT RENIN INHIBITOR (DRI) EFFECT ON GFR AND USE IN RENAL ARTERY STENOSIS SCREENING Abstract #116 CVA AS THE FIRST EVENT OF CARNEY’S SYNDROME Harold Thomas Pretorius, MD, PhD, Nichole Richards, and Michael Harrell Rafael Espinet, MD, and Luis Raul Ruiz Rivera, MD Objective: A new method using a nuclear camera and aВ direct renin inhibitor (DRI) to screen for renal artery stenosis (RAS) in hypertensive patients and to measure the otherwise generally DRIВ increased glomerular filtration rate (GFR). Methods: Same-day basal and 1 hr post 150-300 mg oral Aliskiren (Tekturna) renography used 10-25 mCi Tc99m-DTPAВ intravenousВ for split GFR with a nonlinear relation of renal activity to GFR corrected for body surface area.В Camera sensitivity was corrected using an attenu- Objective: This is a very rare syndrome and it helps me complement my medical knowledge to help patients improve her chance of survival and quality of life. Case presentation: This is a case report of a 45 year old Hispanic woman who had at the age of 33 years a cerebrovascular event. Emboli from a cardiac myxoma caused the CVA for which she underwent surgery. At that time the patient also had hyperpigmented freckles on her face and chest. – 10 – ABSTRACTS – Adrenal Disorders ation coefficientВ 0.12/cm, with lateral viewsВ for simple measure ofВ renal depth. Results: In 9 of 11 patients Tekturna increased GFR by 10% to 60% (p < 0.05).В Both patients with either split GFR increased insignificantlyВ by TekturnaВ had RAS at renal angiography and in one, BP stabilized after renal angioplasty.В The only Tekturna side effect was increased BP to 208/104 forВ < 2 hrs in one RAS case.В Decreased GFR expected in affected kidneys from a Goldblatt mechanism may occur with Tekturna; however, we also found RAS when GFR did not significantly increase as it does in normal kidneys, with or without concurrent renin angiotensin aldosterone system (RAAS) inhibition.В Inaccurate results typical of captopril renography with concurrent RAAS inhibitor therapy are avoided with Tekturna renography, which has been accurate in clinical follow-up, not only with concurrent angiotensin converting enzyme inhibitors or angiotensin receptor blockers, but also with thiazides and alpha or beta or calcium blockers. Discussion: Initial studies of DRI show potential for renal protection; however, the potential of captopril renography never materialized, not only due to technical aspectsВ ofВ earlierВ GFR calculations, but also because of severe and sometimes fatal side effects, especially in patients with RAS.В All RAAS inhibitors are contraindicated in pregnancy and may cause hyperkalemia, particularly in diabetics and with combined RAAS inhibitor use.В Nonetheless,В ifВ the present study results including straightforward, reproducible measure of split GFR, as well as only minor side effects are confirmed inВ further studies, thenВ DRI renography may be widely used in the future. Conclusion: Tekturna,В the firstВ widely available DRI, shows promise for nuclear camera based measure of split GFR in a same-dayВ basal and stimulated study, not only for its potential therapeuticВ increase in GFR; but moreover,В in diagnostic screening for the increasing number of patientsВ with RAS. Case Presentation: A 44 year old African American male presented with signs of chronic heart failure and symptoms of proximal muscle weakness, easy bruising, and poor wound healing for a prolonged period. He also gave a history of progressive swelling of his abdomen, weight gain, decreased libido, persistent fatigue and depression for over a year. He had no typical symptoms of a pheochromocytoma, no palpitations, syncopal episodes or diaphoresis. The diagnosis was confirmed by biochemical screening with elevatedВ 24 h Urinary free cortisol of 369.0Вµg/dl with morning ACTH level less than 5.0 pg/ml, a negative catecholamine screen, and a cortisol level that was not suppressed by high dose dexamethasoneВ suppression test. CT scan of his abdomen and pelvis showed multiple bilateral lobular adrenal masses causing diffuse enlargement of adrenal glands with benign appearance. Histopathological examination following a bilateral adrenalectomy revealed marked enlargement of both adrenal glands with macronodular hyperplasia. Discussion: AIMAH accounts only for less than 1% of all cases of Cushing syndrome and it is characterized by multiple yellow adrenal macronodules within hyperplastic internodular cortex.В Most cases are sporadic; few can be familial autosomal dominant transmission. It has typical histological findings and has been reported to exhibit aberrant expression of gastric inhibitory peptide, vasopressin, catecholamine, luteinizing hormone, Human Chorionic Gonadotropin, leptin and/ or 5-OH tryptamine receptors. Conclusion: Identification of aberrant adrenal receptors offers potential novel pharmacological therapy, but adrenalectomy remains the treatment of choice with preoperative medical therapy to lower cortisol levels in some cases. Cost restrictions limited our ability to perform receptors analysis. Abstract #119 PRIMARY ADRENAL LYMPHOMA Abstract #118 Rene J. Harper, MD, and Carlos Isales, MD ADRENOCORTICOTROPIC HORMONE INDEPENDENT MACRONODULAR ADRENAL HYPERPLASIA (AIMAH) Objective: We discuss a case of adrenal insufficiency and enlarging bilateral adrenal masses. Case presentation: A 60 y/o female presented with weakness, anorexia, nausea, vomiting, abdominal pain, and weight loss of 20 pounds. SheВ had beenВ hospitalized two months PTA for pneumonia requiring mechanical ventilation, and had experienced hypotension and bleeding from a Mallory-Wise tear requiring vasopressors and blood transfusion. During this previous hospitalization a random cortisol at 3:40 AM was 22 mcg/dL and peaked Claudine G Meyer, MD, Almond Drake III, MD, and Sylvester Odeke, MD Objective: To present a rare and often unrecognized cause of Cushing syndrome and review its pre-operative management. – 11 – ABSTRACTS – Adrenal Disorders at 18 mcg/dL sixty minutes after Cosyntropin. A CT scan at that time showed bilateral adrenal masses (right 3.6 x 2.5 cm and left 3.1 x 2.5 cm), extensive alveolar opacities, bilateral pleural effusions, subcentimeter lymphadenopathy in the paratracheal, retroperitoneal and paraaortic regions, and an enlarged spleen measuring 14.5 x 5 x 11 cm.В В She received IV steroids for adrenal insufficiency and was prescribed oral steroids on discharge. On admission she reported noncompliance with oral steroids. Her blood pressure ranged from 81-90 mmHg systolic and 44-60 mmHg diastolic with pulse readings of 80s-90s per minute. There were no palpable lymph nodes, hyperpigmentation, weakness or signs of dehydration. Her abdomen was diffusely tender with a palpable spleen; other physical exam was normal. A random cortisol at 9:00 AM was 3 mcg/dL and peaked at 2 mcg/dL sixty minutes after Cosyntropin. A CT scan now showed markedly enlarged adrenal masses with central necrosis (right 8.7 x 9.6 x 10 cm and left 7.2 x 4.5 x 8.4 cm), retroperitoneal lymphadenopathy (largest 2.2 cm) and multiple, small low-attenuation spleen lesions. She had negative PPD and HIV tests, normal tumor markers and 21-hydroxylase antibodies < 1 U/mL. Diffuse large B-cell lymphoma was confirmed by CT-guided biopsy of the left adrenal mass andВ a bone marrow biopsy did not show tumor involvement. She received 6 cycles of chemotherapy (R-CHOP). A CT scan done after the 4th chemotherapy cycle showed a remarkable decrease in size of the adrenal masses with very little residual tumor, and resolution of pulmonary nodules and effusions, and resolution of the lymphadenopathy and spleen lesions. A PET scan done after the 6th chemotherapy cycle showed no evidence of active lymphoma. Discussion: Primary adrenal lymphoma is a rare condition that often presents with adrenal insufficiency and bilateral adrenal masses but usually without peripheral adenopathy or bone marrow involvement. Prognosis is poor but remission may be achieved with chemotherapy. Conclusion: Primary adrenal lymphoma should be considered in the differential diagnosis of adrenal insufficiency with bilateral adrenal masses. Abstract #120 HUGE ABDOMINAL MASS WITH SPLITTING HEADACHES Marium Ilahi, MD, and Laura AG Armas, MD Objective: To identify signs and symptoms of pheochromocytomas in order to make a prompt diagnosis and initiate treatment. Case Presentation: A 46 yr old male with a history of palpitations presented to an academic endocrine clinic with a one year history of severe episodic headaches. These episodes mainly occurred at night and were associated with pallor, palpitations and nausea. They occurred more commonly when he slept on his right side. The headaches were so severe he was referred to a neurologist. The neurological workup, including head CT, was normal. During one of these episodes his wife measured his blood pressure at 200/90 mm HG, though all other documented blood pressures were normal. This was mentioned during follow-up with his cardiologist for aortic root dilatation. The cardiologist ordered a CT of the abdomen which showed a 14 cm left adrenal mass. A 24 hour urine for metanephrines was elevated at 1614 ug and midnight salivary cortisol, renin, aldosterone and 5-HIAA were all within the normal range. He was started on phenoxybenzamine and placed on a liberal salt diet and his beta-blocker was titrated accordingly. He was sent for surgery and the mass was removed with a maximum dimension of 18 cm and weight of 1450 grams. Pathology consisted of an encapsulated tumor with no vascular, nerve or capsular invasion. Gene testing for MENIN, RET oncogene and VHL were all negative. Discussion: Pheochromocytomas are rare catecholamine secreting tumors which usually present with headaches, sweating and tachycardia. In our patient it is interesting that the tumor was of such a large size and weight. The diagnosis of pheochromocytoma is often overlooked if the patient is sent to multiple specialists and all the classic symptoms are not presented simultaneously. Gene testing was ordered because of the tumor’s size, though all returned negative. Currently the patient is doing well and his headaches have resolved. Also repeat 24 hour urine analysis for fractionated metanephrines and catecholamines have been normal. – 12 – ABSTRACTS – Adrenal Disorders Conclusions: It is not necessary for a patient with pheochromocytoma to present with the classic symptoms of headaches, sweating and tachycardia or hypertension. This diagnosis may be overlooked in individuals who are referred to multiple specialists for a specific symptom. With the large size of the tumor it is likely that the pheochromocytoma was missed for a few years which allowed it to reach it’s final size. Pheochromocytomas may be present in hereditary syndromes which patients may need to be screened for. It is always important to analyze the big picture in order to pick up the correct diagnosis. Recent research has highlighted the role of vascular smooth muscle cell (VSMC) in hemostatsis. Increased intracellular calcium promotes VSMC contraction. Norepinephrine (NE) increases calcium within VSMC by phospholipase C pathway which activates myosin light chain kinase causing contraction. NE also activates Rho kinase, a calcium independent pathway mediating VSMC contraction. The complex interaction of catecholamines on VSMC most likely precipitated stroke in our patient. Selective involvement of cerebral vasculature with sparing of other vascular beds is secondary to differential distributon of endothelial products in different vascular beds. Conclusion: Medications that lower intracellular calcium – nimodipine, are antagonist to endothelin – clazosentan or inhibit Rho-kinase – fasudil hydrochloride, are available and may become standard of care to prevent thombotic injury in hyperadrenergic states. Abstract #121 STROKE IN PHEOCHROMOCYTOMAENDOTHELIAL AND VASCULAR SMOOTH MUSCLE CELL DYSFUNCTION Sudip Nanda, MBBS, Surya Prakash Bhatt, MD, John Pamula, MD, Santo Longo, MD, and Thompson H. Dale, MD Abstract #122 SEVERE IATROGENIC CUSHING’S SYNDROME AS A RESULT OF CHRONIC USE OF ANTI-RASH OINMENTS Objective: Pheochromocytomas cause CNS symptoms through varied mechanisms - uncontrolled hypertension causing intracranial hemorrhage, dilated cardiomyopathy with mural thrombus that embolizes, MEN 2 syndrome with metastasis, NF1 with CNS tumors, Von Hippel Lindau syndrome with hemangioblastomas, multiple cranial aneurysms, malignant thromboembolization from metastatic aortic arch involvement. A patient presented with thrombotic stroke in the absence of these known mechanisms and we propose a hypothesis for the same. Case presentation: A 37 year old female presented with right sided weakness. Her pulse was 52/minute and blood pressure was 130/60mm of Hg. She had motor aphasia with right hemiplegia. Head CT revealed dense left middle cerebral artery infarct. Hemoglobin was 13.4gm/ dL and hematocrit 40.6%. Metabolic panel was normal. Echocardiogram revealed normal valvular and ventricular function without mural thrombus. Carotid dopplers were normal. Hypercoagulable or vasculitic state and systemic malignancy were absent. Abdominal evaluation revealed bilateral pheochromocytomas with plasma normetanephrine 14,031pg/ml and metanephrine 23,136 pg/ml. Discussion: The patient had a stroke secondary to pheochromocytomas. Endothelium plays a central antithrombotic role through nitric oxide, prostacyclin and endothelins. Nitric oxide synthase1 and endothelin1 are preferentially distributed in the CNS. Edgar AvendaГ±o, MD, Ma Alejandra Ramos, Esperanza Valentin, Elva Cardenas, Francisco Gomez-Perez, and Juan Rull Objective: To present a case of severe iatrogenous CushingВґs syndrome due to an abuse of skin ointments. Case report: We present a female patient, who at consultation referred a 17 year history of skin problems that started after she underwent a c-section. After medical evaluation for a papuloeritematous rash in her legs and arms she was prescribed a cream bethametasone formulation with symptom relief. She referred that if she discontinued use of the cream, symptoms recurred so she continued to apply the medication every five minutes, using up to 30g every two days. Her family noticed that her weight increased progressively and her skin was red, they also noted she became isolated, stayed home, stopped working or doing chores around the house because she spent all her time applying the cream every 5 minutes. At consultation she weighed 2 128 pounds with a BMI 26 Kg/M , BP 180/110 Pulse 88xВґ. She was emotionally labile with a moon face, buffalo hump, violet striae in her abdomen, arms and legs. Her skin was red, thin with telangiectasias and presented a generalized scaly pustular dermatosis. Cushing’s syndrome, erythrodermia due to Candida albicans infection, and obsessive compulsive disorder were diagnosed; she was hospitalized for treatment and steroid weaning. At admission her serum – 13 – ABSTRACTS – Adrenal Disorders cortisol was 0.77ng/ml, Na 133 mmol/l, K 3.79 mmol/l, glucose 140 mg/dl, triglycerides 588 mg/dl and total cholesterol 422 mg/dl. She refused to discontinue cream use complaining of extreme irritation and itching so she was given a glycerine based cream and prednisone with dose reduction. Five months later her cortisol has risen to 7.56 ng/ml and is well controlled on NPH insulin. Discussion: We present a woman with a pshychiatric illness who developed Cushing’s syndrome due to chronic exposure to a steroid containing ointment. Her case is particularly interesting because of the prolonged exposure and intensity of her clinical manifestations. Conclusion: Extreme iatrogenous cushing’s syndrome can occur from the exposure to any form of steroids. Treatment of these patients is complex and it is important to convince the patient that continuing to use steroids will preclude a cure. – 14 – ABSTRACTS – Diabetes Mellitus Several reasons including genetic factors could explain these differences. Conclusion: Insulin resistance may not be related to hypertension in Nigerian type-2 diabetic patients. However, larger studies are required to define the relationship between blood pressure and insulin resistance in African populations. DIABETES MELLITUS Abstract #200 RELATIONSHIP BETWEEN ARTERIAL BLOOD PRESSURE AND INSULIN RESISTANCE IN TYPE 2 DIABETIC NIGERIANS. Abstract #201 Adamu Girei Bakari, MBBS, FWACP, and Geoffrey C. Onyemelukwe PROGNOSTIC INDICES OF DIABETES MELLITUS MORTALITY Objective: Cardiovascular disease especially hypertension is commoner among type-2 diabetic patients than the general population. Several reasons have been advanced to explain the higher prevalence of hypertension among type-2 diabetic subjects including the commonality of such risk factors as obesity and sedentary life styles in the aetiology of both conditions. Furthermore, it has been suggested that insulin resistance could be the unifying mechanism for these observations. However, racial factors seem to be important in the role of insulin resistance in the aetiology of cardiovascular disease. Although extensive literature has been generated on the possible role of insulin resistance in the aetiology and sustenance of hypertension among type-2 diabetic subjects else where, there is paucity of such data among Africans generally and Nigerians in particular. Methods: Blood Pressures were measured using standard methods while insulin resistance scores were derived using the homeostasis model assessment method. Results: Forty type-2 diabetic patients and 36 healthy control volunteers were studied. Of the diabetic patients, 13(32.5%) were hypertensive, and 27 (67.5%) were normotensive. The mean insulin resistance scores were respectively 1.96 +1.04 (range 0.49 - 2.92) among diabetic-hypertensive individuals and 2.28 + 1.89 (range 0.39 - 7.6) among normotensive-diabetic patients. The difference between the two groups were however not significant statistically (p = 0.5350). Furthermore, there is no significant relationship between mean arterial blood pressure and insulin resistance (r =+ 0.087, p>0.5) Discussion: The homeostasis model assessment method is cheap, simple, and relatively non-invasive and has been revalidated as a reliable method to assess insulin resistance in clinical practice. In this study there is no significant relationship between mean arterial blood pressure and the HOMA-IR score. This is contrary to observations in western societies where it has been observed that insulin resistance correlates with blood pressure and other cardiovascular risk factors. This observation is however consistent with earlier findings in blacks and Pima Indians. Anthonia Okeoghene Ogbera, MBBS, FMCP, FACE, and Chinenye Sonny Objective: To document the patterns of diabetes mellitus morbidity and mortality, length of hospital stay (LOS) and also to determine the prognostic factors affecting fatal outcomes of DM hospitalization. Methods: A study carried out for a one-year period (January –December 2006) in a tertiary hospital in SouthWest Nigeria. Subjects with diabetes mellitus (DM) were prospectively studied after admission to the medical wards to assess their short term outcome which was defined as death. This was facilitated by gleaning information at frequent intervals from the Wards’ Registers. Case fatality and crude death rates were computed and the prognostic factors for fatal outcomes were determined. The total mortality, causes of death, associated complications and duration of hospital stay were noted. Test statistics included chi test, logistic regression and Students t test. Results: A total of 1,327 subjects were admitted to the Medical wards for the duration of the study and DM related admissions made up 206 (15%) of these with a case fatality rate was 33 (16%)В . The commonest reasons for DM admission were hyperglycaemic emergencies (HE) -88 (40%) and hypertension 44 (21%). The commonest causes of deaths were hypertensive emergencies documented in 15 (46%) and DM foot ulcers (DFU) in 10 (30%) of the subjects. DFU and cerebrovascular disease (CVA) had the highest case fatality rates of 28% and 25% respectively. The mean (SD) and range of duration of LOS of DM admissions were 23(17) days. That for DFU - 51(27) days - was higher than that of DKA, CVA and hypertension admissions and this difference was statistically significant (p values of <0.05 ). DFU, CVD and having Type 2 DM rather than Type 1 DM were highly predictive of fatal outcomes. The odds ratio and 95% CI for these factors were 4.5 (1.5-12.7), 3.0 (0.9-9.92 and 2.1 (0.7-14) respectively. – 15 – ABSTRACTS – Diabetes Mellitus Discussion: An overwhelming majority (94%) of the DM related deaths occurred in those with Type 2 DM and having Type 2 DM had a prognostic impact on DM death. HE were found to be the commonest reasons for DM related admissions and deaths. DFU which was the second commonest cause of death had the highest case fatality rate. The dismal data on DFU outcomes are resultant effects of late presentation, erroneous traditional beliefs and high costs of treatment. The significance of DFU as contributory to a high disease burden is attested to by the findings of prolonged hospitalization. Conclusion: The unacceptable high burden of DM in this report is caused largely by factors that are potentially remediable. Patient education is key to reducing the adverse sequelae of DM. to be healthy enough to stand in lineВ from the early morning hours to receive services. Therefore, patients with significant health or mobility problems would likely not have attended the health fair. Conclusion: Despite the selection bias in our study, it is apparent that 18 months after Hurricane Katrina ravaged the city of New Orleans, the QOL of patients with diabetes remains suboptimal. Abstract #203 ELECTROCARDIOGRAPHIC ABNORMALITIES IN PERSONS WITH TYPE 2 DIABETES IN KADUNA, NORTHERN NIGERIA Fatima Bello-Sani, MBBS, FWACP, and Felicia Ohunene Anumah, MBBS, FNMCP Abstract #202 Objective: Diabetes mellitus is the commonest endocrine disorder in Nigeria. Type 2 Diabetes Mellitus (T2DM) is associated with increased cardiovascular risk, in part due to accelerated subclinical atherosclerosis primarily from dyslipidaemia. Ischaemic Heart Disease (IHD) is a very important chronic complication of diabetes mellitus the most prevalent among cardiovascular diseases and a major cause of morbidity and mortality. This study sets out to determine the most frequent electrocardiographic abnormalities in persons with T2DM in Kaduna (a sub-urban environment). Methods: 150 consecutive persons with T2DM & 150 controls were recruited from the diabetes clinic of ABUTH Kaduna for the study. Relevant history and physical examination findings were recorded in a protocol. The variables studied were: gender, age, smoking habit, physical activity, and waist circumference, and BMI, blood-pressure. Resting electrocardiogram was recorded and abnormalities grouped according to the classification: ST-Tsegment changes, left ventricular hypertrophy (LVH), conduction defects. Serum lipids were also compared. Results: The mean age of the diabetics & controls were not statistically significantly different (50.5В±9.9yrs vs. 51.1В±10.3yrs) respectively. 50% were females. Body mass index (BMI) and the waist circumference were statistically significantly higher in diabetics [(BMI 27.89В±1.78Kg/ M2,Wc 96В±10.2cm) than controls (BMI 24.22В±1.51Kg/ M2,Wc 86В±6.5cm) p<0.05]. 62% of diabetics were hypertensive. 20% of diabetics and 1.5% of control subjects in this study had electrocardiographic evidence of IHD, while 7% of diabetics had LVH respectively. 71% of persons with type 2 diabetes in this study had dyslipidaemia (p<0.05). Conclusion: The various resting 12 lead electrocardiographic findings among persons with type 2 diabetes in QUALITY OF LIFE IN DIABETES PATIENTS IN NEW ORLEANS: 18 MONTHS AFTER KATRINA Teck-Kim Khoo, MD, and Steven Smith, MD Objective: To evaluate the quality of life (QOL)В in diabetes patients in New Orleans. Methods: In August 2005, Hurricane Katrina pummeled southern Louisiana, causing total failure of infrastructure including healthcare. In 2007, the Mayo Clinic was invited to participate in the New Orleans Health Recovery Week, a free medical fair jointly organized by the city and nonprofit organizations.В Because of the high numbers of diabetes patients in the area, diabetology support was specifically requested. Our team included 2 diabetologists, joining 17 other volunteer physicians from across the country.В Patients were invited toВ completeВ the EuroQol EQ-5D Health State Questionnaire, a validated brief multiattribute, preference-based measure of health status. This was calculated into a utilities score of 1 (in best health) to -1 (worse than death). In addition, a Visual Analog Scale, with values from 0-100 was used. This was compared to a baseline population based score from Olmsted County, Minnesota. Results/Discussion: Amongst the patients seen by the two diabetologists, 162 patient surveys were completed, of which 7 were omitted from analysis because of incomplete answers. 155 patient surveys were used for analysis. The New Orleans population had a utilities score of 0.76, in comparison to Olmsted of 0.81 (p=0.004), while the VAS was 65 for New Orleans versus 73 (p<0.0001). Although there is a significant difference between the scores of both groups, the real difference is presumed greater as there is likely a selection bias in this study; patients surveyed had – 16 – ABSTRACTS – Diabetes Mellitus this study reflects non-specific features of cardiovascular diseases in general. The most frequent electrocardiographic abnormalities in type 2 diabetes in this study are ST-T segment depression, left ventricular hypertrophy. Ischaemic heart disease is emerging fast in developing poverty stricken environment like ours and should be routinely looked for. Hypercholesterolaemia and female gender are the strongest and most frequent factors associated with IHD. PGCP 0.9ng/ml or 0.32nmol/L) have been used, most studies conclude that there is a high degree of concordance, ranging between 86 and 89% between c- peptide levels and type of diabetes. BCP and PGCP particularly PGCP have also been found to predict the need for insulin treatment in T2DM (PGCP ≤1.8ng/ml).In this study, 2 of the study subjects clinically diagnosed with type 2 diabetes had PGCP <1ng/ml, and had a lean phenotype thus suggesting a possible misclassification. Further characterisation with antibody testing would have been beneficial in these patients. Ten of the subjects had PGCP values which suggest a need for insulin therapy. Conclusion: Post Glucagon C- peptide levels are useful in reclassifying subjects clinically defined as type 2 diabetes mellitus in Nigeria. Abstract #204 BASAL AND POSTGLCAGON C-PEPTIDE LEVELS IN NIGERIANS WITH TYPE 2 DIABETES MELLITUS Adekemi Olabisi Coker, MBBS, Olufemi Fasanmade, and Efedaye Ohwovoriole Abstract #205 PERFORMANCE OF AMERICAN DIABETES ASSOCIATION QUESTIONNAIRE AMONG NIGERIANS Objective: To study basal C- peptide (BCP) and post glucagon C- peptide (PGCP) levels in Nigerians with type 2 diabetes mellitus. Research Design and Methods: A total of 40 subjects with type 2 diabetes and 20 control subjects were recruited from the Lagos University Teaching Hospital. BCP and 6minute PGCP were determined in all subjects. Results: Mean В±SEM BCP of 2.0В±1.1ng/ml and 1.8В±0.7 ng/ml in controls and subjects with diabetes was comparable. Mean В±SEM post glucagon c- peptide (PGCP) and increment in c-peptide from basal was lower in subjects with diabetes compared with the control subjects (2.9 В± 0.22 versus 5.6 В± 0.5 and 1.1В± 0.2 versus 3.6В±0.32 respectively) p<0.05 and p<0.01. Among the subjects with diabetes, 2 had PGCP levels less than 1ng/ml and mean increment in c-peptide was 0.03 and –0.06 ng/ml while 10(25%) had PGCP < 1.8ng/ml. Discussion: Determination of fasting or basal c- peptide (BCP) and stimulated c-peptide (with glucose or glucagon) levels have been used to determine pancreatic ОІ- cell secretory activity. The c-peptide (CP) response to glucagon correlates well with the stimulated response to mixed meals or other stimulus commonly used to characterize endogenous insulin secretion and has the advantage of a shorter duration and simple standardization. Clinical utilities of c-peptide tests include determining whether pancreatic ОІcell function shows concordance with the clinical classification of diabetes into type 1 and type 2 diabetes. Although different thresholds for BCP (0.6ng/mLor 0.2nmol/L and Abdullah Ndaman Adamu, MBBS Objective: To evaluate the performance of American Diabetes Association Questionnaire among people with systemic hypertension in Nigeria. Methods: Between January and May 2004, screening for type 2 diabetes was conducted among people known to have systemic hypertension who were regular attendees of cardiology and nephrology clinic of Lagos University Teaching Hospital using American Diabetes Association Questionnaire (ADAQ). Oral glucose tolerance test was carried out on all the subjects as a gold standard to establish the diagnosis of diabetes. Result: A total of 207 patients were recruited and 131 of the subjects participated in the whole exercise, giving a participation rate of 63.28%. The subjects were classified into :- 0.7% No RiskВ (0-2), 29.00%High Risk (0-9) and 67.17% Diabetes (>10) based on ADAQ.ADAQ yielded a sensitivity of 100%, specificity of 71.96%, positive predictive value of 44.44% and negative predictive value of 100%. Conclusion: ADAQ performed relatively well among the high risk people with systemic hypertension. A little modification of it to suit racial and socioeconomic differences of people will go a long way in improving its performance for universal use to screen for diabetes. – 17 – ABSTRACTS – Diabetes Mellitus Abstract #206 Abstract #207 DIABETES AND AUTOIMMUNE THYROID DISEASE DIABETIC AND NON DIABETIC SALIVA ALPHA AMYLASE ACTIVITY INCREASED IN ACID MEDIA Aly Abdel Latif Abbassy, MD, FACE, Ibrahim Abdel Rahman, MD, Mohamed Kamal Ghetany, MD, Hazem Shokry, and Nahed Baddor Tarig Sayed Mustafa Arbab, MD, MSc, DIC Objective: To study pH changes during saliva alpha amylase activity in diabetic and non diabetic subjects in relation to glucose yielding. Explain mechanism of action and occurrence of DKA. Methods: 750 fresh saliva samples were collected from 200 diabetic and 50 non-diabetic subjects. All subjects were fasting over night for 12 hours. Glucose oxidase testing was used to detect amylase activity. Three identical 10 mls samples of fresh well-prepared saliva were accepted from each patient for the study. One sample from each subject was used as marker and tested for pH changes and sugar hourly for 24 hours. Each second and third study samples were tested initially for pH and sugar content; 1 ml of flour powder was added in each second sample (250 flour sample). 1 ml of sucrose was added in each third sample (250 sucrose samples). pH changes together with sugar readings were tested hourly in each study sample for 24 hours. Results: 750 (250 marker + 250 flour + 250 sucrose study sample) fresh saliva samples of non diabetics and diabetic patients showed pH of 9 to 7 on immediate testing. 250 marker samples showed no significant change in pH and zero sugar reading for 24 hours. 235 flour, 223 sucrose study samples showed decrease in pH 5 >, in association with glucose detection in samples. 2 flour and 2 sucrose samples showed decrease in pH from 9 to 7 in association with glucose yielding within 24 hours. 8 isolated flour, 11 isolated sucrose diabetic samples, 4 same patient flour and sucrose diabetes samples, 5 flour and 14 sucrose non diabetic samples showed decrease in pH 5 > without glucose yielding in 24 hours (absent amylase activity).В Zero non diabetic samples, same subject showed absent amylase activity for both flour and sucrose. Decrease in pH in study samples was noticed to be associated with increase in glucose yielding. 92% of study samples showed decreased pH 5 > in association with high glucose readings (250 – 500 mg/dl or more). Discussion: Significant but nonspecific elevations of amylase can be seen in DKA (Diabetes Care 26:3193-3194, 2003). Similarity between DKA and this study in terms of increased acidity in the presence of elevated serum amylase, and in association with high glucose from degradation of disaccharides / polysaccharides particles that could exist Objective: There is a well known strong association between type1 diabetes (T1D) and autoimmune thyroid diseases (AITD) but not between type2 diabetes (T2D) and AITD. Methods: To study the correlation between both types (type 1 and type 2) and autoimmune thyroid disorders; 80 diabetic patients (40 T1D “20 males and 20 females” and 40 T2D “20 males and 20 females”) and 20 control subjects were studied. All cases were subjected to history taking, clinical examination with a special emphasis on thyroid examination. Estimation of fasting plasma glucose, HbA1c, plasma C-peptide, GAD65 autoantibodies, antiinsulin antibodies(AIA), TPO antibodies, Anti-Tg, thyroid stimulating immunoglobulin(TSI), FT3, FT4 and TSH were done in addition, Ultrasound-guided fine needle aspiration biopsy to confirm or exclude the presence of thyroid pathology. Results: Revealed significantly elevated BMI, Cpeptide in T2D (confirming IR) than T1D and controls. Anti-GAD and AIA were only positive in T1D. TSH was significantly higher in T1D (50%) than T2D (15%), AntiTPO and Anti-TG were significantly lower in T2D than T1D. BMI was positively correlated with age, C-peptide. Anti-GAD and AIA were negatively correlated with Cpeptide. Anti-TPO and Anti-TG were positively correlated with TSH. HbA1c was positively correlated with rT3 but negatively correlated with T3. Atrophic and Hashimoto’s thyroiditis were only detected in T1D with positive AntiTPO and Anti- TG. Conclusions: Increased prevalence of AITD in T1D. Subclinical hypothyroidism is more common in T1D than T2D that may contribute to the high frequency of symptomatic hypoglycemia in these patients. Autoimmune thyroid antibodies are commonly present in patients with Anti-GAD antibodies. Anti-GAD and AIA are only positive in T1D confirming the role of autoimmunity in its pathogenesis. – 18 – ABSTRACTS – Diabetes Mellitus in slightly larger amounts in the blood of diabetic compared to non diabetic subjects (persorption phenomenon - Gerhard Volkheimer). Conclusion: Saliva alpha amylase activity should be determined in relation to pH media. Saliva alpha amylase is active in acid media. Correction of stomach pH and or abnormal amylase activity could help treat / prevent diabetes and obesity. Discussion: Our results show that the prevalence of vitamin D insufficiency in patients with diabetes seen in a tertiary referral center is extremely high (74.2%). More than half of the subjects in our series were clearly deficient, whereas only about one-fourth had levels considered optimal. Women, patients younger than age 50 years, and those with poorer glycemic control (HbA1c >7%) had somewhat lower levels of 25-OH vitamin D. Although the correlation with these factors was not statistically significant, it may have clinical importance in a selected population such as ours. Conclusion: Vitamin D deficiency is highly prevalent in patients with diabetes treated in a specialty Diabetes Center.В Possible etiologies should be investigated and therapy guidelines formulated for appropriate management. Abstract #208 ASSESSMENT OF VITAMIN D STATUS IN PATIENTS SEEN IN A SPECIALTY DIABETES UNIT Kanakasabai Narasimhan, MD, and Ali Rizvi, MD Abstract #209 Objective: To assess vitamin D status and analyze the presence and degree of vitamin D deficiency in patients with type 2 diabetes seen in a specialty diabetes unit. Methods: We collected data on 97 patients with type 2 diabetes seen in an ambulatory setting in the Diabetes Unit of an academic institution. The following parameters were collected over an 18-week period: serum calcium, serum creatinine, estimated glomerular filtration rate (eGFR), HbA1c, and 25-OH vitamin D. Patients who had advanced concomitant chronic disease or obvious malnutrition, stage 5 kidney disease, known vitamin D deficiency, osteoporosis, or derangements of calcium-parathyroid metabolism were excluded. Data was entered into a Microsoft Excel spreadsheet for analysis. Results: The study included 39 men and 58 women (63 Caucasian, 33 African American, and one Asian) with an average age of 55 years. The mean serum calcium was 9.46 mg/dl (reference range 8.6 to 10.2), mean serum creatinine was 1.06 mg/dl (reference range 0.5 to 1.3), average glycosylated hemoglobin (HbA1c) was 7.52%, and the majority (77/97, or 79%) had eGFR values greater than 60 ml/min. The average 25-OH vitamin D level was 23.3 ng/ ml, with the lowest being 7 and highest 68. The mean values were low in both men (24.4 ng/ml) and women (22.6 ng/ml). В Values were slightly lower in younger patients: thus, the mean 25-OH vitamin D level in patients <50 years (n=34) was 22.9 ng/ml, in patients aged 50-59 years (n=31) it was 25.8 ng/ml, and in persons ≥60 years (n=30), 23.5 ng/ ml. The mean 25-OH vitamin D was 24.3 ng/ml in patients with HbA1c ≤7% (n=44) and 22.54 ng/ml in those with HbA1c >7% (n=53). 49 patients (50.5%) had values of ≤20 ng/ml (“deficient”), the values in 23 patients (23.7%) fell in the 21 to 29 range (“relatively insufficient”), and only 25 patients (25.7%) had levels ≤30 (“sufficient”). AN ASSESSMENT OF LIMITED JOINT MOBILITY OF THE HAND IN BLACK AFRICANS WITH DIABETES MELLITUS AND NON DIABETICS Rosemary Temidayo Ikem, MD, Innocent Ikem, MD, Matthew Olaogun, and Bola Ola, MD Objective: Limited Joint Mobility (LJM) has been described in type 1 diabetic patients. Similar abnormalities are also frequently seen in adult diabetes mellitus (DM) patients. The purpose of this study is to further characterise LJM using quantitative goniometric measurements among type 2 diabetic patients. Methods: Seventy-six patients with type 2 diabetes and 63 normal controls (non DM subjects) matched for age and sex were purposively selected for this study. Visual clinical examination and quantitative goniometric assessment of DM and non DM controls were done. The LJM was graded using the criteria of Silverstein et al. Glyceamic control and proteinuria were also assessed. Results: Our study found a prevalence of 26.3% LJM among type 2 DM patients compared with normal controls with 4.8% LJM. Subjects with LJM within the control group were significantly older than those with LJM within the DM group (p<0.05). Prayer sign was present in 11.8% of DM patients compared with 4.8% of control. The flattening sign demonstrated by the inability to flatten their hands on a flat surface was found to be more in DM patients 10.5% compared 4.8% in the control group. Stage II LJM with 18.4% prevalence was the commonest followed by stage III (7.9%) among DM patients. In our patients, poor glyceamic control was found in 85%, using Fasting Plasma Glucose (FPG) and 70%, using 2hpp. – 19 – ABSTRACTS – Diabetes Mellitus Conclusion: We conclude that black Africans with type 2 DM only have moderately severe cases of LJM. Abstract #211 Abstract #210 ASYMPTOMATIC BACTERIURIA IN PATIENTS WITH DIABETES MELLITUS IN ILE-IFE, SOUTH-WEST NIGERIA QUALITY OF LIFE IN NIGERIANS WITH DIABETIC FOOT ULCER Rosemary Temidayo Ikem, MD, A O Aboderin, MD, Babatunde Odetoyinbo, and Babatope Kolawole, MD Rosemary Temidayo Ikem, MD, Innocent Ikem, MD, and Bola Ola, MD Objectives: To investigate the prevalence and associates of asymptomatic bacteriuria (ASB) in a sample of Nigerian diabetic patients. Method: This is a cross-sectional descriptive and analytic study of consecutive diabetic patients attending the diabetes clinic of the Obafemi Awolowo University Teaching Hospital (OAUTHC), Ile-Ife, South-West Nigeria. Patients were recruited from the Wesley Guild Hospital and Ife State Hospital, both units of OAUTHC, Ile-Ife, Nigeria. 135 diabetic patients and 57 non-diabetic patients (as control). Demographic parameters of participants were recorded.В Significant bacteriuria was determined for each of the mid-stream urine specimen obtained from all the subjects.В Organisms isolated were identified and evaluated for antibiotic susceptibility patterns. Results: There was a significant difference in the prevalence of ASB in the two groups.В Prevalence of ASB was 16% and 3.5% in the diabetic patients and control respectively (p=0.03).В Demographic parameters except age were not related to the presence of ASB.В ASB was found in 54.4% of diabetic patients with poor glycaemia control compared with 2.9% in diabetics with good glycaemia control (p=0.006).В Organisms associated with ASB were Staphylococcus aureus, Klebsiella sp, Escherichia coli and Enterococcus faecalis, however the most predominant was Staphylococcus aureus. These organisms were largely resistant to the common antibiotics tested such as cotrimoxazole and gentamicin but susceptible to nitrofurantoin Conclusions: The prevalence of ASB is high in diabetic patients and poor glucose control can be considered a predisposing factor. Objective: Diabetic foot ulcer (DFU) has a severe negative effect on health related quality of life of individuals with diabetes and existing knowledge about these factors in DFU patients is scarce in sub-Saharan Africa. The purpose of this study was to determine if there was a relationship between depression, Health Related Quality of Life (HRQoL) and cognitive functioning in Nigerian DFU patients. Methods: Thirty nine diabetic patients, including 21 with foot ulcers (focus group) and 18 without foot ulcer but having symptomatic peripheral neuropathy (control group) as measured by insensitivity to Semmes Weinstein 5.07 (10gm) monofilament, were studied in a cross-sectional setting. All subjects completed WHO Quality of Life Scale – Brief Version to assess HRQoL, Beck’s depression Inventory (BDI) to assess depression, and Modified Mini-Mental State Examination (mMMSE) for cognitive function. Discussion: Patients with DFU were significantly impaired in BDI score (p < 0.01) as well as in all domains of HRQoL. There was no evidence of cognitive impairment in these patients. Depression correlated with all domains of HRQoL in them. Conclusion: Patients with DFU are more likely to have poorer health related quality of life (HRQoL) than those without ulcers. Depression is one of the key factors in predicting the outcome of DFU. In DFU patients it adversely affects HRQoL. Further studies are warranted to investigate the impact of improved depression management on HRQoL in patients with DFU. – 20 – ABSTRACTS – Diabetes Mellitus NPH regimens. Discussion: Long acting insulin is generally avoided peri-operatively because of risk of hypoglycemia, but we observed that long acting analog glargine was better than NPH insulin in basal bolus regimens. However limitation of our study is that it is a single centre observational study. Conclusions: There is need of blinded multi centric studies to prove superiority of long acting insulin analog containing regimens in pre and post-operative glycemic control in T2DM patients undergoing major surgery. Abstract #212 GLYCEMIC CONTROL IN TYPE 2 DIABETES MELLITUS PATIENTS UNDERGOING MAJOR SURGERY: COMPARATIVE STUDY OF THREE S.C. INSULIN REGIMENS Sandeep Kumar Mathur, MBBS, MD, DM, Alka Bansal, MD, and Zaffer Yab Khan, MD Objective: Many different regimens of insulin and oral drugs have been suggested for metabolic control during major surgery, but pre-operative glucose control with subcutaneous insulin in semi-urgent situations is logical and well accepted. Among the several insulin regimens which is the best is not certain. Therefore we compared three s.c. insulin regimens in T2DM patients hospitalized for major surgery. Methods: 172 T2DM patients hospitalized for major surgery where it was decided to control hyperglycemia with s.c. insulin because of semi-urgent surgery/oral drug failure participated in the study. The study design was randomized comparative observational study. Preoperative glycemic control was achieved with one of the following regimens: 1. Pre-mix 30/70 insulin (R/N-0-R/N).В 2. R + NPH. Basal-bolus regular & NPH insulin (R-R-R/N).3. R + G. Basal-bolus regular & glargine (R-R-R-G). Insulin doses were adjusted to achieve fasting and post-meal glucose values respectively < 120 and < 180 mg/ dl. Intra-operatively they were treated with glucose –insulin – potassium solution. Post operatively same pre-operative insulin regimen was started. These regimens were compared for following parameters. (1) Time to achieve glycemic target (2) total daily insulin dose (3) incidence of hypo and severe hyperglycemia and (4) complications like renal, infection etc. (5) in hospital mortality. Results: R + G regimen was associated lesser dose of insulin (29.53 В± 9.83 vs. 35.67 В± 12.19 & 37.42 В± 13.5 units respectively for regimen 2 & 1 p <0.005), lesser time to achieve glycemic target (6.75 В± 3.25 vs. 7.37 В± 7.47 & 8.23 В± 6.04 days, p>0.05), lower incidence of hypoglycemia (10.53 vs. 14.81 & 30% p <0.02) and severe hyperglycemia (5.26 vs. 29.63 & 8.33% p <0.005). Incidence of infection (10.53 vs. 18.52 & 15% p >0.05), renal complications (10.53 vs. 11.11 & 15% p >0.05) and mortality (5.26 vs. 14.81 & 15% p > 0.05) were lower with this regimen, but the difference was not statistically significant. Pre-mix 30/70 and R + NPH regimens were comparable for most parameters but hypoglycemia and severe hyperglycemia were more frequent respectively pre-mix 30/70 and R + Abstract #213 THE UKPDS RISK ENGINE AS A USEFUL TOOL FOR CARDIOVASCULAR RISK ESTIMATION IN A MEXICAN POPULATION WITH TYPE 2 DIABETES MELLITUS Paloma Almeda Valdes, MD, Carlos Aguilar-Salinas, Daniel Cuevas-Ramos, Francisco Gomez-Perez, and Juan Rull-Rodrigo Objective: To estimate the utility of the UKPDS risk engine estimating discrimination, calibration, specificity and sensitivity of the model in a Mexican population with type 2 diabetes. Methods: Retrospective study of cases (patients with coronary heart disease or stroke) and controls (patients without them) with at least one year follow up, with all the variables required to calculate cardiovascular risk with the UKPDS risk engine. Results: Cardiovascular risk was estimated in 436 patients, 215 cases and 221 controls, 217 men and 219 women. The estimation was repeated when possible. 436 patients had 1 estimation, 433 had 2 estimations and 289 had 3 estimations. We did not find significant differences between estimations. Mean 10-year coronary risk was 31%. The estimated 10-year coronary risk was greater than 20% in 66.7% of the population. There were 260 cardiovascular events: 215 coronary heart disease events and 45 strokes.В 101 deaths were documented; in 52 (51.4%) coronary heart disease was the cause. The discrimination of the UKPDS model was 0.66 (IC 95% 0.59-0.72) and calibration was 23.8. The sensitivity for a 10-year estimated risk of 20% was 89% andВ specificity 36%. Discussion: Patients with type 2 diabetes have a 2 to 4 fold increased risk for developing cardiovascular disease. A high proportion of diabetics will develop a cardiovascular event during their life time. The increased cardiovascular morbidity and mortality is due to the coexistence of multiple risk factors: elevation of total and LDL choles– 21 – ABSTRACTS – Diabetes Mellitus terol, high blood pressure, hyperglycemia, smoking and low HDL cholesterol. ADA strongly recommends the individual assessment of cardiovascular risk using designed models. The usefulness of the UKPDS risk engine had not been evaluated in Mexican population until this study. Conclusions: The model had moderate discrimination and poor calibration in this Mexican population. The results are similar in other studies done in Europe. The UKPDS risk engine is a useful tool for estimation of cardiovascular risk in Mexican population with type 2 diabetes. improvement of insulin sensitivity in insulin resistant subjects. This rare case exhibits an unexpectedly improvement in glycemic control shortly after using TNF-О± inhibitor despite maintenance of the body weight and diet. A decline in HbA1c for 1%, 7 months after Enbrel injection along with significant decline in medication requirement for glycemic control in this patient strongly suggests the TNF-О± blockade impact on glucose metabolism. Conclusion: This index case emphasizes the importance of TNF-О± on management of diabetes type 2. Cautious should be advised to these patients when start on anti TNF-О± and physicians should be alerted for possible low blood glucose response. Abstract #214 SIGNIFICANT IMPROVEMENT IN DIABETES CONTROL AFTER ADMINISTRATION OF ENBREL Abstract #215 DIABETIC CARDIAC AUTONOMIC NEUROPATHY PROFILE OF WELL CONTROLLED TYPE 2 DIABETIC SUBJECTS WITHIN ONE YEAR OF DIAGNOSIS USING NON-INVASIVE PORTABLE ANSISCOPE Farnoosh Farrokhi, MD, and Nancy McBride, MD Objective: To describe a diabetic case with reduced medication requirement along with improved glycemic control after receiving Embrel injections for psoriasis. Case presentation: 59 years old white female with type 2 diabetesВ for 17 years returned to the clinic complaining low blood glucose levels and hypoglycemia symptoms after administration of Enbrel. She has been treated with twice-daily doses of Metformin 1000 mg, Glyburide 6 mg and Avandia 4 mg since 2005. In Feb. 2007 she was started on Enbrel injections 50 mcg 2 times a week for treatment of psoriasis. Her HbA1c and body mass index (BMI) were 7.9% and 30.99 kg/m2 at that time. She returned to the clinic in June 2007 stating that after few Enbrel injections she noticed hypoglycemia symptoms along with decline in self-measured blood sugars for which she discontinued the evening doses of all her diabetes medications. On that visit her Avandia was discontinued, also her HbA1c and BMI measured to be 7.5% and 29.7 kg/m2 respectively. Few weeks later, due to continuation of low blood sugar levels she decreased Glyburide to 3 mg/day. In Oct. 2007 her HbA1c was 6.9% without any change in the BMI. She denied any change in concomitant medications or diet. Discussion: Enbrel (Etanercept) is Tumor necrosis factor О± (TNF-О±) inhibitor used in treatment of chronic inflammatory diseases. TNF-О± is a proinflammatory cytokine involved in inflammatory and immune responses. Studies have shown that administration of this cytokine to culture cells or in vivo to animals impairs insulin action. Also in humans, acute infusion of TNF-О± has shown to inhibit the insulin stimulated glucose disposal leading to increase susceptibility to insulin resistance. There has been debate on the role of anti- TNF-О± medications and Ali Asghar Jawa, MD, MPH, Mumtaz Hasan, Jawad Zaheer, Muhammad Shahid Jamil, Tahir Rasool, Muhammad Abu Zafar, Syed Ali Imran, and Imteyaz Ahmad Objective: Diabetic Cardiac Autonomic Neuropathy (DCAN) is associated with high risk of cardiovascular morbidity and mortality. Portable ANSiscope is a relatively new device that non-invasively measures the parasympathetic/sympathetic nervous system imbalance in an office setting. The ANSiscope computes a percentage of dysautonomia from a recording of 571 RR intervals recordings for patients at rest in supine position. After analyzing, the ANSiscope generates an ANS index. Based on scoring described by Bellavere et al, five risk categories have been identified using the computed ANS Index. Subjects with ANS index <11%, 11-20%, 21-50%, 51-60 and 61-100% are classified into Healthy, Early, Late, Advanced and Most Advanced Diabetic Cardiac Autonomic neuropathy (DCAN) groups respectively. We investigated prevalence of DCAN amongst well controlled type 2 Diabetic subjects within one year of diagnosis. Methods: All type 2 diabetic subjects with HgbA1c < 7.0 and diagnosed with type 2 Diabetes Mellitus within the past 12 months were included in the study. Informed consent was obtained and subjects were asked to lay supine comfortably for at least 10 minutes before start of the study. EKG electrodes connected to the portable ANSiscope were placed on the chest wall and EKG tracings were recorded – 22 – ABSTRACTS – Diabetes Mellitus for 5 minutes. ANSiscope analyzed the data and calculated an ANS Index. Results: We studied 29 type 2 diabetes subjects, out of which 18 were female, with a mean duration of diabetes of В 9 months (1- 12), mean age of 51 years(30-73), mean BMI of 29 (20-42) and a mean hemoglobin A1c of 6.3% (5.3-7.0). Out of total 29 subjects, 10, 4, 11, 1, 3 subjects were categorized in Healthy, Early, Late, Advanced and Most Advanced Diabetic Autonomic Neuropathy Groups respectively. Conclusions: Our study clearly indicates that despite good glycemic control, almost 2/3 rd of recently diagnosed type 2 diabetes mellitus (T2DM) subjects have some level of diabetic cardiac autonomic neuropathy. This is alarming and further emphasizes the need for earlier diagnosis and aggressive treatment of type 2 diabetes mellitus. В This study also underscores the need for identifying other factors that contribute towards such high level of autonomic dysfunction in subjects with T2DM. We plan to investigate factors and interventions that may reverse or halt the progression of Diabetic Cardiac Autonomic Neuropathy. In future studies, weВ also plan to assess for any correlation between Diabetic Cardiac Autonomic Neuropathy and microalbuminuria and retinopathy. p=0.05 for significance.В Multivariable linear regression was then performed separately for T1 and T2 diabetics. Results: Charts of T1 and T2 diabetics age 18 or older were reviewed until 200 complete records were obtained. Exclusion criteria included dialysis and transplant patients. At least one missing glucose value was noted in 51 of the first 200 (25.5%) records examined.В Only two cases of glucose <60 mg/dl were documented. В T1 diabetic median preoperative glucose was 233 mg/dl (range 48-444 mg/dl) and median postoperative glucose was 156 mg/dl (range 93-380 mg/dl). T2 diabetic median preoperative glucose was 133 mg/dl (range 71-315 mg/dl) and median postoperative glucose was 155 mg/dl (range 55-318 mg/dl). Type of diabetes (p=0.004), insulin use (p=<0.0001), and oral medication use (p=0.002) were significantly related to glucose change while all other variables were not.В Regression analysis for T2 diabetics was significant only for insulin use (p=0.02) which decreased glucose change by 24.6 mg/ dl. No variables significantly predicted glucose change in T1 diabetics as the regression was confounded by 100% of all T1 diabetics being on insulin and none on oral medications. Discussion: Incomplete perioperative glucose records were found in 25.5% of the first 200 diabetics examined.В Perioperative glucose control in T2 diabetics was reasonable given no specific targets exist. The only predictor of glucose change in this group was insulin use. Glucose control in T1 diabetics was suboptimal preoperatively, and no predictors of glucose change were found for this group. Conclusion: Perioperative glucose management in our study was not optimal particularly in T1 diabetics. Our data support the need to develop diabetic perioperative glucose protocols to ensure proper glucose testing and to improve perioperative glucose control. Abstract #216 DIABETIC PERIOPERATIVE BLOOD GLUCOSE CONTROL: A COMPARISION OF BLOOD GLUCOSE MEASUREMENTS IN THE PREOPERATIVE AND POSTOPERATIVE SETTING Kelli Karches, MD, MPH, James McCallum, MD, and Nitasha Bakhru, MD Abstract #217 Objective: Hyperglycemia in the perioperative setting is associated with poor surgical outcomes, yet no specific targets for perioperative glucose management exist.В This study was designed to examine perioperative glucose control and variables that may influence it. Methods: A retrospective chart review using diagnosis codes identified 200 Type 1 (T1) and Type 2 (T2) diabetics who had a general anesthetic surgical procedure at Scripps Green Hospital between April-September 2006.В Variables examined were pre- and postoperative point of care blood glucose, type of diabetes mellitus, insulin, oral, or no medication use, age, gender, BMI, ethnicity, and postoperative hospitalization.В Univariate analysis using 2 sample Wilcoxon tests examined variables with respect to average glucose change (postop-preop) for each group using ACUTE CHOLECYSTITIS TEMPORALLY ASSOCIATED WITH INITIATION OF TREATMENT WITH EXENATIDE Sri Prakash L. Mokshagundam, MD, Suresh Lohano, and Vasdev Lohano Objective: В We report a patient with type 2 diabetes mellitus (T2DM) who presented with abdominal symptoms shortly after the initiation of exenatide (Byetta) therapy and was found to have acute cholecystitis requiring cholecystectomy. Case Presentation: A 51-year old South Asian lady with history of T2DM presented with symptoms of epi– 23 – ABSTRACTS – Diabetes Mellitus during the time frame. Other parameters examined in the present study included maternal age, delivery date, selfdeclared First Nation status, rural or urban residence and previous history of GDM. The data were analyzed using multivariate logistic regression models. Results: The prevalence of GDM during the 20 year period was 2.92%. Statistically significant increases in the prevalence of GDM were detected over the time, from 1.95% in 1985-86 to 3.72% in 2003-04 (p<0.01). The trend of increase in the prevalence of GDM in Manitoba sustained after modifications in the diagnostic criteria of GDM in the Canadian Diabetes Association Clinical Practice Guidelines. The prevalence of GDM was substantially higher in First Nation women (6.94%) than that in non-First Nation women (2.36%, p<0.01). The prevalence of GDM was higher in pregnant women living in rural regions (3.12%) compared to those in urban areas (2.70%, p<0.01). The prevalence of GDM in pregnant women who were ≥35 years old (5.92%) was greater than those <35 years of age (2.60%, p<0. 01). The prevalence of recurrent GDM in First Nations was 48.12% compared to 42.39% in non-First Nations pregnant women (p<0.01). Adjusted odds ratios (95% confidence interval) of GDM for First Nation status, advanced maternal age and previous history of GDM were 2.20 (2.00, 2.42), 2.38 (2.24, 2.54) and 25.09 (23.15, 27.19). The adjusted odds ratio for rural residence was 0.77 (0.74, 0.82), but had an interaction of 1.66 (1.48, 1.86) when associated with First Nation status. Conclusion: The results of the present study indicate that the prevalence of GDM increased in Manitoba during the 20 year time frame. First Nation status, advanced maternal age and a history of GDM are independent risk factors for GDM in Manitoba. Further research to determine the cause and consequence of the increase in prevalence of GDM is required (Supported by Canadian Institutes of Health Research and The Lawson Foundation). gastric pain, nausea and vomiting after a meal. Her past medical history was significant for T2Dm, hypertension, severe pancreatitis in 2003, vitamin D deficiency, and aspirin induced gastritis. She had been on metformin and pioglitazone for her diabetes mellitus and was started on Exenatide 5 micrograms bid, about 1 week before the episode. Physical examination was significant only for tenderness in the right upper abdominal quadrant. Liver function tests, creatinine, amylase and lipase were normal. Ultrasound of the abdomen showed mild distension of gall bladder with small amount of sludge. She underwent laparoscopic cholecystectomy the following day. Resected gall bladder showed acute and chronic cholecystitis with intramural abscesses. Discussion: Exenatide has been increasingly used in management of T2DM. A common side effect of the medication is abdominal discomfort, which is usually mild and often resolves over time. Recently, however, several reports of pancreatitis associated with the use of exenatide have prompted the FDA to issue warning about this potential effect. The mechanisms leading to pancreatitis are unclear. It is not known whether exenatide increases risk of cholelithiasis, which could lead to both pancreatitis and cholecystitis. Gall bladder disease is common in subjects with obesity and T2DM. However, the temporal relationship between the start of exenatide and the development of symptoms of gall bladder disease in our patient, raises possibility of a causative link. Conclusion: Clinicians using exenatide for the management of diabetes should carefully evaluate any significant abdominal symptoms and consider the possibility of gall bladder disease. В Abstract #218 GESTATIONAL DIABETES IN MANITOBA DURING A TWENTY YEAR PERIOD Abstract #219 Naji Jameel Aljohani, MD, Garry Shen, MD, Brenda Rempel, MD, Sora Ludwig, Margaret Morris, Kelly McQuillen, Mary Cheang, and Robert Murray PATTERN OF DIABETES IN NORTHERN NIGERIA Objective: Gestational diabetes mellitus (GDM) is associated with postnatal obesity and type 2 diabetes. We conducted a retrospective database study to determine the prevalence of GDM in the province of Manitoba in the years 1985-2004 and its relationship with advanced age, ethnicity, rural residence and history of GDM of pregnant women. Methods: Manitoba Health collected computerized data on 324,605 deliveries by 165,969 Manitoban women Adamu Girei Bakari, MBBS, FWACP, and Geoffrey C. Onyemelukwe Objective: Genetic and environmental factors are known to play significant roles in the pathogenesis and presentation of diabetes mellitus. The pattern of this disorder may therefore vary from one location to the other depending of genetic factors, other confounding disease conditions and peculiarities in life styles. This report describes the pattern of diabetes in the sahelian northern Nigeria. – 24 – ABSTRACTS – Diabetes Mellitus Methods: A 10 year prospective review of cases of diabetes mellitus seen in a Teaching hospital. Diabetes was diagnosed and classified using the WHO criteria. Results: A total of 747 patients with a male to female ratio of 2.38:1 were seen. Type 2 diabetes mellitus is the commonest form of the disorder occurring in 575 (77.0%) of patients. Type-1 diabetes occurred in 117 (5.7%), while 41(5.5%) of patients had secondary diabetes. Chronic Liver disease was the commonest cause of secondary diabetes mellitus in this population. Gestational diabetes was found in 14(6.5%burden of diabetes among the females in this series. Type 2 diabetes mellitus is the commonest form of the disorder encountered. On the other hand, chronic Liver disease was the commonest cause of secondary diabetes mellitus in this population. Discussion: As was the case in other studies in Nigeria, and globally, type 2 diabetes mellitus is the commonest form of diabetes mellitus in this study. Chronic liver disease was the commonest cause of secondary diabetes in this environment accounting for 36.6%of cases in the secondary diabetes group. This finding is noteworthy as hepatitis B viral infection is endemic in this region as evidenced by Hepatitis B surface antigen (HBsAg) rates. An HBsAg rate of 40% and 10% has been demonstrated in children under the age of 5 years and adults above 30 years of age respectively. The role of liver disease in increasing hepatic glucose output and insulin resistance culminating in glucose intolerance has been extensively discussed. Further studies on the probable role of hepatitis B Viral infection in the aetiology of diabetes mellitus are required especially in HBsAg endemic areas Conclusion: Liver disease is a significant cause of secondary diabetes in this environment. Background: Vitamin B12 deficiency causes peripheral neuropathy in subjects with type 2 diabetes mellitus. Vitamin B12 deficiency can occur either due to nutritional deficiency or due to lack of intrinsic factor and subsequent vitamin B12 malabsorption in pernicious anemia. Additionally, Metformin use in type 2 diabetic subjects has been associated with nutritional deficiency. In order to ascertain the type of vitamin B12 deficiency, performing a Schilling test has been the standard of care. However, Schilling test is a cumbersome and relatively expensive procedure. We decided to test a different approach. All subjects with biochemically proven Vitamin B12 deficiency would be supplemented orally with methylated Cyanocobalamin, chemically known as Mecobalamin. Mecobalamin is the activated form of Vitamin B12 and is absorbed more efficiently. Subjects would receive 1500 Microgram of Mecobalamin per day orally for 3 months followed by repeat Vitamin B12 levels measurement. Those subjects who would remain deficient in Vitamin B12 will be offered 7 injections of intramuscular supplementation of Mecobalamin given every other day for 14 days. Vitamin B12 levels would be measured again after three months of receiving intramuscular supplementation with Mecobalamin. Those subjects who will correct their Vitamin B12 deficiency by oral supplementation alone will be labeled as having nutritional Vitamin b12 deficiency. Those who require intramuscular injections in order to correct the deficit will be presumed to have pernicious anemia. Methods: After obtaining informed consent, we measured vitamin B12 levels in 44 subjects with type 2 diabetes mellitus not taking metformin. 23/44(52%) subjects with type 2 diabetes mellitus had normal vitamin B12 level and 21/44 (48%) subjects had low vitamin B12 level defined as Vitamin B12 levels less than < 200 MCG/dL. 10/21 vitamin B12 deficient subjects with type 2 diabetes mellitus decided not to participate in the intervention phase and 1 subject expired due to unrelated medical condition. 10/21 subjects with type 2 diabetes mellitus agreed for oral mecobalamin therapy for 3 months followed by measurement of vitamin B12 levels. If they persistently had low vitamin B12 levels after 3 months, they would be treated with intramuscular injection of mecobalamin and Vitamin B12 levels measured after 3 months of first injection. Results: 10/10 subjects with type 2 diabetes mellitus and a mean age of 50 years (35-65) completed the study. All subjects normalized their vitamin B12 level (> 200 MCG/dL) 3 months after initiation of oral mecobalamin therapy. Hence none of these subjects needed to be treated with intramuscular mecobalamin therapy. Abstract #220 VITAMIN B12 DEFICIENCY IS COMMON IN SUBJECTS WITH TYPE 2 DIABETES MELLITUS NOT TAKING METFORMIN AND IS NUTRITIONAL IN NATURE Ali Asghar Jawa, MD, MPH, Mumtaz Hasan, Muhammad Shahid Jamil, Jawad Zaheer, MD Syed Ali Imran, Ghazanfar Jawa, and Umair Javaid Chaudhary, MD Objective: To assess frequency of vitamin B12 in subjects with type 2 diabetes mellitus. Additionally, we decided to investigate whether the vitamin B12 deficiency was due to nutritional deficiency or due to malabsorption of Vitamin B12 in pernicious anemia. – 25 – ABSTRACTS – Diabetes Mellitus Conclusions: Our study clearly shows that almost half of T2DM subjects not taking metformin have Vitamin B12 deficiency. 1/4th of these subjects have vitamin B12 deficiency that is readily correctable with oral supplementation alone. This is a novel finding and stresses the need for aggressive and early diagnosis and treatment to avoid neurological complications of Vitamin B12 deficiency. Also, it would not be unreasonable to empirically treat type 2 diabetes subjects with signs and symptoms of peripheral neuropathy with 3 months of oral supplementation with Vitamin B12 or its activated form, Mecobalamin.В respiratory alkalosis which occurs in pregnancy. Fetal IQ and incidence of fetal congenital heart defects have been inversely related to Гџ hydroxybutyrate and FFA levels. Fetal loss in DKA is caused by decreased uteroplacental blood flow due to osmotic diuresis leading to volume depletion. Maternal hypokalemia can lead to fetal hypokalemia leading to myocardial suppression and arrhythmia. Maternal hypophosphatemia can cause decrease in 2, 3-DPG leading to impaired delivery of O2 to fetus. Fetal hyperinsulinemia due to maternal hyperglycemia can cause increase in O2 requirement by stimulating the metabolic pathway. Conclusion: This case illustrates the need to consider euglycemic DKA in pregnancy and the deleterious effects of uncontrolled DM and DKA on the fetus. Abstract #221 “EUGLYCEMIC” DKA IN PREGNANCY AND ITS EFFECTS ON FETUS Abstract #222 Veena Watwe, MBBS, and Hamdee Attallah, MD ADDITION OF COLESEVELAM HCL IMPROVES GLYCEMIC CONTROL IN PATIENTS WITH POORLY-CONTROLLED TYPE 2 DIABETES MELLITUS WITH SULFONYLUREA-BASED THERAPY: A POOLED ANALYSIS Objective: To describe a case of euglycemic DKA in type 1 DM and effects of uncontrolled DM on the fetus. Case: A pregnant 26-yr-old African American woman with longstanding type 1 DM presented at 30 wks gestation with frequent nausea and vomiting. В She has had multiple DKA admissions due to noncompliance with insulin since the first trimester. On admission, fingerstick glucoses were 132-150 mg/dl and ketoacidosis was confirmed by the presence of a serum bicarbonate 7, anion gap 21, and ++ ketones in the serum and urine.В No identifiable precipitating factors for DKA were identified, and the acidosis resolved completely with reinstitution of insulin. Diabetes-associated complications included overt nephrotic syndrome noted since the first trimester, pregestational uncontrolled hypertension and longstanding retinopathy. At presentation, BP = 170/80, RR = 30 and Kussmaul respiration was present. Other findings included generalized edema with 3-4+ pitting the lower extremities. At 32 5/7 weeks, a 1.3 kg male infant was delivered by cesarian section with abdominal situs inversus and congenital hypoplastic left heart syndrome. The baby died at 1 month of age. Discussion: DKA has been associated with a fetal loss rate of 9 %, and most DKA episodes occur in second and third trimester and often despite relatively lower glucose concentrations. “Euglycemic” DKA, in which diabetic ketoacidosis appears when glucoses are below 180 mg/dl, has been described in the literature. Factors contributing to increased risk of DKA in pregnancy are increasing insulin resistance due to increase in hormones like HPL, cortisol and prolactin, decreased GI motility with increased absorption of carbohydrates, accelerated starvation as the fetus and placenta use up large stores of glucose, lower buffering capacity with bicarbonate ions due to compensation of the Vivian Andrew Fonseca, MD, FACE, Allison B. Goldfine, MD, Kenneth E. Truitt, MD, and Michael R. Jones, PhD Objective: Colesevelam HCl (COL) is a bile acid sequestrant with a new additional indication as an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus (T2DM). The glucose-lowering efficacy of COL in patients (pts) with poorly controlled T2DM (A1C 7.5%-9.5%) was evaluated in 3 randomized, double-blind studies in which COL was added to metformin (26 wks), insulin (16 wks), or sulfonylurea (SU)-based therapy (26 wks), respectively, as monotherapy or in combination with other antidiabetic agents. Each of the primary studies demonstrated a significant reduction in mean A1C with COL vs placebo (PL) by study end (-0.54%,В -0.50%, -0.54%, respectively; P<0.001 for all). Here we report the results of a pooled analysis of the efficacy data for all pts who received SU in the 3 primary studies. Methods: A total of 653 pts on SU-based therapy (alone or combined with other oral antidiabetic agents) were randomized in the primary studies to add-on therapy with COL 3.75 g/day (n=326) or PL (n=327). Efficacy endpoints included change from baseline to study end in A1C and fasting plasma glucose (FPG). In addition, the proportion of pts who achieved a reduction in A1C≥0.7% or a reduction in FPG≥30 mg/dL from baseline to study end was evaluated. – 26 – ABSTRACTS – Diabetes Mellitus Results: Compared with PL, COL added to SU therapy resulted in significant reductions in mean A1C and FPG by study end. The mean change from baseline in A1C was -0.35% in the COL group (mean baseline A1C 8.2%) vs +0.18% in the PL group (mean baseline A1C 8.3%), resulting in a treatment difference of -0.53% by study end (P<0.001). The mean change from baseline in FPG with COL was -1.4 mg/dL (mean baseline FPG 174.1 mg/dL) vs +12.2 mg/dL with PL (mean baseline FPG 172.4 mg/ dL), resulting in a treatment difference of -13.6 mg/dL at study end (P=0.001). In addition, significantly more pts in the COL group achieved a reduction in A1C≥0.7% (35.0% vs 16.5%; P<0.001) or FPG≥30 mg/dL (29.1% vs 21.7%; P=0.029) from baseline to endpoint vs the PL group. Conclusion: The addition of COL in pts with T2DM inadequately controlled with SU-based therapy significantly improved glycemic control. Several mechanisms have been proposed for the glucose-lowering effect of COL, including reductions in glucose absorption and effects on glucose metabolism via nuclear receptors in the intestine and/or liver. The exact mechanism(s) remains to be confirmed. obesity (27% were overweight and >65% were obese).В Overweight or obese T2DM respondents were significantly less likely to report excellent health (31% and 18%, respectively), compared with overweight or obese HR respondents (42% and 30%, respectively), p<0.001.В There were no differences between T2DM and HR groups overall for вЂ�contemplating exercising’ and вЂ�exercising regularly’ but more obese respondents in the T2DM and HR groups were вЂ�contemplating exercising’ (20.4% and 20.8%, respectively), and fewer obese respondents were currently вЂ�exercising regularly’ (21.4% and 23.3%) В than the overweight (9%-13% contemplating and 33%-34% exercising regularly) and normal weight (8%-9% contemplating and 38%-40% exercising regularly) groups, p<0.001 for each.В More obese respondents in both the T2DM and HR groups attempted weight management (83% and 78%, respectively) than normal or overweight respondents (28%-61%), p<0.001.В However, a larger proportion of obese T2DM respondents tried to lose (82.7%) or maintain weight (82.2%), compared with obese HR respondents (78.4% and 77.6%, respectively), p<0.001. Conclusions: Differences in attitudes and behaviors for exercise and weight management within T2DM and HR groups were largely associated with differences in BMI category.В Obesity had a negative impact on current health, on the likelihood of exercising regularly, and on weight management for those with or at risk for diabetes. Abstract #223 INFLUENCE OF OBESITY ON HEALTH ATTITUDES AND BEHAVIORS AMONG INDIVIDUALS WITH OR AT RISK FOR TYPE 2 DIABETES MELLITUS Abstract #224 AN OBSERVATIONAL STUDY OF THE GLYCEMIC CONTROL IN HOSPITALIZED PATIENTS ON ARTIFICIAL ENTERAL FEEDING Helena W. Rodbard, MD, FACP, MACE, James R. Gavin III, Kathleen M Fox, and Susan Grandy Objective: This investigation evaluated the role of obesity in health attitudes and behaviors for weight management and exercise among individuals with type 2 diabetes mellitus (T2DM) and those at high risk for T2DM. Methods: Self-reported attitudes toward health, exercise behaviors, and weight management were assessed in the US longitudinal SHIELD study from the mailed 2004 survey for respondents with T2DM or high risk (HR) for diabetes defined as >3 of the following: abdominal obesity, 2 body mass index >28 kg/m (BMI), self-reported diagnosis of dyslipidemia, hypertension, or history of cardiovascular disease.В Respondents were stratified into 3 categories 2 of BMI (kg/m ): <25 (under/normal weight), 25.0-29.9 (overweight), and >30 (obese).В Comparisons across BMI groups were made using analysis of variance; comparisons between T2DM and HR were made using chi-square tests. Results: T2DM (n=3917) and HR (n=5465) were similar for age (mean=59 years), race (>85% white), and Fadi Adel Nabhan, MD, Norma Lopez, MD, Alexandra Reiher, MD, James Sincaroe, Nicholas Emanuele, and Mary Ann Emanuele Objective: This study is aimed at evaluating the prevalence of adequate glycemic control in hospitalized patients on artificial enteral tube feeding (TF) and appropriate insulin management in these patients Methods: This is an observational study on hospitalized patients at Loyola University Medical Center.В We included patients who were on TF for at least 8 continuous hours/day.В Medical records were reviewed on 5 random days to assess the blood glucose (BG) measurements of all eligible patients. В Some patients were represented on more than one day, so we utilized the concept of a patientday, defined as a 24-hour period where a given patient’s glucose measurements were evaluated. В Glycemic control – 27 – ABSTRACTS – Diabetes Mellitus was considered optimal if BG was 70-180 mg/dL.В Primary outcome was the percentage of BG measurements between 70 and 180 mg/dL. Result: Seventy-three eligible patients, resulting in 108 patient-days, were studied.В В Thirty-four patient-days were on intravenous insulin drips, 17 were on insulin glargine and the remaining 57 patient-days were either on no insulin or insulin as needed.В Overall, the mean percentage of BG measurements recorded at target, >180 mg/dL and <70 mg/dl were 83.9%, 14.1% and 1.5% respectively. В Those with a history of DM were less likely to have BG measurements at target (p<0.002) and more likely to be hyperglycemic (p<0.014) than those without a prior history of DM. While on intravenous insulin, 91.3% of BG measurements were at target compared to 54.1% on subcutaneous insulin glargine (p<0.001).В В Among patients receiving insulin glargine, those with renal failure were less likely to achieve BG measurements at target than those with normal renal function (p<0.006) and more likely to be hyperglycemic (p<0.015).В The use of glucocorticoids and mechanical ventilation were not correlated with the achievement of target glycemic control.В Mean percentage of BG measurements at target in patient-days on no insulin or insulin only as needed was 88.4% suggesting their lack of need for insulin.В В В В Discussion: Our data revealed that the overall prevalence of optimal glycemic control in hospitalized patients receiving TF was high. However, this was mainly noted in those who were on intravenous insulin drips or those whose hyperglycemia was so mild that they either did not require insulin or were only treated with minimal insulin as needed.В В Patients who required insulin more consistently but were on subcutaneous insulin glargine achieved less optimal glycemic control.В В Since the use of insulin by intravenous drips may not be practical outside of intensive care units, more studies to determine the optimal mode(s) of subcutaneous insulin deliver are warranted.В В Our study also showed that a previous history of DM or renal failure were associated with achieving less optimal glycemic control. Conclusion: Prevalence of optimal glycemic control in patients on artificial enteral feeding in our entire study cohort was high at 83.9%, and was better in those without an antecedent history of diabetes and with normal renal function. The use of continuous intravenous insulin administration was superior to subcutaneous insulin glargine. Abstract #225 CONTINUOUS GLUCOSE MONITORING SYSTEM AS AN INDICATOR OF GRAFT DYSFUNCTION IN ISLET TRANSPLANTATION Lisa Gorn, DO, Raquel N. Faradji, MD, Shari Messinger, PhD, Kathy Monroy MD, David A. Baidal MD, Tatiana Froud MD, Camillo Ricordi MD, and Rodolfo Alejandro MD Objective: To evaluate the effects of islet transplant (ITx) on glycemic control via the continuous glucose monitoring system (CGMS) and its utility as an indicator of graft dysfunction (GD). Methods: Glycemic control was assessed in 25 subjects with type 1 diabetes:12В underwent ITx and 13 were controls. Weight, BMI, insulin use, HbA1C, 90min glucose after a mixed meal tolerance test, and fasting C-peptide/ glucose ratio (CPGR)В were followed.В Mean interstitial glucose (MG), standard deviation (SD), glucose variability (GV), and percent time in hyperglycemia (%GT>140 mg/dl), hypoglycemia (%GT <54 mg/dl), and normoglycemia (%GT 54-140 mg/dl) were measured in 72 hr periods from CGMS in the controls at baseline and ITx group at 3,6,9,12,15, and 18 months after ITx, and analyzed as indicators of GD.В Linear mixed model regression assessedВ if CGMS findings at the time of GD were significantly different than those at preceding timepoints. Results: MG andВ GV were significantly lower in the ITx group at all times except 3 and 15 months.В Compared to controls, percent time in hypoglycemia was significantly lower in the ITx group at all times.В There was no association between insulin use and time in hypoglycemia in the ITx group.В Time in normoglycemia wasВ increased in the ITx group at all times except 15 months. Decreased time in hyperglycemia was significant at 6,9,12, and 18 months in the ITx group. HbA1C, 90min glucose, and CPGRВ were significantly improved at all times after ITx. MG, SD, GV, and %GT>140 mg/dl were indicators of GD, and increased by 19.4 mg/dl,15.1 mg/dl,19.8 mg/dl, and 19.4% respectively when GD occurred compared to preceding timepoints. Discussion: CGMS is an indicator of GD with changes in patterns of glycemia found within 3 months of GD.В Use of real time CGMS should be considered for earlierВ detection andВ prediction of GD. – 28 – ABSTRACTS – Diabetes Mellitus glycemic control (1,5-AG was recently included in the new International Diabetes Federation guideline for management of postmeal glucose as an emerging technology to measure PPG).В Data from this retrospective analysis indicate that 1,5-AG revealed underlying treatment effects on postprandial glucose control which were not readily apparent by A1C measurements, confirming the role of 1,5-AG as a PPG marker. Conclusion: 1,5-AG may be a useful complement to A1C to reflect PPG in diabetic patients treated with agents that target PPG. Conclusions: Benefits up to 18 months post-ITx were apparent, regardless of insulin independence, including decrease in hypoglycemia, maintenance of glucose stability, and increase in normoglycemia. MG, SD, GV, and %GT>140mg/dl were indicators of GD. Abstract #226 THE USE OF 1,5-ANHYDROGLUCITOL (GLYCOMARK) TO MONITOR NEW CLASSES OF THERAPIES FOR MANAGING POSTMEAL GLUCOSE IN PATIENTS WITH DIABETES Abstract #227 Steven Wittlin, MD, Hirotaka Ishibashi, MS, Eric Button, MS, MBA, Scott Foster, PhD, Toshikazu Yamanouchi, MD, and Antonio Ceriello, MD LONG TERM INSULIN INDEPENDENCE AND IMPROVEMENT OF FIRST PHASE INSULIN RELEASE AFTER SUPPLEMENTAL ISLET INFUSION UNDER EXENATIDE TREATMENT IN SUBJECTS WITH ISLET GRAFT DYSFUNCTION Objective: To evaluate the use of 1,5-anhydroglucitol (1,5-AG) to monitor new therapies for PPG. Methods: Retrospective analysis of clinical drug studies utilizing 1,5-AG. Results: 1,5-AG has recently been used in clinical studies with several new classes of therapies for managing postmeal glucose (amylin analogs, glucagons-like peptide-1 [GLP-1] derivatives. dipeptidyl peptidase-4 [DPP4] inhibitors, alpha-glucosidase inhibitors). In the case of sitagliptin phosphate, a DPP-4 inhibitor, 1,5-AG increased by 4.45 ug/ml in the sitagliptin group (n=75) compared with a decrease of 0.33 ug/ml in the placebo (n=76), for a between-treatment group difference in 1,5-AG of 4.78 ug/ ml (95% CI: 3.76, 5.80; p<0.001) over a 12-week period and consistent with improvement in PPG control.В In a study with miglitol, an alpha-glucosidase inhibitor, comparing a placebo group (n=84) to a miglitol-treated group (n=158) over 12 weeks,1,5-AG mean levels did not change significantly from baseline (4.62 ug/ml) to study end in the placebo group.В In the miglitol-treated group, 1,5-AG increased from 4.79 ug/ml to 10.46 ug/ml from baseline to study end, consistent with changes in PPG control.В After 4 weeks, the mean 1,5-AG was 9.15 (p<0.001 compared to baseline levels).В Discussion: A1C measurement is a critical component of diabetes management; however, a key limitation of A1C as a measure of glycemia is the lack of timeliness -- it does not detect underlying blood glucose excursion levels in moderately controlled diabetic patients (A1C < 8) as it is a measurement of mean glucose levels over the longerterm.В In contrast, the 1,5-anhydroglucitol (1,5-AG) assay responds rapidly and sensitively to serum glucose levels above the renal threshold and has been demonstrated as a valid marker of postprandial hyperglycemia and short-term Raquel NoemГ Faradji, MD, Thipaporn Tharavanij, Tatiana Froud, Shari Messinger, Kathy Monroy, Antonello Pileggi, David A. Baidal, Davide Mineo, Cristiane Leitao, Pablo Cure, Aleida Saenz, Andrea Curry, Gennaro Selvaggi, Camillo Ricordi, and Rodolfo Alejandro Objective: To assess the effects of Exenatide (EXN) on supplemental islet infusions (SI). Methods: SI was performed in 9 subjects with graft dysfunction after previous islet transplantation under Edmonton-like protocol. Five underwent SI in 2003 without exenatide (SI-C group) and four received SI under EXN in 2006 (SI-EXN group). Clinical and metabolic profiles were assessed every 3 months up to 18 months. The analysis was done by 2-way ANOVA and t-test. Results: The SI-EXN group had been on this drug for median time of 171 days (range 155-197) pre-SI without achieving insulin independence (IND). Both groups had similar baseline characteristics except duration of graft dysfunction before SI which was longer in SI-EXN group (664В±83 vs 326В±93, p=0.03). The SI-C and SI-EXN groups received a mean of 8713В±4714 and 5613В±970 IEQ/ kg, respectively (NS). Only 3/5 of SI-C patients achieved IND for 303, 403 and >1670 days after SI. All subjects in the SI-EXN group achieved IND for more than 443, 621, 641, 654 days. At 18 months IND was 20% in SI-C group and 100% in SI-EXN group. Comparing pre and post-SI, only the SI-EXN group had significantly lower A1C at 3, 6 and 12 months (6.7В±0.2, 5.5В±0.1, 6.1В±0.2, and 6.2В±0.8%, respectively). Mixed meal stimulation index (AUC C– 29 – ABSTRACTS – Diabetes Mellitus within 2ВЅ hours starting at 10 p.m. The CGMS tracing (see figure) demonstrated that the cumulative effect of these late night boluses on day #1 В lowered his subcutaneous glucose from 200 at midnight to <40 mg/dL shortly after 2 a.m. on day #2. When his parents called EMS his measured CGMS glucose was ~10 mg/dl. Since the patient was otherwise healthy, we concluded that this case represents hypoglycemic death. Discussion: The patient had a long standing history that could be characterized as “zealous perfectionism” to achieve tight glycemic control. Strenuous evening physical activity predisposed him to nocturnal hypoglycemia.В His recent episodes of severe hypoglycemia lowered his threshold for counterregulation. The Dead in Bed Syndrome describes a scenario where otherwise healthy young persons with T1DM are found dead in the morning. Autopsies are unrevealing and the post mortem diagnosis of hypoglycemia is problematic. This syndrome may account for 6% of deaths of patients under age 40 with T1DM. The literature suggests that death is probably caused by a cardiac arrhythmia. Strategies to prevent this outcome include increasing glucose targets to raise the threshold for hypoglycemic counterregulation and the use of real-time subcutaneous glucose sensors with alarms for hypoglycemia. Conclusion: This case may be the first time CGMS has recorded hypoglycemia resulting in death. Unfortunately the device he wore did not have a real-time glucose display or alarms for hypoglycemia which may have prevented this tragic outcome. peptideГ—100/ AUC glucose) was increased at 3, 6, 9 and 12 months (p<0.05). Intravenous glucose tolerance test (IVGTT) showed significantly increased acute insulin and C-peptide responses to glucose at 3, 6, 9, 15 and 18 months in SI-EXN group (p<0.05). No significant differences of these parameters were seen pre and post-SI in the SI-C group. At 18 months post-SI, body weight was not different from baseline in both groups. No serious adverse events from EXN treatment were observed. Discussion: Comparing with conventional SI, adjuvant EXN treatment had better metabolic profiles and longer IND. IVGTT indicated the improvement in first phase insulin release (FPIR) followed by better glucose control. This study confirmed better islet function in SI-EXN group. These changes may be due to prevention of apoptosis and reduction of islet stressors (decreased glucagon, glucose) leading to better engraftment. Conclusion: Supplemental islet infusions under EXN treatment appear to be beneficial as there is improvement FPIR and long term graft function that leads to long term insulin independence. Abstract #228 HYPOGLYCEMIC DEATH INCIDENTALLY RECORDED BY CGMS Robert Jay Tanenberg, MD, FACP, Christopher Alan Newton, and A.J. Drake III, MD, FACE Objective: Demonstrate the current and potential uses of a continuous subcutaneous glucose sensor to detect potentially fatal nocturnal hypoglycemia T1DM patients Case Presentation: A 23 year old man with T1DM for 12 years had recently begun insulin pump therapy to improve his glycemic control and reduce frequent hypoglycemic reactions. In June 2005, his family called the EMS for severe hypoglycemia associated with a seizure. He was treated in the emergency department and released. His A1C was 6.4% and his nighttime basal rates were adjusted to prevent further episodes. Despite this change, he had another severe hypoglycemic episode the next week and a continuous glucose monitoring system (CGMS, Medtronic DiabetesГ”) was ordered. Less than 24 hours after the patient was placed on the monitor, he was found unconscious by his family at 9 a.m. Unfortunately, with this episode he did not respond to D50 administered by EMS and was pronounced dead on arrival in the ED.В The insulin pump and CGMS were removed by the diabetes nurse. Downloaded data showed the patient worked out after supper, but took 5 insulin boluses totaling 7.35 units Abstract #229 EFFECT OF RESVERATROL, A COMPONENT OF RED WINE, ON GLUT1-MEDIATED GLUCOSE TRANSPORT Kimberly Martin, MD, Ming Jing, MD, PhD, and Faramarz Ismail-Beigi, MD, PhD Objective: To examine the effect of resveratrol on Glut1-mediated glucose transport. Methods: Clone 9 cells, C2C12 cells and human erythrocytes were employed.В Resveratrol and 5’-aminoimidazole-4-carboxamide-1-beta-d-ribofuranoside (AICAR) were added to the culture medium.В Resveratrol’s effect on phosphorylation of AMPK was assayed by Western blot.В Glucose transport was measured by cytochalasin B (CB)inhibitable 3-OMG uptake.В The effect of resveratrol on CB binding to erythrocyte ghosts was determined in the presence and absence of glucose. – 30 – ABSTRACTS – Diabetes Mellitus Results: Incubation of Clone 9 cells (a rat liver cell line expressing only the Glut1 isoform) with resveratrol (0.1 to 500 mM for 1 hr) revealed that AMPK phosphorylation is slightly inhibited at low concentrations and stimulated (1.5 to 2.2-fold) at concentrations of resveratrol above 100 mM.В However, the addition of resveratrol to the same cells markedly inhibited glucose transport (EC50 of ~25 mM), regardless of whether AMPK phosphorylation was augmented or suppressed.В Glucose transport was inhibited while AMPK phosphorylation was stimulated within 1 minute after exposure of cells to 100 mM resveratrol.В Addition of 2 mM AICAR, a known stimulator of AMPK and glucose transport in these and in other cells, to resveratrol-treated Clone 9 cells stimulated AMPK phosphorylation but had no effect on the suppressed rate of glucose transport.В The effect of resveratrol on activation of AMPK and inhibition of glucose transport was also observed in C2C12 cells.В Addition of resveratrol to human erythrocyte ghosts, which exclusively express Glut1, completely blocked the glucose displaceable binding of cytochalasin B to erythrocyte membranes. Discussion: Resveratrol is a naturally occurring polyphenol found in grapes that has been reported to have cardioprotective, anti-inflammatory, and anticancer properties.В More recently, investigations have demonstrated that this compound stimulates AMPK activity and appears to have anti-diabetic capabilities through the activation of Glut4mediated glucose transport in skeletal muscle.В Our results, however, demonstrate that resveratrol inhibits Glut1-mediated transport.В Further studies are needed to verify these results using in vivo models. Conclusions: Our findings indicate that resveratrol suppresses Glut1-mediated glucose transport by presumably acting directly to inhibit the Glut1 glucose transporter.В Given that Glut1 transporters are highly expressed in brain, retina and placenta, we tentatively recommend that this agent be used with caution in humans.В В В This work was supported by the Metabolism Training Program (T32 DK007319) and by DK-061994. – 31 – Abstract #230 THE GLUCOSE-LOWERING EFFECTS OF COLESEVELAM HCL IN PATIENTS WITH TYPE 2 DIABETES MELLITUS INADEQUATELY CONTROLLED WITH METFORMIN-BASED THERAPY: A POOLED ANALYSIS Harold Bays, MD, Kenneth Truitt, MD, and Michael Jones, PhD Objective: Colesevelam HCl (COL) is indicated as an adjunct to diet and exercise for improving glycemic control in adults with type 2 diabetes mellitus (T2DM). This pooled analysis evaluated the glucose-lowering efficacy of COL in T2DM patients (pts) inadequately controlled (A1C 7.5%-9.5%) with metformin (MET). Pts were derived from 3 randomized, double-blind studies wherein COL was added to MET, insulin, or sulfonylurea, respectively, administered alone or combined with other oral anti-diabetes agents (OAD). MET was the primary OAD in the MET study (26 wks) and constituted a concomitant OAD in the insulin (16 wks) and sulfonylurea study (26 wks). In these separate studies, the addition of COL reduced A1C by ‑0.54% (MET), ‑0.50% (insulin), or ‑0.54% (sulfonylurea) vs placebo (PL) by study end (P<0.001 for all). Methods: In this pooled analysis of the 3 primary studies, 696 MET pts were assigned COL 3.75 g/day (n=355) or PL (n=341), in addition to their other anti-diabetes agent(s).В Efficacy endpoints in this analysis included change from baseline in A1C and fasting plasma glucose (FPG). Additional analyses included the proportion of pts who achieved a reduction in A1C≥0.7% or a reduction in FPG≥30 mg/dL from baseline to study end. Lipids and weight were not analyzed in this pooled analysis. However, LDL-C was significantly reduced in each of the primary studies (P<0.001 vs PL). Weight did not significantly change with COL in any of the primary studies. Results: Demographic and baseline characteristics (age, weight, BMI, A1C, and FPG) were comparable between the COL and PL groups. By study end, A1C was reduced by ‑0.42% in the COL group while A1C increased by 0.08% in the PL group, resulting in a placebo-corrected change from baseline of ‑0.50% (P<0.001).В FPG decreased by ‑4.6 mg/dL in the COL group and increased by 11.1 mg/ dL in the PL group, resulting in a treatment difference of ‑15.7 mg/dL (P<0.001).В Furthermore, the addition of COL to MET therapy resulted in a significantly higher proportion of pts achieving a reduction in A1C≥0.7% (38.3% vs 19.4%; P<0.001) or a reduction in FPG≥30 mg/dL (30.1% vs 22.0%; P=0.015) from baseline to endpoint vs PL. ABSTRACTS – Diabetes Mellitus Conclusion: COL administered to T2DM pts with inadequately controlled blood glucose on MET-based therapy significantly improved glycemic control. Conclusion: Kidney function remained stable after islet transplantation alone and it continues to be a safe procedure for treatment of unstable type 1 DM as long as aggressive treatment of conventional risk factors for diabetic nephropathy is provided. Abstract #231 UNCHANGED RENAL FUNCTION AFTER CLINICAL ISLET TRANSPLANTATION Abstract #232 ACANTHOSIS NIGRICANS IN A SUB-SET OF TYPE 2 DIABETIC PATIENTS IN AN URBAN HOSPITAL IN NIGERIA Cristiane Bauermann Leitao, MD, Pablo Cure, Shari Messinger, Antonello Pileggi, Oliver Lenz, Tatiana Froud, Raquel N. Faradji, Gennaro Selvaggi, Warren Kupin, David Baidal, Thipaporn Tharavanij, Davide Mineo, Karina Bernetti, Eva Herrada, Camillo Ricordi, and Rodolfo Alejandro Akinyele Taofiq Akinlade, MBBS, and Anthonia Ogbera, MBBS, FACE Objective: This study is to determine the prevalence of Acanthosis (AN) and the associated features in our patients with Type 2 diabetes Mellitus (DM) Methods: 171consecutive patients drawn from our Diabetes center were examined for AN and other essential data were obtained through interviewer administered questionnaires. Primary endpoints were the prevalence of Acanthosis Nigricans and the accompanying type 2 DM risk factors Results and Discussion: The mean age (SD) of the study subjects was 58 (12) years with a range of 21-85 years. A significant proportion of the patients-70% were obese. Mean BMI of the study was 28.4kg/m2 with mean body weight being 74kg (SD 15). The male-female ratio of the subjects was 1:2. The mean fasting blood sugar (FBS) of the study was 162.64mg/dl (SD 76.42). The prevalence of AN in this study was 24% and three-quarters of these subjects with AN were women. A family history of DM was seen in 26% of those with AN while 74 % had no family history. This difference was statistically significant (?= 7.9, p<0.01). Mean FBS of those with AN was 174.5mg/dl, majority 33 (80.5%) of whom are on oral hypoglycemic agents (OHA) and their mean FBS was 156.1mg/dl. This is better than the 166.89mg/dl for the 6 (14.6%) patients with AN but on either insulin alone (9.8%) or both insulin/OHA (4.9%). More than half of patients (53.7%) with AN are obese while 31.7% are overweight. A small proportion (14.6%) had a normal BMI despite having AN but no underweight patient had AN. Those with AN have more of generalized and centripetal obesity as compared to those without AN and was statistically significant (?= 9.95, p<0.04). Of the obese patients with AN, 18 (81.8%) are also hypertensive, representing a significant clustering of the associated features of insulin resistance in our DM patients. Objective: To determine the clinical course of kidney function after islet transplantation and identify clinical, laboratory and immunosuppressive factors associated. Methods: A retrospective cohort study was conducted in 35 subjects submitted to pancreatic islet transplantation as treatment for unstable type 1 diabetes mellitus (DM). Demographic, anthropometrical and laboratory data, as well as immunosuppressive and anti-hypertensive therapy were recorded. Kidney function was assessed by serum creatinine and albuminuria and estimated glomerular filtration rate (eGFR) was calculated by MDRD formula. Results: Overall eGFR remained stable during follow-up. Even subjects with low eGFR and/or microalbuminuria (n=10) at baseline maintained stable values posttransplantation (61.13В±3.25 vs. 63.32В±4.36 ml/min/1.73 2 m , P=0.500). Six (20%) normoalbimunuric subjects progressed to microalbuminuria, but sustained macroalbuminuria was not detected. A1c was normal in all patients after transplant (pre: 7.45В±0.11 vs. post: 6.09В±0.09%, P <0.001). A mild increment in LDL-cholesterol levels after transplantation was found (pre: 93.3В±3.3 vs. post: 101.6В±2.3 mg/dl, P=0.008). BP remained stable during the follow-up (pre: 121.7В±2.3/71.9В±1.6 vs. 119.3 В± 1.6/71.5В±1.0 mm Hg, P >0.05), at the expense of increasing the number of antihypertension medications/patient (0.34В±0.48 vs. 0.71В±0.86, P=0.002). After multivariate adjustments, age was the only risk factor for low eGFR (OR=1.78, 95%CI 1.22–2.61). Similarly, LDL-cholesterol (OR=2.90, 95%CI 1.37–6.12) and previous microalbuminuria (OR=6.42, 95%CI 1.42– 29.11) were risk factors for macroalbuminuria development. Tacrolimus was a protective factor against macroalbuminuria (OR=0.12, 95%CI 0.06-0.26). Discussion: The better kidney prognosis found could be attributed to healthier kidney status at baseline associated with prompt treatment of renal side effects. – 32 – ABSTRACTS – Diabetes Mellitus Conclusion: The prevalence of AN in DM in this report is 24%. Its presence is related to generalized and centripetal obesity, a family history of DM and being female. Cluster of these factors points to the likely presence of insulin resistance. AN occurring with obesity and hypertension are prominent features of our type 2 DM patients. Majority of them are on OHA and have poor glycemic control like other patients with AN on insulin or insulin/OHA combination; putting them at greater risk for atherosclerotic cardiovascular disease. group (7.52 В±0.30 vs. 7.53 В±0.32 [mean В± sem]; p=0.98). However, when we stratified the hemoglobin A1C categorically adjusting for age, patients in the NSTEMI group were 3.6 times more likely to have an A1C over 8.0% compared to control patients (p=0.03). We did find a significant inverse correlation between HDL-C and peak troponin inВ a univariate analysis. Conclusion: We found no difference in the last measured mean A1C in diabetic patients presenting to the intensive care unit with NSTEMI compared to other intensive care unit diabetic patients without NSTEMI. However, when A1C was categorized into those with вЂ�controlled’ versus вЂ�uncontrolled’ (cutoff value of 8%), NSTEMI patients were over three times more likely to have a high (over 8) hemoglobin A1C value when adjusted for age. HDL-C was inversely related to the peak troponin when examined individually. Discussion: High Hemoglobin A1C as a risk factor for Acute NSTEMI can be further investigated in large scale prospective studies. Hyperglycemia as a potential cause for direct myocardial injury has been studied in animal models and human cell culture lines. Providers should followВ establishedВ guidelines forВ A1C monitoringВ andВ A1CВ targets for therapy. Thiozolidinediones are a class of drugs which were approved as they improved glucose control. Recent studies have highlighted their negative cardiovascular effects. This studyВ raises the question; Can we really consider blood sugar control and cardiovascular events as mutually exclusive ?There are however some significant limitations to our study. Our study does not distinguish between Type 1 and Type 2 Diabetes Mellitus. Our study does not differentiate the subjects with respect to the duration of diabetes. The last measured A1C was not categorized based on the time lag between measurement and the event. Our study was underpowered in the multiple linear regression analysis. There were significant number of persons with renal failure who may have influenced both the peak troponin as well as the A1C levels. Conclusion: We found no difference in the last measured mean A1C in diabetic patients presenting to the intensive care unit with NSTEMI compared to other intensive care unit diabetic patients without NSTEMI. When A1C was categorized into those with вЂ�controlled’ versus вЂ�uncontrolled’ (cutoff value of 8%), NSTEMI patients were over three times more likely to have an uncontrolled hemoblogin A1C value when adjusted for age. HDL-C was inverserly related to the peak troponin when examined individually. Abstract #233 IS THERE AN ASSOCIATION BETWEEN LAST MEASURED GLYCATED HEMOGLOBIN (HbA1C) AND ACUTE NON-ST SEGMENT ELEVATION MYOCARDIAL INFARCTION IN DIABETIC INDIVIDUALS? Prasanna Santhanam, MBBS, Bruce Chertow, and Todd W. Gress Objective: Diabetes mellitus (DM) is an independent risk factor for the development of acute myocardial infarction (AMI). Prior work has revealed an association between the admission serum glucose and mortality in patients with AMI. The purpose of the study was to examine if there existed some relationship between the last measured Hemoglobin A1C in the clinical setting (within six months)and the acute coronary syndrome specifically Non ST segment Elevation Myocardial Infarction (NSTEMI) in persons with Diabetes Mellitus. Methods: We identified 1128 patients admitted to our intensive care unit between January 1, 2006 and June 30, 2007. Of these, 36 with NSTEMI were found to have a measured A1C within the last 6 months and comprised our case group. From the same time period, we selected 42 diabetic controls without NSTEMI admitted to our intensive care unit with a measured A1C within the last 6 months. The hemoglobin A1C was divided into those below 8% (вЂ�controlled’) and those at or above 8% (вЂ�uncontrolled’). We performed a multiple linearВ regression analysis simultaneously adjusting for potential confounding variables, which included age, systolic blood pressure, diastolic blood pressure, hemoglobin,HDL-Cholesterol, and LDLCholesterol levels. Results: We found that the mean hemoglobin A1C in the NSTEMI group was no different than the control – 33 – ABSTRACTS – Diabetes Mellitus betes7. This study has a prospective component (with support of our local Diabetes Association) and has attempted to look at the pattern of diabetes in Rivers State. Our study confirms that diabetes is a health problem in Rivers State, though rate (0.3%) is much lower than that reported in the 1997 national survey (3.03% Vs 2.2%). However the current study focused on overt diabetes. The few number of diabetics from some LGAs is probably a reflection of the awareness level and nearness to the study centres rather than an actual magnitude of the disease. The non-availability of facilities for chromosomal/ genetic studies in our environment may have resulted in inclusion of more вЂ�Other specific type’ into the вЂ�Type 2’ category. The diet of most of the patients consisted of one or two bulky carbohydrate meals (derivatives of yam, cassava and maize) eaten with vegetable soup and occasional meat and fish. Some ate cereals such as beans, rice and bread. The diet of the elites comprised in addition, animal protein. No one admitted to more than occasional consumption of alcohol, and usually on social occasions. The proportion of type 2 subjects with chronic complications (neuropathy 56.3%; erectile dysfunction 36.3%, nephropathy 9.2% and retinopathy 7.3%) at diagnoses reflects the fact that Type 2 diabetes has an asymptomatic pre-clinical phase which is not benign. This underscores the need for primary prevention and population screening to detect the disease early and institute therapy. Hypertension and diabetes mellitus: Hypertension frequently co exists with diabetes, there is an increased prevalence of hypertension among diabetic patients but there is also high propensity among hypertensive patients to develop type-2 diabetes. When occurring together the two disease entities appear to aggravate one another worsening both the diabetes and cardiovascular end points.В Data from UK Prospective Diabetes Study (UKPDS) revealed that every 10mm.Hg reduction in the level of systolic BP is associated with a nearly 12% lower incidence in myocardial infarction, down to a systolic BP level of <120mm.Hg.В Progressive lower diastolic BP also reduces CV risk progressively. The Hypertension Optimal Treatment (HOT) trial showed that number of major cardiovascular events dropped in line with increasing astringent target diastolic BP-target.В These findings are reflected in the BP-target for diabetic patients of < 130/80mm of Hg as now recommended by European Society of Hypertension, JNC7 report and American Diabetes Association. Conclusion: Diabetes mellitus is a substantial health problem in Rivers State, though crude prevalence (0.3%) is much lower than that reported in the 1997 national survey (0.3% vs 2.2%) Type 2 diabetes has an asymptomatic pre-clinical phase which is not benign, considering the pro- Abstract #234 THE PATTERN OF DIABETES MELLITUS IN RIVERS STATE, NIGERIA Sunday Chinenye, MBBS, FWACP, Doris Uchenna MBBS, FWACP, FMCP, Chioma Unachukwu BSc, MBBS, FWACP, and Anthonia Ogbera MBBS, MPH, FMCP Objectives: To determine the types of diabetes mellitus seen in Rivers State. Ascertain the clinical and biochemical features of our newly diagnosed diabetics. Methods: Cross-sectional study of people living with diabetes attending our local diabetes association meetings, and diabetes clinic at the University of Port Harcourt Teaching Hospital (UPTH) during the period Jan 2001 to Dec 2005, were recruited with informed consent. The subjects were old and new diabetics from the settings above. Physical and biochemical examinations were undertaken to detect the main outcome variables viz: Demographic/ Anthropometrics of subjects, Hypertension ( Taken as BP ≥140/90mmHg on at least two different occasions), Neuropathy (Sensory, motor and/or autonomic) diagnosed by established clinical criteria., Retinopathy (Checked for by fundoscopy, confirmed by an Ophthalmologist), Diabetes mellitus: Defined as FPG ≥7.0mmol/L and/ or 2 Hour PG ≥11.1mmol/L, Nephropathy: Frank proteinuria detected with Multistix test strip or an albumin excretion rate >200Вµg/ min using “Micral test” strip on an early morning urine sample was regarded as demonstrating nephropathy. Results: A total of 10,518 people living with diabetes mellitus were seen during the period from the 23 local governments (LGAs) of Rivers State. There were 5,350 females (50.9%) and 5,168 males (49.1%) giving F:M ratio of 1.04: 1. The majority of subjects were adults (93.9%) aged 20 years and above. 830 of the subjects were seen regularly and evaluated for clinical / biochemical characteristics, modes of therapy and complications on initial presentation (see tables). These comprised 25 type 1 diabetics (3.0%), 780 type 2 (94.0%), 10 (1.2%) вЂ�Other specific types” and 15 (1.8%) with Gestational diabetics. At diagnosis, the type 2 subjects (780) had the following complications viz: neuropathy 439 (56.3%), erectile dysfunction 283 (36.3%), nephropathy 72 (9.2%), and retinopathy 57 (7.3%).В Discussion: Previous reports on diabetes in our environment were retrospective hospital based studies which dealt mainly with pattern of foot ulcer and childhood dia– 34 – ABSTRACTS – Diabetes Mellitus portion of new cases with established complications, thus underscoring the need for primary prevention and population screening to detect the disease early and institute therapy. factors found in this study are similar to findings in other parts of the world with high prevalence of GDM. Conclusion: The prevalence of GDM among the study group was 14%. The predominant risk factors for GDM were multiparity, macrosomia, stillbirth, previous C/ S, glycosuria and hypertension. Most (83%) of the women found to have GDM had risk factors for GDM. Abstract #235 PREVALENCE AND RISK FACTORS FOR GESTATIONAL DIABETES MELLITUS AMONG NIGERIAN WOMEN Abstract #236 Andrew Enemako Uloko, MD, Fabian Puepet, FMCP, Christiana Ukoli, FMCP, and Patrick Daru, FWCOG MOST NEWLY DIAGNOSED TYPE 2 DIABETES MELLITUS SUBJECTS MEET INTERNATIONAL DIABETES FEDERATION 2005 DEFINITION FOR METABOLIC SYNDROME Objective: To determine the prevalence of gestational diabetes mellitus (GDM) and to assess the risk factors associated with it. Methods: In a cross sectional study spanning three months, pregnant women from second trimester upwards attending the antenatal clinics of the Jos University Teaching Hospital (JUTH), Jos, NigeriaВ were consecutively recruited regardless of risk factors for diabetes mellitus. Relevant bio-data and history of risk factors of GDM were obtained from each participant via a structured interviewer-administered questionnaire. Physical examination including anthropometric indices was carried out on each subject. Urinalysis and a 2-hour 75g OGTT were performed. The WHO diagnostic criteria for GDM was used to interpret the OGTT. Multivariate analysis using logistic regression was applied to determine the independent risk factors associated with GDM. p < 0.05 was considered to be statistically significant. Result: A total of 180 pregnant women with a mean (SD) age of 28.16 (5.23) years, age range 20-45 years participated in the study. Mean (SD) gestational age was 33 (7) weeks. The prevalence of GDM based on the WHO diagnostic criteria for GDM was 14%. Risk factors for GDM were present in 83% of the women with GDM. The predominant risk factors for GDM were multiparity, macrosomia, stillbirth, previous caesarean section, glycosuria and hypertension. The independent risk factors associated with GDM were macrosomia [OR = 3.20, (95% CI 1.005 – 9.773) p = 0.04], C/S [OR = 12.42, (95% CI = 2.9252.77) p = 0.001], and systemic hypertension [OR = 12.10, (95% CI =2.93-49.92) p = 0.001]. Discussion: A GDM prevalence of 14% found in this study is slightly higher compared to earlier reports of 11.6% by Olarinoye et al in south-western Nigeria, though the diagnostic methods are different. This prevalence may also mirror the rising prevalence of diabetes in Nigeria (2.2% in 1997, 5% projected prevalence in 2005). The risk Ali Asghar Jawa, MD, MPH, Tahir Rasool, Muhammad Abu Zafar, Prof., Mumtaz Hasan, MD (S.I.), Jawad Zaheer, MD, Ghazanfar Jawa, and Syed Ali Imran Objective: To assess the prevalence of Metabolic Syndrome amongst newly diagnosed subjects with type 2 diabetes mellitus using the International Diabetes Federation 2005 definition. Methods: According to International Diabetes Federation 2005 definition, metabolic syndrome is defined as ethnic-specific central obesity (Waist circumference > 80 cms in females or > 90 cms in males for southeast Asians) and presence of 2 out of the following 4 risk factors: Systolic Blood Pressure >130 mm Hg or Diastolic Blood Pressure > 85 mm Hg or known hypertension, Fasting Blood Glucose > 100 mg/dL or known type 2 diabetes mellitus, Serum Triglycerides > 150 mg/dL or on lipid lowering medications,В or HDL < 50 in females or < 40 in males. We performed a retrospective chart review of all newly diagnosed type 2 diabetes subjects presenting to the Hamza Foundation Diabetes Centre from January 1December 31, 2005. 89 new cases presented for new onset diabetes management. Medical records were reviewed and baseline data including Height, Weight, BMI, Waist Circumference, HDL-Cholesterol, Serum triglycerides, Systolic and Diastolic Blood pressure at the time of presentation were tabulated. All data was analyzed using SPSS 13.0 Results: 64/89 subjects with newly diagnosed type 2 Diabetes Mellitus met International Diabetes Federation 2005 Criteria for Metabolic Syndrome. 50/64 subjects were female. Mean age was 46 years (30-70), mean waist circumference was 98 cms (80-120) and mean BMI was 29 (20-40). Biochemical profile of these subjects showed a mean A1C of 8.8% (5-16), mean HDL-Cholesterol of 39 mg/dL (25-59) and mean Triglycerides of 281 (85-1487). – 35 – ABSTRACTS – Diabetes Mellitus Discussion: One rare form of fungal sinusitis is chronic invasive sinusitis that usually takes weeks to months to develop. Patients usually have visual changes not associated with fever, chills, nasal congestion or rhinorrhea. Few cases have been reported, most of them have type 2 diabetes which is relatively well-controlled. They usually present with orbital apex syndrome characterized by ptosis, periorbital edema and cranial nerve III, IV and VI deficits as seen in this patient. Conclusion: This is the first case of chronic invasive fungal sinusitis in type 1B diabetes that has been reported which responded well to treatment. This infection usually has an indolent course but a poor prognosis. A combination of medical and surgical treatment is usually required as in this case. The Systolic Blood Pressure at the time of diagnosis was 130 mmHg (100-170) and Diastolic Blood Pressure was 84 mmHg (70-100). Conclusions: The results of this study indicate that almost 3/4th of newly diagnosed newly diagnosed type 2 diabetics have Metabolic Syndrome as defined by the new IDF definition. This finding underscores a great need for earlier detection and treatment of metabolic syndrome before clinical diabetes develops. Abstract #237 CHRONIC INVASIVE FUNGAL SINUSITIS IN A 28 YEAR-OLD WITH TYPE 1B DIABETES Juan Carlos Varon, MD, and Alina Khan Ronal Goldberg Abstract #238 Objective: To report an unusual case of chronic invasive fungal sinusitis in a young woman with type 1B diabetes. Case presentation: A 28 year old non-obese Asian woman with type 1 diabetes Mellitus presented to the hospital complaining of progressive right eye pain and frontal headaches, without fever or chills, as well as diplopia for approximately one month. The patient was diagnosed with type 1 diabetes 7 years prior to presentation when she presented with diabetic ketoacidosis. Since then, she had been on insulin treatment and presented with diabetic ketoacidosis on 2 occasions after stopping insulin for 2-3 months. The absence of islet cell antibodies, GAD54 autoantibodies and a low C-peptide level of 0.4 pm/ml with plasma glucose of 230 mg/dl, confirmed a diagnosis of Type 1B diabetes. Before presenting to the hospital, she had discontinued her insulin therapy for 6-7 months but continued to monitor her diabetes at home and her finger sticks were about 200 mg/dl. On admission, her blood glucose was 660 mg/dl, but without features of diabetic ketoacidosis. Notable on physical examination were the presence of right sided ptosis and cranial nerve III,В IV andВ VI paralysis. A CT Scan of the head and sinuses revealed bilateral sinusitis with bony destruction, highly suggestive of a fungal infection. The patient was then started on empiric broad spectrum antibiotics as well as antifungals which may have contributed to the fact that the culture results were negative. She subsequently underwent endoscopic bilateral ethmoidectomy, sphenoidectomy and orbital exploration. The histology of the sinus and bone showed both acute and chronic inflammation as well as dichotomously branching septate hyphae at 45В o angles which is characteristic of Aspergillus infection. Post-operatively the patient was started on high-dose liposomal amphotericin-B and oral vorizonazole, with good response. INPATIENT HYPERGLYCEMIA MANAGEMENT AND OUTCOMES Megan Elizabeth Mcgarvey, MD, Maida Soghikian, MD, and James McCallum, MD Objective: Despite the large body of evidence linking hyperВglycemia with poor hospital outcomes, there is onВgoing debate about the value of achieving glyceВmic control targets in the non-ICU setting. We sought to evaluate glycemic control and outcomes for patients hospitalized in a non-critical care setting prior to the institution of a basal/ bolus subcutaneous insulin protocol. Methods: We conducted a retrospective review of all paВtients admitted in a one year period to non-Вcritical care wards. ICD-9 codes were used to idenВtify diabetic and nondiabetic patients at the time of admission, track inpatient complications, length of stay, total costs of stay, discharge destination, and mortality rates. Recorded finger-stick glucoses (FSG) were evaluated. All data was subjected to statistical review using both chi square and two-sided T tests. Results: Fewer patients with diabetes were admitted to the hospital in comparison to non-diabetic patients (3,021 diabetic vs.13,268 non-diabetic admissions). Diabetic patients were more likely to be readmitted than the non-diabetic patients (29% vs. 24%, p<0.0001). 24% of patients admitted with diaВbetes had a pre-admission HbA1C greater than 7%. There was a significantly higher percentage of the diabetic patients admitted with a diagnosis of infection (24% vs. 16%, p<0.0001) and of cardiovascular complications (19% vs. 9%, p<0.0001). Only 40% of diabetic inpatients’ FSG values were within the American Diabetes Association’s (ADA) recommended goal of 70139 mg/dL, while 57% of obtained values were in the – 36 – ABSTRACTS – Diabetes Mellitus hyperglycemic range and 3% were in the hypoВglycemic range. When compared to the non-diabetic patients, we found that patients with diabetes more often developed infection (9.5% vs. 4.5%, p= 0.005) and renal complications (9.1% vs. 5.9%, p=0.05) during their hospitalization. Fewer diabetics were discharged directly to home (69% vs. 72%, p<0.0001). Diabetic patients more often were disВ charged home with home health care (15% vs. 13%, p = 0.012). 15% of diabetics vs.12% of non-diabetics were discharged to a skilled nursing facility (p=0.012). There was no significant difference in inpatient mortality between the two groups. Patients with diabetes stayed on average a half a day longer and incurred approximately $1300 more in hospital cost. Discussion: Intervention with a standardized insulin protocol may improve glycemic control, and improve overall patient outcomes. Conclusion: Our institution was poorly compliant with ADA guidelines. Compared to non-diabetics, our diabetic patients had poorer outcomes, longer length of stays and incurred higher costs. the outpatient A1Cs was 7.778, and the mean inpatient A1C was 7.711, with a difference of 0.067 (p=0.91). Correlation of mean outpatient and inpatient A1Cs was 0.68 (p<0.001). 124 (56%) of the admission A1Cs remained in the same category as the mean associated outpatient A1C, 49 (22%) dropped to a lower category after admission, and 47 (21%) rose to a higher category (p<0.01). Discussion: Although A1Cs have been used to assess mean glucose levels over three month intervals, A1C is a time-weighted measure of glycemic control, most influenced by mean blood glucose during the previous 4-5 weeks. We compared admission A1Cs with prior stable outpatient A1Cs to determine if potential hyperglycemia from illness in the weeks prior to admission significantly raised the admission A1C. A1Cs from 60 days prior to admission were excluded since the inpatient A1C would assess glycemia over this time period. Conclusions: Inpatient A1Cs obtained during one week after hospital admission did not significantly change from mean stable outpatient A1Cs from the previous year. Admission inpatient A1Cs may be an accurate indicator of stable outpatient glycemic control in this population of patients. Further studies with greater power are needed to determine if the slight decrease in the mean A1C upon hospital admission is significant. Abstract #239 THE EVALUATION OF HEMOGLOBIN A1C IN STABLE DIABETICS PRE AND POST ADMISSION Abstract #240 Aysha Emily Inankur, MD, and Brian Burke, MD, FACP EXENATIDE LEADS TO REDUCTION IN LIVER ENZYMES IN DIABETICS INDEPENDENT OF WEIGHT LOSS Objective: To examine the relationship between A1Cs measured upon hospital admission and stable outpatient A1Cs measured during the year prior to admission in subjects with diabetes mellitus (DM). Methods: Medical records of patients with DM admitted onto medical and surgical wards of the Dayton, Ohio VA Hospital from October, 2003 through October 2007 were reviewed. Admission A1Cs were included if they were preceded by two stable outpatient A1Cs. Stable outpatient A1Cs differed <1.0 and were obtained within a 10 month period <12 months and >60 days prior to admission.1 A1C levels were standardized by the Diabetes Control and Complications Trial reference method. Admission A1Cs were compared to the mean of two prior outpatient A1Cs by the pared t-test. Outpatient and inpatient values were categorized as <6.00%, 6.00-6.99%, 7.00-7.99%, and ≥8.00%. Categories were analyzed by the Pearson chi-square test. Results: During the period of review, 18,908 admissions occurred to medical and surgical wards. Of these admissions, 6,379 involved a prior diagnosis of DM type 1 or 2. Of this group, 1,922 had an inpatient A1C ≤7 days of admission. 220 of these inpatient A1Cs were preceded by ≥2 stable outpatient A1Cs as defined above. The mean of Deepti Bulchandani, MD, Jagdish S Nachnani, MD, Crystal Eaton, LPN, and Mitchell Hamburg, MD, FACE Objective: Exenatide is a peptide receptor of the GLP1(Glucagon like peptide 1) receptor which promotes insulin secretion. Raised liver enzymes in diabetics has been postulated to be due to Non alcoholic fatty liver disease (NAFLD) which is one of the commonest liver diseases and has been associated with Type 2 diabetes mellitus(DM) and insulin resistance. Exenatide has been shown to reverse hepatic steatosis in the animal model of fatty liver. However, there have been no studies looking at the association of liver enzymes with the use of exenatide. Methods: From January 2007 till date, 29В eligible patients who had completed exetanide for a period of one year were included in our study. The patients were continuing their sulfonylurea/metformin treatment per their treating endocrinologist. Demographic, anthropometric and laboratory were retrospectively collected. Paired t test and Pearson’s correlation coefficient was used for comparison. – 37 – ABSTRACTS – Diabetes Mellitus A two tailed p value of 0.05 was considered statistically significant. Results: There were 29 patients in our study cohort. The mean age (+/- standard deviation) of the patients was 55.5(8.1) years. 59% of the patients were males. The mean weight, HgBA1C, AST and ALT was 239 +/- 51 lbs, 8.2 +/- 1.3%, 31.3 +/- 15.6 units/L and 37.5 +/- 16.0 units/L respectively prior to starting exetanide therapy. 12/29 patients had either AST or ALT > 35 units/L. The mean decrease in weight at one year was 10. 8 lbs (p=0.005) and the mean decrease in HgBA1C was 0.7(p=0.001). The mean decrease at one year in AST was 6.5 units/L (p=0.04) and ALT was 11.9 units/L (p=0.001) respectively. There was no correlation with reduction in AST(p=0.51) or ALT(p=0.50)with change in weight. Out of the 12 patients with raised liver enzymes, in 7 patients the liver enzymes returned back to normal. Discussion: NAFLD has emerged as the most common chronic liver disease in United States. Diabetes has been implicated as a risk factor in NAFLD. In fact the commonest reason for aymptomatic raised liver enzymes in diabetics has been postulated to be NAFLD. In our study exetanide has been shown to reduce liver enzymes after one year of treatment. It may possible that this could be an independent effect of exetanide or it could be secondary to the loss of weight accompanied with the use of exetanide. However, it our study, change in weight did not seem to be correlated with the reduction in liver enzymes and the effect was probably secondary to the use of exetanide. Conclusions: In patients with Type 2 DM, exetanide treatment leads to decrease in AST and ALT along with a mean reduction of weight and HgBA1C. It is possible that exetanide may be a possible therapy option in NAFLD in patients with raised liver function tests though further prospective studies will be needed to delineate that association. 2007 were reviewed. Patients older than 18 years of age and confirmed DKA or HHS (according ADA criteria) were included in this study.В Subjects were retrospectively classified as having type 1 diabetes (T1D), type 2 diabetes (T2D) irrespective of their insulin useВ or had new-onset diabetes. We found 96 episodes of DKA and 9 episodes of HHS between January 2001 and January 2007 (91.4% and 8.6%, respectively).В 61%В of the patients were male, the age (mean В± SD) was 44.7 В± 15.6 years, 57.1% of the patients had a family history of diabetes, and 55.3% of the patients had a prior diagnosis of diabetes. In 44.7% of the patients this was the first manifestation of diabetes. Discontinuation of treatment was the precipitating factor in 41%, infections in 17.1% and, an intercurrent illness in 2% of the patients. No identifiable causes were found in 40% of the patients. During the six years of the study, only five episodes of DKA in five T1D patients were observed.В The mean В± SD results of laboratory blood tests were: glucose 496.62 В± 173.14 mg/dL, pH 7.17 В± 0.15, bicarbonate 8.46 В± 6.31 mEq/L, serum osmolality 304.27 В± 21.07 and, anion GAP 25.72 В± 7.97 mmol/L.В 70% of DKA episodes were severe. Discussion: The incidence of DKA/HHS among T2D patients has been increasing in the last years especially among the non-Caucasian ethnicities. Peru has one of the lowest T1D incidence, this phenomenon could explain why less than 5% of the DKA episodes were observed in patients with T1D. Also, it might reflect inadequate availability of primary health care services and be caused by delayed diagnosis of T2D. Conclusion: Our study suggests that in countries were the incidence of T1D is low, a significant proportion of DKA cases occur in patients with T2D, especially in patients with new-onset disease. Most of these episodes were severe, and were related to non-compliance in treatment or had no identifiable cause. Abstract #242 Abstract #241 HYPERGLYCEMIC HYPEROSMOLAR STATE AND RHINO-ORBITAL MUCORMYCOSIS IN A PATIENT WITH NEW-ONSET DIABETES MELLITUS HYPERGLYCEMIC CRISES IN PERUVIAN PATIENTS WITH TYPE 2 DIABETES Miguel E. Pinto, MD, Ximena Guevara, MD, and Jaime E. Villena, MD Miguel E. Pinto, MD, Ximena Guevara, MD, and Jaime E. Villena, MD Objective: To describe the clinical and laboratory characteristics of hyperglycemic crises in Peruvian patients with diabetes. Case Presentation: The clinical charts at Cayetano Heredia Hospital (Lima, Peru) of all diabetic patients with diabetic ketoacidosis (DKA) or hyperglycemic hyperosmolar state (HHS) between January 2001 and January Objective: To reportВ the case of a man with new-onset diabetes mellitus who developed hyperglycemic hyperosmolar state and rhino-orbital mucormycosis. Case Presentation: A 74-year-old man with 2-week history of polydipsia, polyuria, weight loss, and diplopia came to the Emergency Service. He had noВ personal his– 38 – ABSTRACTS – Diabetes Mellitus tory of diabetes. Physical examination showed a swelling of his left cheek, ocular protrusion and purulent discharge from his left eye. His vital signs showed a blood pressure of 150/90 mmHg, heart rate of 90 beats/min, oral temperature of 37.3 ВєC, and BMI of 25.5. When he was admitted to the hospital, the glucose level was 700 mg/dL, serum bicarbonate was 20.4 mEq/L, arterial pH was 7.40, corrected sodium was 157 mEq/L, potassium was 4.9 mEq/ L, chloride was 106 mEq/L, calculated serum osmolality was 334 mOsm/Kg, and urine ketones were positive. The diagnosis of hyperglycemic hyperosmolar state (EHH) was established, and appropriate medical treatment was started with IV insulin, hypotonic solutions, and broad spectrum antibiotics. A CT scan showed cellulitis in the left orbit with severe swelling of all extra ocular muscles and pansinusitis. Patient underwent aggressive surgical debridement of the sinuses and nasal cavity, and exenteration of the left orbit. On histopathologic examination, the orbital tissue was found to contain a fungus ball with nonseptate hyphae with right-angle branching, consistent with mucormycosis. IV amphotericin B was started. Further laboratory working showed an HbA1c of 14%, microalbuminuria of 292Вµg/ mg and normal funduscopy. Cultures were positive to Rhizopus sp. PatientВ hadВ a favorable glycemic control with NPH insulin. Oral posaconazole was added because patient developed renal insufficiency associatedВ with amphotericin B. Patient was discharged from hospital with no specific therapy for diabetes, because his glucose level was in the normal range,В and oral posaconazole. Discussion: Mucormycosis often develops in immunocompromised patients, particularly in patients with diabetic ketoacidosis. In many cases, this could be the first manifestation of the disease. The metabolic acidosis offers an added advantage to this fungal infection, the acidic milieu reduces the binding of iron to transferrin and thereby a more favourable conditions for fungal multiplication arises. Conclusion: We report the case of a patient with newonset diabetes mellitus with a rhino-orbital mucormycosis and hyperglycemic hyperosmolar state. Although mucormycosis is a fatal infection, early diagnosis and aggressive treatment, that includes surgical procedures, may decrease mortality. Abstract #243 RESOLUTION OF DIABETES AFTER EXTIRPATION OF BENIGN HEPATIC FIBROHISTIOCYTOMA Miguel E. Pinto, MD, Ximena Guevara, MD, and Jaime E. Villena, MD Objective: To report the clinical evolution of a man with new-onset diabetes who resolved his disease after the extirpation of a benign hepatic fibrohistiocytoma. Case Presentation: A 54-year-old man with a 1-week history of polydipsia, polyuria, and fever was referred to our emergency unit. Initial laboratory work-up showed: glucoseВ of 700 mg/dL,В pH of 7.09,В bicarbonate of 3.9 mEq/L, and urine ketones were positive. There wasВ no history of diabetes.В Diabetic ketoacidosis (DKA) diagnosis was established and aggressive treatment withВ IV insulin, hydratation, and antibiotics was started. Te HBA1c level was 11.1%В Physical examination showed fever and hepatomegaly with a palpable mass in the left hepatic lobe. The daily insulin requirements were high with an average over 320 UI/day.В Computed tomography showed a heterogeneous mass in the left hepaticВ lobe. The initial management was difficult becauseВ high doses of insulin were needed (daily average insulin dose of 105 UI, daily average fasting glucoseВ of 252 mg/dL) and fever was persistent throughout hospitalization (daily average temperature of 38.4 C).В After 27 days of hospitalization, extirpation of his hepatic mass was done. This was a 670 grams encapsulated mass. Pathologic anatomy was compatible with a benign fibrohistiocytoma and immunohistochemical stain was positive for glucagon. One day after surgery, fever was gone andВ daily averageВ glucoseВ was 95 mg/dL. Patient’s clinical evolution was favorable and e was discharged from hospital with no specific therapy for glucose control and without complaints. After four weeks of discharge, patient was with no antidiabetic treatment and glucose was normal. Discussion: Fibrous histiocytoma is a pleomorphic sarcoma composed of histiocyte-like and fibroblast-like elements. The majority of tumors occurs in the extremities, retroperitoneum and head/neck. The hepatic location is extremely rare. In this case, infection of the mass was ruled out because no necrosis was found in the surgical piece and cultures were negative. No association with secondary diabetes has been described in medical literature. – 39 – ABSTRACTS – Diabetes Mellitus Conclusion: To our knowledge, this is the first case reported in the English medical literature that describes the association of a benign hepatic histiocytoma with diabetes. We suggest that probably this mass secretes some substances that impaired insulin sensitivity as a paraneoplasic syndrome like glucagon. Conclusion: Overall glyburide appears safe and effective for the treatment of gestational diabetes mellitus during the second and third trimester of pregnancy. Abstract #245 EFFECTIVENESS OF AN INTENSIVE TRAINING PROGRAM COMBINED WITH INSULIN PUMP THERAPY Abstract #244 GLYBURIDE TREATMENT IN GESTATIONAL DIABETES MELLITUS: HOW SAFE AND EFFECTIVE Andrew John Behnke, MD, FACE, Ruth Beel, RN, and Melissa Benzon, RD Objective: To examine the effectiveness of an intensive education program in patients with poorly controlled diabetes mellitus using insulin pump therapy. Methods: Sixteen (16) patients with diabetes mellitus were identified as having poor glucose control and requiring insulin therapy.В The majority (9/16) had Type one diabetes. The average Hgb A1C at the beginning of the program was 8.6.В These patients were educated with an intensive program including multiple office visits and culminating in a 24-hour continuous physician supervisedВ monitoring period with insulin pump administration. Levels of glycosylated hemoglobin were monitored before, during, and up to six months after the education program and insulin pump starts. Result: Average levels of Hgb A1C reduced to 7.7%, 7.3%, and 7.3% at the time of the insulin pump administration and 24-hour monitoring period, three months, and six months later respectively. The percent of individuals achieving the AACE recommended level of Hgb A1C ( < 6.5 %) increased from a baseline of 6.3% to 14.3% at three months and 37.5% at six months. Discussion: Patients with poor glucose control are at high risk for multiple diabetic complications and may benefit from insulin pump therapy.В The combination of insulin pump therapy with a novel intensive education approach including a continuously monitored 24-hour period significantly reduced levels of Hgb A1C.В A significantly more number of these individuals met AACE goal levels of glucose control which persisted up to six months after the education period. Conclusion: In patients with poorly controlled diabetes requiring insulin, the combination of an insulin pump and an intensive education program significantly reduced levels of glycemia and resulted in an increase in the number of patients meeting AACE goals of glucose control. Besa Bushati, MD, Vipul Shah, MD, and Jann Johnston, MD Objective: To study the safety and effectiveness of glyburide in the treatment of gestational diabetes mellitus. Methods: Retrospective chart review of all patients with gestational diabetes mellitus (GDM) in endocrine practice in 2005. 58 women were identified. All were instructed in diet and home glucose monitoring. Glyburide or insulin were initiated if diet failed to control postprandial glucose values <120 mg/dl. Choice of therapy was up to patient preference. Groups were compared for age, weight at first visit, parity, final hemoglobin A1C (HbA1C), reported hypoglycemia, mode of delivery, pregnancy complications and baby weight. Statistical analyses consisted of applying univariate parametric and nonparametric measures. Results: 41/58 or 71% patients were treated with diet only. For the 17 who required pharmacologic therapy, 12/17 (71%) chose glyburide compared to 5/17 (29%) who chose insulin injections. There was no significant difference between any group regarding parity, weight, age, pregnancy complications or baby weight. Mean HbA1C: Diet 5.38 + 0.41%, Glyburide 5.45 + 0.46%, Insulin 5.92 + 0.94% (p-value 0.08). C-section rates were: Diet 9/41 (22%), Glyburide 9/12 (75%), Insulin 3/5 (60%) (pvalue 0.03). Reported hypoglycemia for Diet 5/41 (12%), Glyburide. 8/12 (67%) Insulin 1/5 (20%) (p-value <0.001). No severe hypoglycemia was reported. Discussion: Glyburide for the treatment of GDM does not appear to be associated with more fetal complications or difference in baby weight. C-section rates were higher as well as increased episodes of hypoglycemia however this is a known side effect of glyburide and insulin therapy. Oral glyburide was preferred to insulin injections and appears to be safe and effective for use in the second and third trimester. – 40 – ABSTRACTS – Diabetes Mellitus Abstract #246 Abstract #247 CLINICAL USE OF BRAIN NATRIURETIC PEPTIDE (BNP) IN PATIENTS WITH TYPE 2 DIABETES WHO ARE TAKING TZD’S THE RELATIONSHIP AMONG HOMOCYSTEINE, URINE ALBUMIN/CREATININE RATIO AND DEGREE OF RETINOPATHY IN PATIENTS WITH TYPE 2 DIABETES Andrew John Behnke, MD, FACE Nanny Natalia Mulyani Soetedjo, MD, Helen C. Tarigan, and I. Gusti N. Adhiartha Objective: To examine the clinical utility of Brian Natriuretic Peptide (BNP) in patients with type two diabetes receiving Thiazolidinedione (TZD) therapy. Methods: Patients who had Type 2 diabetes and were receiving TZD therapy with either pioglitazone or rosiglitazone were identified in a clinic setting.В Levels of BNP were measured in 90 consecutive patients.В Data were collected regarding levels of glucose control,В adverse events and estimates of cardiac function. Result: The proportion of patients receiving either pioglitazone or rosiglitazone was even ( 49 % rosiglitazone and 51% pioglitazone). Baseline characteristics were similar in both groups. В Most patients ( 57%) had reached ADA goal of Hgb A1C <7.0 and 27 % reached AACE goals of < 6.5 %. The number of patients having a BNP level of greater than 100 pg/ml was 6.4%.В Significantly more patients receiving pioglitazone had elevated BNP levels (62.5 % vs. 12.5 % on rosiglitazone).В Patients with elevated BNP levels had hadВ several significant cardiac events including cardiac bypass and myocardialВ infarction. Discussion: Previous studies have demonstrated the clinical utility of BNP levels in screening patients with Diabetes for occult heart dysfunction. BNP levels in patients with type two diabetes receiving TZD therapies were generally lower than 100. Of those that were elevated,В further investigation revealed significant cardiac dysfunction.В More patients had elevated BNP levels if they were treated with pioglitazone vs. rosiglitazone. Conclusion: A) TZD therapy in patients with type 2 diabetes is associated with A1C levels at ADA goal rates in a majority of patients and AACE goals in nearly 1/3 of patients. B) Most patients in this study had low levels of BNP on TZD therapy C) There were more patients with significantly high BNP (>100) on Pioglitazone vs RosiglitazoneВ D) BNP may be used clinicallyВ to assist in the management of Type 2 diabetes in patients who are receiving TZD therapyВ Objective: Increased plasma levels of homocysteine (tHcy) considered as independent risk factor for atherosclerotic disease in subjects with normal tolerance. There are controversies concerning plasma tHcy levels in type 2 diabetes. Whether hyperhomocysteinemia contributes to the development of diabetic microangiopathy is still debated. Thus the aim of this study is to evaluate whether there is relationships among homocysteine, urine albumin/ creatinine ratio (UACR) and retinopathy in type 2 diabetic patients. Methods: We observed type 2 diabetic patients who visited our outclinics between February 2007 and July 2007 who had creatinine serum <1.4 mg/dL, no history of: cardiocerebrovascular disease, diabetic ulcers, and severe infection. Urine albumin level was tested by immunoturbidimetry method, urine creatinine level was measured using Jaffe method and homocysteine level was measured by fluorescence polarization immunoassay (FPIA) method. Result: Baseline data for the cross-sectional study were obtained from 49 patients, between 40 and 79 years of age. The history of diabetes were between 8 months and 17 years. Their mean tHcy levels are 11.27 (4.15-98.29) Вµmol/L. All patients have perifer neuropathy. Mean of UACR levels are 42 (0.02-724.92) mg/g. Eight patients have Proliferative Diabetic Retinopathy (PDR), 31 patients have Non-PDR and 10 patients normal. Discussion: There are no significant differences between group with high tHcyВ (>10 Вµmol/L) and low tHcy levels for UACR and stage of retinopathy. No significant correlation between tHcy and UACR, but there are significant correlation between stage of tHcy and stage of retinopathy with p<0.01 and stage of retinopathy and stage of UACR with p<0.01. Conclusion: Plasma tHcy levels in this study are mild hyperhomocycteinemia. tHcy and UACR seem to be correlated with stage of retinopathy in patients with type 2 diabetes. – 41 – ABSTRACTS – Diabetes Mellitus decreased synthesis of gamma-aminobutyric acid, temporary ischemia and hyperviscosity. Conclusion: Hemiballism is a rare neurologic manifestation of hyperglycemia.В Awareness of this association is important, since the movement disorder may be the sole presentation of a clinically significant hyperglycemia.В В Additionally, hyperglycemic hemiballism may be reversible with glycemic control. Abstract #248 A RARE NEUROLOGIC MANIFESTATION OF HYPERGLYCEMIA: CASE REPORT OF A PATIENT WITH HYPERGLYCEMIC HEMIBALLISM Sara Elisabeth Lubitz, MD, and Julie Probst-Riordan, MD Objective: To describe a case of hemiballism associated with hyperglycemia Case Presentation: A 79 year old female presented with uncontrolled movement of her arm.В Exam was significant for flailing of the left upper extremity that ceased with sleep and worsened with agitation; the remainder of her neurologic exam was normal.В Laboratory evaluation revealed a glucose of 421 mg/dl, normal anion gap, and negative urinary ketones.В Although the patient had no known history of diabetes mellitus, HbA1c was 16.1%.В CT brain showed high-density material within the right basal ganglia.В MRIВ was significant forВ increased T1 signal and decreased T2 signal within the right lentiform nucleus without associated mass effect, diffusion restriction, or susceptible artifact and interpreted as compatible with the diagnosis of diabetic hemiballism. The patient was treated with intravenous insulin and neuroleptics.В Two months later her glucose was controlled (HbA1c 6.9%) with lowdose sulfonylurea without resolution of the movement disorder. Discussion: Hemiballism is a rare hyperkinetic movement disorder characterized by unilateral, irregular, involuntary flinging movements of the limbs caused by lesions of the basal ganglia.В Hyperglycemic hemiballism was first described by BedwellВ in 1960 in a woman who presented with arm flailing in the setting of hyperglycemia.В As the blood-glucose abnormality was corrected, the hemiballism resolved only to recur episodically with lapses in glycemic control. Today, it is largely a neuroradiologic diagnosis characterized by high signal on T1-weighted MRI images in the putamen contralateral to the movements, with similar changes found in the globus pallidus and the caudate. Twothirds of patients also have high signal abnormalities on T2 weighted sequences or densities in the striatum on CT scan.В The patients typically are elderly females with no history of diabetes mellitus who present with involuntary movements and severe non-ketotic hyperglycemia.В The hemiballism may be the only manifestation of the hyperglycemia.В After correction of the hyperglycemia, the movements usually resolve in hours to days.В However, 20% of patients have persistent hemiballism.В The pathogenesis remains uncertain. Potential etiologies include petechial hemorrhage, – 42 – Abstract #249 EVIDENCE THAT NEW SCREENING TESTS ARE NEEDED FOR SCREENING FOR TYPE II DIABETES Lee Pletts Goscin, MD, PhD Objective: Numerous studies have shown 50% of patients with first diagnosis of Diabetes 2 have coronary artery disease (CAD). Complications of Diabetes 2 take ten years to develop.В Eight million people in the U.S.A. are estimated to have undiagnosed Diabetes 2. Cases with undiagnosed diabetes are presented. Case Presentations: Case #1 A 43-year-old, thin woman had three risk factors for Diabetes.В She requested a glucose tolerance test which showed blood glucose of 195 at two hours.В She required daily NSAID or COX II inhibitors for arthritis. This patient did diet and exercise for 15 years until she developed Type II Diabetes with a Hemoglobin A1C of 6.3.В In four months of Actos 15 plus Metformin 500, and a statin, diet, and exercise the patient’s Hemoglobin A1C is 5.4.В Now at 60 years old, she has four risk factors for CAD:В family history, Hypertension, Elevated LDL and DM. Case #2: A 55- year-old RN, survivor of breast cancer has two risk factors for Diabetes with symptoms and В Impaired Fasting Glucose.В A two-hour glucose tolerance test shows glucose of 255 at 90 min. and 279 at 120 min. Case #3: An asymptomatic 58-year-old man had an abnormal CT of the Coronary Arteries.В Cardiac catheterization showed three blocked coronary arteries..В He underwent 3 vessel coronary artery bypass..В His two brothers died suddenly at ages 52 and 53 within a year apart recently. His father died at 50 after heart trouble. The patient had no previous history of metabolic syndrome, high blood pressure, smoking, stress, alcohol.В His fasting blood sugar in this cardiac workup was 180. On day one post surgery the fasting glucose was 150 and HgA1c was 5.4.В His LDL of 117 had been treated for seven years with a statin. Case #4: An obese (BMI В 31) woman age 52 with fasting blood sugars in the 90s seeks a second opinion of ABSTRACTS – Diabetes Mellitus does she have Diabetes?В Another Endocrinologist did a two-hour glucose tolerance test on her two years ago and said she did have Diabetes.В She has lost approximately 10 pounds, В with diet and exercise. В Now her fasting blood sugars isВ 90 andВ the HgA1C is 5.4. Discussion: With Diabetes and Metabolic Syndrome being risk factors for CAD, should endocrinologists and primary care physicians be identifying IGT, IFG, Metabolic Syndrome or DM 2 more aggressively and sooner to decrease C AD as well as diabetic complications?.В An expensive CT of the coronary arteries В В was the starting abnormal test which may have saved an asymptomatic patient’s life. These cases В represent only the tip of the iceberg for redefining our standards and methods of identification of people with Type 2 Diabetes.В Also treatment goals may need to be lowered with more aggressive therapies.В Conclusion:В These cases support a strong argument that can be made for increased detection of DM in young people based on clinical suspicion and the number of risk factors for DM and CAD. by measuring reflection index (RI), a ratio of the heights of the diastolic and systolic components of digital volume pulse (DVP) obtained by using a photoplethysmograph device. Results: Mean values of clinical characteristics in 68 selected subjects were, age 49.9В±2.0 years, body mass index 26.1В±1.0 kg/m2 and duration of diabetes 7.4В±1.0 years. Before study, these parameters as well as glycemic and other laboratory measurements were comparable in all 4 groups (control, RG, EN, RG+EN). After 12 weeks, fasting and post prandial plasma glucose, glycated hemoglobin, fasting insulin and insulin resistance (HOMA-IR), and systolic and diastolic blood pressure improved significantly (p<0.001) in all subjects treated with RG compared to controls. However in subjects on EN alone, there were significant improvements in blood pressure levels but not in glycemic control and insulin levels. In subjects treated with RG+EN, reduction in heart-brahial (hb) PWV (-10.1%), brachial-ankle (ba) PWV (-13.7%) and carotidfemoral (cf) PWV (-16.3%) was significantly (p<0.01) greater than in those on RG alone (hbPWV -8.1, baPWV -9.4 and cfPWV -11.3%). Similarly, RI has also improved significantly (p<0.01) in subjects treated with RG+EN than in those on RG alone (-11.5 Vs.-8.5%). Conclusion: In spite of no discernible effect of enalapril on glycemia, insulin levels or lipids, it has an additive effect on the beneficiary role of rosiglitazone in improving the vascular functions in type 2 diabetes. Enalapril in combination with rosiglitazone was effective in improving vascular function and to possibly decrease cardiovascular complications in patients with type 2 diabetes mellitus. Abstract #250 ENALAPRIL WITH ROSIGLITAZONE IMPROVES VASCULAR FUNCTION IN TYPE 2 DIABETES MELLITUS Sreekanth Reddy Reddem, MBBS, Yashmaina Sridhar, Paturi Bhanu Teja, P. Usharani, P.V. Rao, and M.U.R. Naidu Objective: To assess the effect of enalapril therapy with and without rosiglitazone on vascular function in patients with type 2 diabetes mellitus in a prospective, randomized, double-blind, controlled, and parallel comparative study. Methods: Sixty-eight subjects with type 2 diabetes on stable doses of two oral hypoglycemic agents (metformin 500-750 mg tid and gliburide 5-10 mg bid) attending the Diabetes Care facility at the Nizam’s Institute of Medical Sciences University Hospital in Hyderabad, India, were consecutively recruited. They were randomized into control (n:15), rosiglitazone alone (RG n:17), enalapril alone (EN n:18) and RG+EN (n:18) groups. All subjects in test groups received either rosiglitazone 2 mg bid, enalapril 5 mg bid or both, for 12 weeks. This study was approved by the Institutional Ethics Committee and all patients gave their written informed consent to participate. Vascular function was measured by pulse wave velocity (PWV), an indicator of arterial stiffness using a non-invasive pulse wave analyzing device. Vascular tone was also quantified Abstract #251 DECREASED HOSPITAL ADMISSIONS FOR DKA IN A HIGH RISK PEDIATRIC POPULATION Mark A. Kummer, MD, and Sandra G. Hudson, ARNP Objective: Escambia County, Florida is the poorest county in Florida and the 17th poorest in the USA. After receiving permission from the IRB, a retrospective review of hospital readmissions in the under 18 yr age group for diabetic ketoacidosis was undertaken in May 2006 to assess the quality of the Pediatric Diabetes Program. In 2004, 62 children with known diabetes were readmitted for ketoacidosis: in 2005, there were 61admissions. This reflects 24 admissions for every 100 children followed in the outpatient clinic. Methods: This study targeted high risk patients with the primary goal of decreased hospital admissions over the – 43 – ABSTRACTS – Diabetes Mellitus next year - July 2006 to June 2007. Patients were identified as high risk if they had an admission for DKA in the past year or an hemoglobin A1c above 12% in the clinic. There was considerable overlap in the groups, but not exclusive. This project was accomplished within the limits of the clinic without any new monetary support. All patients from these groups were approached to participate in a high risk protocol which included: monthly clinic visits, weekly review of blood sugars, a review with both the dietitian and diabetes educator, and a visit with the social worker at enrollment to ensure that the patients had adequate diabetes medications and supplies as well as a review of family concerns. Counseling was recommended to all patients and families to identify blocks in compliance with treatment recommendations. A case management team meeting of physicians, nurse practitioners, educators and social worker was held monthly to discuss all current patients and the need to enroll additional high risk patients. Results: Upon enrollment, all families and patients were asked to sign a statement that identified them as being at high risk for diabetes complications or death from diabetic ketoacidosis. They were asked to commit to the blood sugar testing, reporting of blood sugars and clinic visits. During the time of the study, hospital readmissions for DKA dropped to 41 despite a total increase of patients seeking care. Because of a rise in new diabetes patients attending clinic and the decreased number of hospital admissions, the rate of admissions per 100 clinic patients dropped to 13 from 24. During the 2nd quarter of 2006, there were 30 patients with an A1c > 12% whereas, in the 2nd quarter of 2007, the number had dropped to 7 patients. Conclusion: This method has proven effective in lowering hospital admissions over the short term without significant increase in costs to the clinic or hospital. Secondary benefits have been improved coordination and consistency of the care plan for the most complicated patients and fewer patients with very high hemoglobin A1c levels in the clinic. Also, a new sick day management guideline was developed for all clinic patients because of the effectiveness identified in this high risk group. thetic deep pain, disturbingВ sleep and quality of life which brings the mostВ referralsВ to someВ clinics for therapy. It is called “dying back” axopathy because of its ascendance overtime from the toes upward. It predicts foot ulcers with 89% sensitivity. But until now there has been no clinical practical grading scale for its quantification which is clearly needed by the busy clinician (NCNS is not practical in every patient. research grading system exists but difficult to do inВ practice). We devised a practical grading scale, easy to do in the first office visit and every follow up visit within 2 minutes. This is a report ofВ its practical application. Methods: We tested 102 consecutive patients with the 128 Hz tuning fork. We recordedВ the loss of vibration sensationВ at the first office visit and every follow up visit at 10 levels from the hip downward: 1-toes and foot bottom (T),В 2-mid footВ (F),В 3-ankle (A),В 4-lower third of the shin (LS), 5-mid shin (MS),В 6-upper third of shin (US), 7-Knee(K), 8-thigh (TH), 9-hips (H), 10-above the hip (AH). All normal sensory vibration patients were termed NL. Each patient had intermediate outcome measures (FBS, PPG, HgA1C, etc.) tested before and after therapy (which included metabolic control, Trazadone, and adjuvant analgesic). В Results: At baseline, loss of sensory vibration was found in 58 patients (56.8%) at the following variable levels: 1-toes: 8(%13.8)В 2-foot: 8(%13.8) 3-ankle: 8(%13.8) В 4-lower shin: 4(%6.8)В 5-mid shin: 8(%13.8)В 6upper shin: 4(%6.8)В 7-knee: 10(%17.2)В В 8-thigh: 3(%5)В 9hip: 2(%3) 10-above hip: 1(%1.7). В Average FBS was 255, average HgA1C wasВ 9.7%В В В В .В В В В After therapy, loss of sensory vibration clearly improved within 2-4weeks and up to 4 months: 12 patients became normal (NL), 3 were unchanged, 2 became worse. The other 40 have improved at the following variable levels:1-toes: 11(%19).В 2-foot:В В 9 (%15.5).В В В 3-ankle: 5(%8.6)В В 4-lower shin: 4(%6.8)В 5-mid shin: 6(%10) 6upper shin: 2(%3).В 7-knee: 2(%3) 8-thigh: 0В 9-hip: 0 10above hip: 0. Average FBS became 154, HgA1cВ 7.85%. Comparing baseline with after therapy for the total group: FBS decreasedВ 101, HgA1c decreased 1.85%, improvement in sensory vibration by one level was seen in 19 patients (%33),В two levels 16 pt’s (%27.5), three levels 4 pt’s (%6.8), four levelsВ 4 pt’s (%6.8), uncertain level 11 pt’s (%19). When looking at any level of improvement it was seen in 53/58 original patients with neuropathy (91%) Discussion: The striking improvement seenВ in most patients was a very important objective sign to patient and physician. Patients see В improvement correlated with metabolic control, making patients more committed to treatment plan. ItВ guides physician in increasingВ intensity Abstract #252 HOW TO QUANTIFY DIABETIC POLYNEUROPATHY Saad Sakal, MD, FACE Objective: Loss of vibration sensation is an early sign inВ diabetic polynueropathy (DPN), reported in 30% of diabetics by phys. exam,70% by NCVS, as a burning paras– 44 – ABSTRACTS – Diabetes Mellitus levels in the general populace. Results: 365 complete records of type 2 DM patients were identified for the periodВ December 2006 to November 2007.В Mean HBA1c was 7.78+/- 2.73%. The range of HBA1c was 4.0% - 16.7%.В 208 of the HBA1c results were > or = 7.0%, representing a level of 57.0% being in poor control.В Less than 5% of the patients were able to doВ more than 1В HBA1c tests in the year under review due to financial constraints. In comparison 10 male and 10 female adults (volunteers) with normal OGTTs were tested and their HBA1c ranged from 4.0 -5.8%, the mean being 4.59%. Discussion: Glycated Hemoglobin is a relatively expensive test which few patients with DM can afford to do especiallyВ in resource poor countries like Nigeria where more than 50% of the population lives on less thanВ one US dollar per day and less than 10% of the population is covered by health insurance of any kind. Despite limited resources it is interesting that more than 40% of out-patient managed type 2 DM patients have good glycaemic control. Larger local studies require to be carried out to evaluate the correlation between these HBA1c levels and morbidity and to see the effect of different pharmacological and non pharmacological intervention on the HBA1c levels. Conclusion: Diabetes is a major health burden that requires strict glycaemic control to prevent complications. The targets can be achieved with simple and affordable medication and lifestyle modifications which are readily available even in resource poor countries. More widespread use of this simple tool is to be encouraged to help manage DM better. of therapy. TheВ significant percent ofВ reversible componentВ likely relates to glycemic/metabolic control despite diabetesВ duration of years, seems easily documented as early as 2-4 weeks and descending gradually further toward the toes reversing the “dying-back” axopathy in a welcome “living-back” phenomena. we believe this grading scale of sensory vibration (Sakkal Scale) an extremely easy to do, time saving (less than2 minutes), reproducible, correlates well with patient symptoms, metabolic control, easy to document in the chart, to follow up, it improves communicationВ in research and stimulate patient and physician to improve care. Division to 10 levels (metric system) makes the scale easier to administer. In practice most patients (86%) will fall in the first 7 grades. Choosing the absolute loss of vibratory perception for the scale improves application, avoidВ inter observers confusion. Conclusion: Documenting the level of the loss ofВ sensory vibrationВ in diabetic neuropathy is an objective, accurate, easy to implement, time saving, reproducibleВ clinical grading tool ( Sakkal Scale ) which correlates well with patient symptoms and metabolic control В . It improves communication in research and clinical care in most patients with diabetic polynueropathy. Abstract #253 TYPE 2 DIABETES MELLITUS SUBJECTS DIAGNOSED WITHIN ONE YEAR MANIFEST AUTONOMIC DYSFUNCTION SIMILAR TO THOSE WITH DIABETES OF LONGER DURATION Abstract #254 Olufemi Adetola Fasanmade, MBBS, FWACP, Adekunle Adeyemi-Doro, Anthonia Ogbera, Sandra Iwuala, and S.B. Bamiro HBA1C LEVELS IN PERSONS WITH TYPE 2 DIABETES MELLITUS IN LAGOS, NIGERIA Objective: This cross sectional non interventional study was carried out to determine the degree of glycaemic control of patients with type 2 diabetes attending a federal tertiary hospital in the Lagos metropolitan area of Nigeria in West Africa. Methods: All the availableВ medical records of patients with type 2 diabetes mellitus who had been sent for HBA1c testing were studied and basic health statistics and levels of HBA1c were extracted and analysed using Microsoft excel statistical software. (Tests were done using electrophoresis and the effect of Hemoglobin S noted to be minimal). Results (NGSP/DCCT calibrated) were expressedВ as mean +В SD. The number who were within the levels of good control (</=В 7%)В were ascertained. A control (non diabetic) group of volunteers was also tested to ascertain the HBA1c Olufemi Adetola Fasanmade, MBBS, FWACP, Adekunle Adeyemi-Doro, Anthonia Ogbera, and Sandra Iwuala, S.B. Bamiro Objective: This cross sectional non interventional study was carried out to determine the degree of glycaemic control of patients with type 2 diabetes attending a federal tertiary hospital in the Lagos metropolitan area of Nigeria in West Africa. Methods: All the availableВ medical records of patients with type 2 diabetes mellitus who had been sent for HBA1c testing were studied and basic health statistics and levels of HBA1c were extracted and analysed using Microsoft excel statistical software. (Tests were done using electrophoresis and the effect of Hemoglobin S noted to be minimal). – 45 – ABSTRACTS – Diabetes Mellitus Mellitus (DM) was defined by the current ADA guidelines or the need for anti-DM medications, at the time of preLT evaluation, and at 1 week, 4 months and 1 year postLT.В Exclusion criteria included: known DM pre-LT, renal failure prior to LT, prior history of a solid organ transplant, or the initial use of immunosuppressant other than Tacrolimus. Result: A total of 122 patients met study criteria. The overall incidence of NODM post-LT was 95% at 1 week (n=114), 38% at 4 months (n=38) and 34% (n=37) at 1 year. Intriguingly, of the 35% (n=43) of patients were classified as NODM at both1 week and 4 months post-LT, 85% (n=35) remained diabetic at 1 year post-LT. The odds ratio for NODM in subjects with alcoholic liver disease was 8 fold of that autoimmune hepatitis. In univariate analysis the significant predictors of NODM (p < 0.05) were the etiology of liver disease, family history of diabetes, severity of liver disease (MELD score), male gender. Age, race and body mass index were not significantly associated with NODM. Discussion: The rationale for identifying NODM at 1 week, 4 months and 1 year post-LT is to account for the steroid treatment regimen.В In general, patients undergoing LT, receive steroid boluses immediately post-LT, then are discharged home on a tapering steroid dosage, to be discontinued at 4 months. Conclusion: Patients undergoing LT are at high risk for developing NODM. Those who have diabetes at 4 months post LT are very likely to continue to have diabetes at 1 year. The risks for persistent NODM at 1 year post-LT include: underlying etiology, notably alcoholic liver disease, family history of DM, male gender and high MELD score. Results (NGSP/DCCT calibrated) were expressedВ as mean +В SD. The number who were within the levels of good control (</=В 7%)В were ascertained. A control (non diabetic) group of volunteers was also tested to ascertain the HBA1c levels in the general populace. Results: 365 complete records of type 2 DM patients were identified for the periodВ December 2006 to November 2007.В Mean HBA1c was 7.78+/- 2.73%. The range of HBA1c was 4.0% - 16.7%.В 208 of the HBA1c results were > or = 7.0%, representing a level of 57.0% being in poor control.В Less than 5% of the patients were able to doВ more than 1В HBA1c tests in the year under review due to financial constraints. In comparison 10 male and 10 female adults (volunteers) with normal OGTTs were tested and their HBA1c ranged from 4.0 -5.8%, the mean being 4.59%. Discussion: Glycated Hemoglobin is a relatively expensive test which few patients with DM can afford to do especiallyВ in resource poor countries like Nigeria where more than 50% of the population lives on less thanВ one US dollar per day and less than 10% of the population is covered by health insurance of any kind. Despite limited resources it is interesting that more than 40% of out-patient managed type 2 DM patients have good glycaemic control. Larger local studies require to be carried out to evaluate the correlation between these HBA1c levels and morbidity and to see the effect of different pharmacological and non pharmacological intervention on the HBA1c levels. Conclusion: Diabetes is a major health burden that requires strict glycaemic control to prevent complications. The targets can be achieved with simple and affordable medication and lifestyle modifications which are readily available even in resource poor countries. More widespread use of this simple tool is to be encouraged to help manage DM better. Abstract #256 Abstract #255 DIABETIC AND NON-DIABETIC SALIVA ALPHA AMYLASE ACTIVITY INCREASED IN ACID MEDIA THE INCIDENCE AND RISK FACTORS OF NEW ONSET DIABETES MELLITUS POST LIVER TRANSPLANTATION Tarig Sayed Mustafa Arbab, MD, MSc, DIC Mae Sheikh-Ali, MD, Lina Aguirre, MD, Shon Meek, MD, PhD, Rebecca McNeil, PhD, and Andrew Keaveny, MD Objectives: To study pH changes during saliva alpha amylase activity in diabetic and non diabetic subjects in relation to glucose yielding. Explain mechanism of action and occurrence of DKA.В Methods: 750 fresh saliva samples were collected from 200 diabetic and 50 non-diabetic subjects. All subjects were fasting over night for 12 hours. Glucose oxidase testing was used to detect amylase activity. Three identical 10 mls samples of fresh well-prepared saliva were accepted from each patient for the study. One sample from Objective: 1-To determine the incidence of new onset diabetes mellitus (NODM) in patients who have undergone liver transplantation (LT)В 2-To follow the progression and transition of NODM over the first year post-LTВ 3-To identify risk factors for the development of NODM post-LT Methods: A retrospective review of 275 LTs was conducted at the Mayo Clinic in Jacksonville from 2004 to 2005.В Patients were followed for 12 months. Diabetes – 46 – ABSTRACTS – Diabetes Mellitus cose yielding in 24 hours (absent amylase activity).В Zero non diabetic samples, same subject showed absent amylase activity for both flour and sucrose. Decrease in pH in study samples was noticed to be associated with increase in glucose yielding. 92% of study samples showed decreased pH 5 > in association with high glucose readings (250 – 500 mg/dl or more). Discussion: Significant but nonspecific elevations of amylase can be seen in DKA (Diabetes Care 26:31933194, 2003). Similarity between DKA and this study in terms of increased acidity in the presence of elevated serum amylase, and in association with high glucose from degradation of disaccharides / polysaccharides particles that could exist in slightly larger amounts in the blood of diabetic compared to non diabetic subjects (persorption phenomenon - Gerhard Volkheimer). Conclusion: Saliva alpha amylase activity should be determined in relation to pH media. Saliva alpha amylase is active in acid media. Correction of stomach pH and or abnormal amylase activity could help treat / prevent diabetes and obesity. each subject was used as marker and tested for pH changes and sugar hourly for 24 hours. Each second and third study samples were tested initially for pH and sugar content; 1 ml of flour powder was added in each second sample (250 flour sample). 1 ml of sucrose was added in each third sample (250 sucrose samples). pH changes together with sugar readings were tested hourly in each study sample for 24 hours. Results: 750 (250 marker + 250 flour + 250 sucrose study sample) fresh saliva samples of non diabetics and diabetic patients showed pH of 9 to 7 on immediate testing. 250 marker samples showed no significant change in pH and zero sugar reading for 24 hours. 235 flour, 223 sucrose study samples showed decrease in pH 5 >, in association with glucose detection in samples. 2 flour and 2 sucrose samples showed decrease in pH from 9 to 7 in association with glucose yielding within 24 hours. 8 isolated flour, 11 isolated sucrose diabetic samples, 4 same patient flour and sucrose diabetes samples, 5 flour and 14 sucrose non diabetic samples showed decrease in pH 5 > without glu- – 47 – ABSTRACTS – Hypoglycemia HYPOGLYCEMIA Abstract #301 Abstract #300 TIME FACTOR IN INSULIN OVERDOSE ADULT NESIDIOBLASTOSIS IN A PATIENT WITH PAST EVIDENCE OF INSULINOMA Monica Agarwal, MD, and Steven Elbein Objective: Hypoglycemia induced by exogenous insulin often occurs accidentally in diabetic patients but many cases of insulin overdose are self inflicted by depressed persons with intent of suicide.В We report a case of patient who injected a massive dose of insulin with prolonged hypoglycemia.В Case: 47y/o Caucasian male with depression and Type 2 diabetes on insulin presented to emergency room (ER) with low blood glucose.В Earlier that night the patient had injected subcutaneously 11,000 units of Neutral Protamine Hagedorn insulin in the abdomen. He had purchased 10 ml syringes on the internet. As an hour passed by after injecting insulin, he changed his mind and decided that he needed to go to ER.В He presented to ER after raising his glucose by drinking pancake syrup. In the ER, his blood glucose was 48 mg/dL; serum insulin level was 6194 uIU/dL. He received intermittent boluses of D50 and was started on D10. Over the first 24 hours he required 450 gms of glucose intravenously in addition to generous oral intake.В His blood glucose ranged from 50 to 75 mg/dL. He required intravenous glucose for eight days. Insulin levels were measured for nine days. The insulin decay curve was nonlinear as suggested in the literature. Discussion: To our knowledge this is the first case reported of NPH insulin overdose of this magnitude. This case is unique as the patient injected 11,000 units of NPH insulin and required intravenous dextrose for eight days.В Intermittent hypoglycemia continued for 232 hours. The serum insulin level was not related with the severity of the hypoglycemia. The intensity of hypoglycemia seems to be independent of the dose or the type of insulin, but the duration of hypoglycemia and dose do appear to be related.В The time course of our patient reflects that relationship. The prolonged hypoglycemia could be related to delayed absorption from the injection site. The buffering effect of antibodies present in many diabetic patients may delay clearance. The case confirms the exceptionally long half life of insulin in such settings. In insulin overdose the serum glucose level should be carefully monitored and glucose infusion rate accordingly adjusted because insulin levels are continuously changing.В The patients who attempt suicide with insulin may repeat the attempt using the same method so other therapeutic approaches should be considered. Eshraq Nazir Aljaghbeer, MBBS, Sant P Singh, MD, and Ahmad Khraisat Sidney Cruz, MD Objective: To report a case of recurrent hyperinsulinemic hypoglycemia, secondary to adult nesidioblastosis, in a patient with previous evidence of insulinoma. Case presentation: In 1978, a 22 year old woman was diagnosed with insulinoma. A 2 cm solitary insulinoma was enucleated and patient remained asymptomatic. In 2002, she experienced progressive neuroglycopenic symptoms after meals. In 2003, patient presented to ER unconscious, plasma glucose was 28mg/dl, insulin 64mIU, proinsulin 28pmol/l, c-peptide 1.1ng/ml and plasma sulfonylurea was negative. Localization studies were negative for insulinoma, patient underwent partial (80%) pancreatectomy. Histological examination was characteristic for nesidioblatosis. Post-operative recovery was uneventful. Two months later, 5 hour OGTT was normal.В Subsequently, during three and a half years of follow-up, the patient remained euglycemic. Discussion: Nesidioblastosis is a descriptor of the morphologic findings of B cells associated with hyperinsulinemic hypoglycemia in the absence of an insulinoma. These morphologic abnormalities include; hypertrophic islets’ B cells, close association of islet cells with small pancreatic ducts and an abnormal aggregation of islets. It is the most common cause of Persistent Neonatal Hyperinsulinemic Hypoglycemia. In adults, Insulinoma is the most common cause. A relationship between the hyperfunction pathology conditions of B cell was not identified as yet. В Adult patients with nesidioblastosis characteristically present with neuroglycopenic symptoms within a short period of meal ingestion, but have negative hypoglycemic response to a 72-hour fast. After excluding an insulinoma by imaging studies, selective arterial calcium-stimulation test (SACST) can be helpful in differentiating nesidioblastosis from insulinoma. Diagnosis requires histopathological verification. Treatment is operative reduction of the B cell mass with guidance by SACST. Conclusion: Nesidioblastosis should be considered in a patient with previous evidence of insulinoma, presenting with recurrent hyperinsulinemic hypoglycemia. We raise the question of a common etiology causes both disorders. – 48 – ABSTRACTS – Hypoglycemia Conclusion: Insulin overdose and suicidal intent is more common than thought and should be considered in diabetic patients with unexplained hypoglycemia. Physicians should be prepared for persistent and recurrent hypoglycemia. Delay in therapy is an important prognostic factor. are not different from a typical insulinoma, the diagnosis, however, is usually delayed until proinsulin measurement is made. As in other reported cases, measurements of proinsulin, but not insulin, established the diagnosis. Abstract #302 RESTORATION OF HYPOGLYCEMIA AWARENESS AFTER ISLET TRANSPLANTATION Abstract #303 ABNORMAL EXPRESSION OF THE PRO-PROTEIN CONVERTASES 1/3 (PC1) AND PC2 IN HUMAN INSULINOMAS, THE SO CALLED “PROINSULINOMAS” Cristiane Bauermann Leitao, MD, Pablo Cure, Antonello Pileggi, David A. Baidal, Thipaporn Tharavanij, Davide Mineo, Karina Bernetti, Raquel N. Faradji, Tatiana Froud, Aleida Saenz, Camillo Ricordi, and Rodolfo Alejandro Daniel Cuevas-Ramos, MD, Francisco J. GГіmez-PГ©rez, Paloma Almeda-ValdГ©s, Xeily Zarate-Diaz, Alejandro Zentella-Dehesa, Jose Luis Ventura-Gallegos, Norma Uribe-Uribe, and Juan Rull Objective: To determine if optimal metabolic control achieved by islet transplantation has sustained effects on hypoglycemia unawareness. Methods: A retrospective cohort study was conducted in 29 subjects followed before and after allogenic islet transplantation as treatment for unstable type 1 diabetes mellitus. Hypoglycemia unawareness was accessed through a validated questionnaire (Clarke score; score = 0 if no reported hypoglycemia; score ≥4 = hypoglycemia unawareness) before and at end of follow-up. A stratified statistical analysis was performed based on graft function: off-insulin (n = 8), graft dysfunction (back on insulin and stimulated C-peptide ≥0.3 ng/ml, n = 13) and graft failure (stimulated C-peptide <0.3 ng/ml, n = 8, 5.5 В± 6.2 months after failure). Results: The hypoglycemia score was lower after islet transplant (1.11 В± 1.52 vs. 5.41 В± 1.52, P <0.001) and an increment in the threshold for hypoglycemic symptoms was observed (60.28 В± 7.9 vs. 42.5 В± 18.7 mg/dl, P = 0.001), as expected. Lower hypoglycemic score values were correlated with better beta cell function (r = -0.522, P = 0.004 and r = 0.605, P = 0.001 for stimulated C-peptide and glucose levels, respectively). These results were sustained even after patient’s stratification based on islet function (off-insulin–pre: 5.63 В± 2.00 vs. post: 0.00 В± 0.00, P <0.001; graft dysfunction–pre: 5.31 В± 1.49 vs. post: 1.23 В± 1.59, P <0.001 and graft failure-pre: 4.86 В± 1.35 vs. post: 2.14 В± 1.57, P = 0.004). Discussion: The recovery of awareness found in offinsulin and graft dysfunction groups was predictable and probably related to islet function. In patients with graft failure it is possible that the due to avoidance of hypoglycemia during the early post-transplant period lead to reestablishment of alert hypoglycemic symptoms. Objective: The mechanism of the over production of proinsulin by proinsulinomas is unknown. Since the normal processing of proinsulin to insulin involves PC1/3 (75%) and PC2 (15%), the aim of the study was to analyze the expression of PC1/3 and PC2 in one proinsulinoma and one benign insulinoma. Methods: Western blot with anti-PC1/3 and anti-PC2 antibodies was done in both islet-cell tumors; and used normal pancreatic tissue from each patient, from mice and an islet-cell culture (RINmsf) as control. Results: Immunoblot in both tumors’ cells detected specific molecular bands for PC1/3 at 80kDa and for PC2 at 65kDa. An increased expression of PC1/3 (3-fold) and PC2 (15-fold) was detected in both tumors but not in controls. Interestingly, we found a second specific band expression for PC1/3 of lower molecular weight (75kDa) only in the proinsulinoma. Discussion and Conclusions: The immunoblot results indicate that in both tumors, the activity of PC1/3 and PC2 is increased. In addition, we found an abnormal expression of PC1/3 only in the proinsulinoma. It is plausible that a structural alteration of PC1/3 explains a lower molecular weight and enzymatic activity of this protein, and therefore a defective processing of proinsulin to insulin. The decreased activity of PC1/3 is not overcome by the overexpression of PC2 and, the proinsulinoma, in turn, releases more proinsulin to the circulation. Although the results need confirmation, the enzymatic abnormality of PC1/3 found in this study seemed to be exclusive of proinsulinomas. If confirmed, a new subtype of islet-cell tumors with different physiopathology and diagnostic approach should be considered. Although the clinical behavior and treatment – 49 – ABSTRACTS – Hypoglycemia Conclusion: Stable metabolic control achieved with clinical islet transplantation restores hypoglycemia awareness and these effects have persisted even after islet graft failure. 72-h fasting test has been illustrated in some patients with insulinoma. It is also possible that early in the treatment of panhypopituitarism and central adrenal insufficiency with corticosteroid, patients might have relative hyperinsulinemia resulting in misleading 72-h fasting test. An inconclusive fasting test should be interpreted in the light of clinical picture. Abstract #304 RECURRENT HYPOGLYCEMIA IN HYPOPITUITARISM TREATED WITH CORTICOSTEROID. Abstract #305 PROINSULIN-SECRETING ISLET-CELL TUMOR AS A CAUSE OF ORGANIC HYPOGLYCEMIA, OUR FOURTH CASE Tasma Harindhanavudhi, MD, Tanyanan Tanawuttiwat, MD, Tarita Thomas, MD, Barnard San Gabriel, MD, Tahira Yasmeen, MD, Dan Mihailescu, MD, and Joseph Kowalczyk, MD Daniel Cuevas-Ramos, MD, Francisco J. GГіmez-PГ©rez, Paloma Almeda-ValdГ©s, Xeily Zarate-Diaz, Norma Uribe-Uribe, and Juan Rull Introduction: Fasting hypoglycemia is a serious condition which can potentially cause substantial morbidity and even death. Frequently, there is difficulty in diagnosis, localization and management due to failure to recognize each of the clinical syndromes. We describe a case of hypoglycemia related to endogenous hyperinsulinemia in a patient with panhypopituitarism. Case description: A 60 years old lady with neurosarcoidosis previously treated with prednisone presented with generalized seizures associated with hypoglycemia. Physical examination was unremarkable. Laboratory data showed low blood glucose. Patient was also found to have panhypopituitarism. She was treated with stress doses of hydrocortisone for adrenal insufficiency, followed by levothyroxine replacement. However, she continued to have hypoglycemic episodes. 72-h fasts revealed a low glucose level of 40 mg/dl with concomitant inappropriately elevated insulin (7 uIU/ml), pro-insulin (19.5 pmol/L) and C-peptide (3.7 ng/ml) levels. Similar results were obtained during a spontaneous hypoglycemic episode 5 days after admission which also was consistent with endogenous hyperinsulinemia. Sulfonylurea screen was negative. The possibility of a coexistent insulinoma was considered. Abdominal CT scan, MRI, endoscopic ultrasound and octreotide scintigraphy, were all unable to localize a tumor. She was transferred to a tertiary center where repeat imaging studies including celiac-splenic angiogram failed to show any focal tumors. Patient also underwent a second 72h fasting which was reported within the normal limits. She was discharged home on hydrocortisone and levothyroxine replacement therapy and so far remained asymptomatic. Discussion: Insulinoma is the most common cause of hyperinsulinemic hypoglycemia. A “normal” standard Objective: To report a case of a proinsulinoma. Case presentation: a 46-year-old woman was studied for organic hypoglycemia. The patient had a five year history of dizziness, confusion, seizures and a weight increment of 26 lbs. В She underwent a supervised fast that produced symptomatic hypoglycemia (20mg/dl) after 7 hours. During the entire fast test, insulin, using an ultraspecific assay, remained lower than 3ОјU/ml (2.2В±0.7) when glucose was <50mg/dl. Urinary sulphonylureas were negative and C-peptide was high normal (3.3В±0.7ng/ml, 0.8-3.9). Circulating proinsulin was persistently and significantly high (>200В±0.0pmol/L, nl<18) during the test. An abdominal MRI and endoscopic ultrasound confirmed the presence of a 2.5 cm tumor in pancreatic head. The patient underwent surgical resection. Interestingly, the immunohistochemistry staining for proinsulin was stronger than insulin inside the tumor. Discussion: The biological activity of proinsulin is estimated to be only 5-10% of that of insulin. Nevertheless, some authors suggest that the hyperproinsulinemic state amplifies the biological activity of this peptide and, consequently, serum glucose levels decrease. This appears to be a reasonable explanation for the findings in our patient. We were surprised that of our last consecutive cases of organic hypoglycemia, 4 out of 5 appeared to be proinsulinomas. This fourth case shares similar clinical and biochemical characteristics of the other three previously reported. Conclusion: The measurement of proinsulin levels may disclose the etiology of organic hypoglycemia in patients with islet-cell tumor and normal intact insulin levels. – 50 – ABSTRACTS – Hypoglycemia puted tomography was performed and found with a small lesion at the tale of the pancreas. During exploratory laparotomy, a lesion (1.2x0.5x0.7cm) found by palpation and small portion of the tale of the pancreas (1.5x0.6x0.6cm) was removed. After the surgery, half hour, and one hour later the blood sugar levels were138 and 132mg/dL, respectively. One month after the surgery, a repeat fasting blood sugar was found on 49mg/dL, insulin 66.2uIU/mL, and C-peptide 9.4ng/mL, with recurrence of symptoms. The pathology failed to report any endocrine tumor, but it did revealed findings consistent with the adult form of nesidioblastosis. The patient was started in Diazoxide with improvement В in glycemia and symptoms. The possibility of a more extensive pancreatectomy is being discussed. Discussion: Nesidioblastosis is the most common cause of neonatal hyperinsulinemia but is rare in adults accounting for 0.5-7% of all causes of hyperinsulinemia. Pathologic findings are primarily islet cell hyperplasia that is found in close contact with acinar ducts. Our patient’s history and findings were consistent with these pathologic findings, but they have also been described in nontumor pancreatic tissue of patients with insulinomas. As the report failed to demonstrate pathologic findings of an insulinoma, and the patient had recurrence of symptoms and biochemical evidence of hyperinsulinemic hypoglycemiaafter the lesion was removed, we made a diagnosis of nesidioblastosis. Conclusion: Although a very rare disorder in adults, nesidioblastosis should be considered as a differential diagnosis when evaluating a patient with hyperinsulinemic hypoglycemia, even in the presence of a pancreatic mass. Abstract #306 NESIDIOBLASTOSIS: A RARE CAUSE OF NONINSULINOMA PANCREATOGENOUS HYPOGLYCEMIA SYNDROME IN ADULTS Marielba Agosto, MD, Monica Santiago, MD, Jose Garcia Mateo, MD, Margarita Ramirez, MD, Myriam Allende, MD, and Vilma Rabell, MD Objective: To report a case of an adult male patient in Puerto Rico with nesidioblastosis. Case Presentation: A 54-year old man referred after he was found with a fasting glucose of 40mg/dl during work up for hypoglycemia. The patient refers that since one year ago, had been experiencing weight gain, intermittent cold sweats, dizziness, blurred vision, and tumescence, which were relieved with carbohydrates ingestion. The episodes occurred both at fasting and postpandrially, and he denies insulin administration. Medical history was negative for peptide ulcer disease or gastrointestinal surgical procedures, family history was negative for endocrine tumors and physical examination was unremarkable. Repeated fasting blood sugar 39mg/dL(60-100 mg/dl), with concomitant insulin levels:24.09uIU/ml(1.9-23 uIU/ml), proinsulin levels:34.1pmol/L(1.8-18pmol/L), b-hydroxybutarate 0.5 mmol/L (> 2.7mmol/L), C-peptide: 4.4 ng/mL (1.1-5 ng/mL), a negative serum sulfonylurea screen and negative serum insulin antibodies. An insulinoma was considered to be the etiology, but abdominal magnetic resonance, computed tomography, and indium octreotide scan were all negative. An abdominal arteriogram with a com- – 51 – ABSTRACTS – Lipid Disorders experiments have shown competitive inhibition of binding between HCV and LDL receptor by LDL thus low LDL actually helps the virus to gain entry into the hepatocyte. Deficiency of MTP also causes low Apo B and that could be involved in the pathogenesis of steatosis in chronic Hepatitis C. No significant difference has been seen in the levels of triglycerides. Conclusion: Lower LDL cholesterol and BMI is seen soon after the HCV infection is diagnosed regardless of degree of fibrosis. The cardiovascular benefits of this are still unproven. LIPID DISORDERS Abstract #400 UNDETECTABLE LDL CHOLESTEROL IN DIABETIC WITH HEPATITIS C Suchitra V. Zambare, MD, and Hamdee Attallah Objective: To understand the interactions between chronic hepatitis C and lipid metabolism. Case-Presentation: A 56-year-old African American male with Hepatitis C related to prior IV drug abuse was seen for evaluation and treatment of recently diagnosed type 2 diabetes mellitus. В He was originally on NovoLog 70/30 mix 15 units twice daily and metformin 500 mg twice a day but experienced repeated hypoglycemic episodes on this regimen. He denied polyuria or polydipsia. He had loss of appetite, fatigue and weight loss for the last 3 months. Insulin was gradually tapered off because of his symptoms, and his HbA1c was 6%. Abstract #401 STATINS IN CLINICAL PRACTICE: USE OR OVERUSE? Mohsen Eledrisi, MD, FACE, Analyn Crisostomo, Omran Joosub, Elsayed Bakry, and Mohammed Sultan Objective: Statins are commonly prescribed in clinical practice. We aimed at assessing the appropriateness of prescribing statins by physicians. The guidelines recommended by the national cholesterol education program adult treatment panel (ATP-III) were used as a quality control tool to determine if statin therapy was properly indicated. Methods: The study was conducted at the National Guard medical city in the eastern region of Saudi Arabia. Patients using statins were identified from the pharmacy’s computerized system of physicians’ prescriptions. Medical charts of those patients were reviewed and data collected on, age, sex, medical conditions, LDL-cholesterol levels, risk factors of coronary heart diseases (CHD), including family history of CHD, smoking history, and HDL levels, and indication for initiating statins. Target LDL-cholesterol levels and need for drug therapy was assessed according to ATP-III guidelines. Results: A total of 885 patients were identified. Patients’ primary diagnosis was as follows: hypertension 77 %, diabetes 13 %, coronary artery disease 1 % and dyslipidemia 9 % (had 0-1 risk factors). Using the ATP-III criteria for initiating drug therapy, statins were appropriately prescribed for 30 % of patients with hypertension, 95 % of patients with diabetes, and 100 % of patients with CHD. All clinical decisions to start statins for patients with the diagnosis of dyslipidemia were not supported by evidence (those patients had LDL levels that did not meet the criteria for drug therapy). Discussion: Dyslipidemia is well-recognized as an important risk factor for coronary heart disease. Statins have shown significant impact on cardiovascular disease PHYSICAL EXAMINATION: BP:120/ 70, P: 80, R/R: 20, BMI 23.8. Examination was unremarkable except for the appearance of fatigue and a thin body habitus. LABS: Electrolytes normal, BUN12mg/dL (7-20), Cr 0.6mg/dL (.6-1.3), Cholesterol 50mg/dL (100-200), triglycerides 12mg/dL(35-160),HDL 26mg/dl (>39) LDL could В not be calculated. Total bili 0.4mg/dL (0-1.5), alk phos 52u/L (50-185), albumin 3.3g/dL (3.5-5.2), AST 23u/ L (0-60), ALT 40u/L (0-65), Apo-lipoprotein-B < 35mg/ dL (52-109) Discussion: Studies have reported 5 times higher prevalence of hypocholesterolemia and hypo-betalipoproteinemia in patients with HepatitisC infection than the general population. The mechanism by which HCV infection may lower serum cholesterol is not known. Microsomal Triglyceride Transfer Protein (MTP) is necessary for assembly and secretion of VLDL cholesterol from the hepatocytes. It has been demonstrated that hepatic overexpression of HCV core protein causes a marked reduction of MTP activity and results in decreased secretion of VLDL cholesterol. These are the mechanisms postulated to explain the lower VLDL and LDL cholesterol production that can occur with hepatitis C infection. Particles of HCV exist bound within lipoprotein particles. It is suggested that the LDL may protect the virus from the inactivating antibodies. Thus a reduction in serum LDL cholesterol may serve as a defense mechanism against hepatitis C infection. On the contrary it has been reported that HCV binds to the LDL receptor in order to gain entry into the hepatocyte and – 52 – ABSTRACTS – Lipid Disorders and are one of the most commonly used drugs worldwide. The National Cholesterol Education Program adult treatment panel (ATP-III) recommends specified target levels for LDL-cholesterol that vary according to the patient’s risk for coronary heart disease. Our data showed that in this Saudi population, statins were appropriately prescribed for patients with CHD, CHD equivalent and those at high risk for CHD (2 or more risk factors). However, in the majority of lower risk patients (those with 0-1 risk factors) the use of statins was not supported by evidence. Conclusion: In this study, clinical decisions were appropriate to initiate statins in the majority of patients with diabetes, those with CHD and those with 2 or more CHD risk factors. However, most patients with 0-1 risk factors were prescribed statins with no justification. Physician education and focused quality improvement programs are needed to improve the patterns of statins prescriptions. Discussion: ABL (Bassen-Kornzweig syndrome) is a rare autosomal recessive disease. Clinical manifestations result from malabsorption and defective transport of lipids and fat soluble vitamins (A, D, E, and K). In our patient ABL presented as a failure to thrive in infancy with steatorrhea. В An unusual feature of this case was that the patient had no neuromuscular or ocular manifestations, possibly related to initial compliance with vitamins during childhood. Her family history revealed normal lipid profiles in both parents indicating an unusual inheritance of this disorder. Patient had no prenatal care and was noncompliant with vitamin therapy. Vitamin K deficiency was responsible for the coagulopathy in this patient causing postpartum hemorrhage. Fortunately our patient had a normal neonatal outcome despite several abnormal fetal effects reported with fat-soluble hypovitaminosis. Conclusion: This is the first reported case in literature with life threatening postpartum bleeding in a patient with abetalipoprotenemia. Expecting patients with ABL should be counseled. Clinicians should make sure that laboratory studies (serum retinol levels, coagulation panel) are normalized and maintained for a favorable pregnancy outcome. Abstract #402 ABETALIPOPROTENEMIA WITH POSTPARTUM HEMORRHAGE Seema Haq, MD, Mary Baker, Hal Scofield, and Sadaf Saghier Abstract #403 Objective: The purpose of this case report is to review the management of abetalipoprotenemia (ABL) and its impact on pregnancy and fetal outcomes. Case Presentation: A primigravid 24-year-old with history of abetalipoprotenemia presented with early postpartum hemorrhage and hemodynamic instability after vaginal delivery at 37 weeks of gestation. Infant was delivered at home by midwife with proper delivery of placenta. Patient denied any history of coagulation disorders, excessive bleeding with surgical procedures, menorrhagia or being on any medications. Her family history was unremarkable. Physical examination revealed a pale, lethargic, tachycardic (pulse rate 110 beats/min), afebrile, and hypotensive (BP 70/40 mmHg) patient.В Abdomen was mildly distended and non-tender. Genital examination revealed left vulvular hematoma at the episiotomy site oozing bloody serous fluid. Laboratory studies showed INR 7.7 (0.9-1.2), PT 72.4 (9.5-12), PTT 83.6 (24-34) and hemoglobin 5 gms (12-16), acanthocytosis and normal platelet count. She had abnormal lipid and lipoprotein profile consistent with history of ABL. Patient was stabilized with PRBC, IV fluids and subcutaneous vitamin K. Perineal hematoma was managed conservatively. Infant evaluation was reported normal by the pediatrician. Patient did well and was discharged home on modified regimen of fat-soluble vitamins. HYPERLIPIDEMIA IN SYSTEMIC LUPUS ERYTHEMATOSUS Sudip Nanda, MBBS, Rohini Handa, MD, and Surya Prakash Bhatt, MD Objective: Premature atherosclerosis is increasingly recognized in systemic lupus erythematosus (SLE) and other autoimmune disorders. Hyperlipidemia in SLE is due to both the disease and its treatment. We hypothesized that patients with SLE have a high frequency of hyperlipidemia and aimed to estimate its frequency and determinants. Methods: 103 consecutive SLE patients fulfilling the American College of Rheumatology 1997 criteria were included in this cross-sectional observational study conducted at a tertiary referral center. Patients with diabetes mellitus; age<16 years; overlap syndromes; pregnancy; statin use; with other defined causes of hyperlipidemia like hypothyroidism, liver disease and familial were excluded. Variables studied included age, sex, BMI, menopausal status, smoking, alcohol use, nephrotic syndrome, disease duration, and use of steroids and hydroxychloroquine (HCQ). SLE Disease Activity Index (SLEDAI) assessed the disease activity with SLEDAI>16 being severe disease. – 53 – ABSTRACTS – Lipid Disorders and beta-blocker use, and disease severity. Nephrotic syndrome was more common in patients with hyperlipidemia (16.1% vs 2.9%; p=0.03). Severe disease, present in 25%, was associated with significantly elevated TG (210В±118 vs. 154В±109 mg/dl, p=0.03). Those on steroids and HCQ had a lower apo B compared to those on steroids only (81В±29 vs. 108В±46 mg/dl, p=0.01). Discussion and Conclusion: Hyperlipidemia is a frequent occurrence in this young, predominantly pre-menopausal cohort of lupus patients. It should be routinely tested and aggressively treated. Fasting lipid profile included total cholesterol, LDL-C, VLDL-C, HDL-C, TG, ApoA and ApoB. Borderline high for any one of the 5 lipid parameters of the NCEP-ATP III guidelines was used to define hyperlipidemia. Results: Mean age was 32.9+10.7SD years. 97(94%) were females of whom 88.7% were pre-menopausal. 68(66%) patients had hyperlipidemia. 30(44%) had elevated LDL-C, 40(59%) had elevated VLDL-C, 41(60%) had hypertriglyceridemia and 33(49%) had low HDL-C. There were no significant differences between those with hyperlipidemia and those without, in age, sex, presence of lupus nephritis, duration of disease, oral prednisone HCQ – 54 – ABSTRACTS – Metabolic Bone Disease PREVALENCE OF VITAMIN D DEFICIENCY AMONG ACUTE HIP FRACTURE PATIENTS IN A NEW ENGLAND HOSPITAL hip fractures.В History of a previous fracture as a risk factor for future fractures is still under-recognized in the medical community.В Increased awareness can lead to efforts to modify risk factors including vitamin D deficiency.В Identifying and treating these patients with vitamin D may help prevent future fractures and the significant morbidity associated with them. Akta Patel Mukherjee, MD, and Suzanne Rieke, MD Abstract #501 Objective: To determine the prevalence of vitamin D deficiency in patients presenting with acute hip fracture in a New England Hospital. Methods: This study was a retrospective analysis of 117 patients who presented with acute hip fracture from November 2004 to January 2006 to Lahey Clinic in Burlington, Massachusetts.В An endocrinology consultation assessed risk factors for osteoporosis including a 25hydroxyvitamin D (25OHD) for all of these patients. Results: Ninety patients (76.9%) with acute hip fracture were women, and mean age was 80.3 years.В With a 25OHD of <30ng/ml, 109 patients (90.6%) presenting with acute hip fracture were vitamin D insufficient.В Seventythree patients (62.4%) were vitamin D deficient, with a 25OHD <20ng/ml.В Mean serum calcium was 8.5mg/dl among all patients.В The mean parathyroid hormone level in the 15 patients assessed was 57.8pg/ml.В Fifty patients (42.7%) reported a history of osteopenia or osteoporosis, and 63 subjects (53.8%) had a history of previous fracture.В В Twenty-four patients (48%) with osteoporosis prior to admission were vitamin D deficient compared to 49 patients (73.1%) without osteoporosis.В However, of the 63 patients with a history of fracture, 43 subjects (68.3%) were vitamin D deficient compared to 30 of 54 patients (55.6%) without a fracture history. Discussion: The health consequences of vitamin D deficiency have been increasingly recognized, including the greater risk of fractures.В Our study demonstrates the continued high prevalence of vitamin D deficiency among patients presenting with a hip fracture.В The majority of patients presenting to our hospital with hip fracture, even with history of a previous fracture, were vitamin D deficient.В Patients with osteoporosis or osteopenia were less likely to be vitamin D deficient, because they are often advised to start calcium and vitamin D.В However, history of fracture is not identified as an osteoporosis risk equivalent that is aggressively treated with vitamin D. В The new emphasis on fracture risk assessment will help address this issue and identify patients at high risk of complications from vitamin D deficiency. Conclusion: This study reinforces the high prevalence of vitamin D deficiency in patients presenting with FLUORESCENCE-GUIADED PARATHYROIDECTOMY IN SECONDARY HYPERPARATHYROIDISM: FIRST CASE OF LATIN AMERICA METABOLIC BONE DISEASE Abstract #500 Pedro E Morales, MD, Franklin GarcГa, MD, Lavi Jasson, MD, and Monsalve Laura, MD Objective: Develop the technique of the fluorescence – guiaded parathyroidectomy in patients with secondary hyperparathyroidism. Case presentation: Female patient, 29 years old, with systemic lupus eritematous since 10 years. Chronic renal failure since 5 years, with dialysis since 2 years. Se refers bone pain, 1 year of evolution, and deformation in fingers of hands. Also, diagnosis of multinodular goiter the last year. Serum parathormone in 6500 pg/ml, alkaline fosfatase 380 U/L, serum calcium 10.5 mg/L, serum phosphorus 4.0 mg/L. Ultrasound of neck showed thyroid increased and nodular image suggesting right superior parathyroid gland. Photosensitization was with 5-aminolevulinic acid, dose 30 mg/Kg, diluted in 250 cc of water, oral way, 4 hour before the procedure. The patient stayed in dark room. We did total thyroidectomy, total parathyroidectomy and transcervical subtotal timectomy. The surgical procedure begins with cervicotomy. Then, exposition of posterior side of thyroid lobules. First, we used white light without recognize the parathyroid glands. Then, we used blue light wavelength between 380-440 nm (D-Light System, Karl Storz Co) by 3 minutes and we can recognize 4 structures with selective red fluorescence corresponding to 4 parathyroid glands. The pathology analysis showed 4 parathyroid glands (the same structures identified with fluorescence) with hyperplasia; the thyroid gland showed adenomatous hyperplasia; the timic specimen showed not alterations. The evolution of patient was satisfactory. Only one adverse effect: skin reaction auto-limited in 10 days. Discussion: The surgery treatment of secondary hyperparathyroidism requires the recognition of all parathyroid glands. In some cases, this situation is not easy and is necessary the use of methods for the localization of the glands, principally in cases of ectopic tissue. The fluores– 55 – ABSTRACTS – Metabolic Bone Disease cence-guiaded parathyroidectomy showed the capability of recognizes, in selective form, the parathyroid glands. This technique not requires special training, not uses radiations and is not necessary expensive equipments, only the surgeons and the blue light source. Also, the 5-aminolevulinic acid is a natural product, with few adverse effects. This case is the first fluorescence-guiaded parathyroidectomy in Latin America. The firsts reports in the world were in Germany. In the medical literature, there aren’t cases with this technique in United States. Conclusion: The fluorescence-guiaded parathyroidectomy in patients with secondary parathyroidectomy is an effective technique. May be the use of this technique will be for cases of primary hyperparathyroidism or reoperation where the anatomy is altered. However, the model of secondary hyperparathyroidism is very good for observe and study the technique. Finally, this is an important contribution of the region. Discussion: Based on the above presentation & investigations patient. was diagnosed as having Primary Hyperparathyroidism due to parathyroid adenoma but did not have overt hypercalcemia due to associated vitamin D deficiency. Patient was operated & left lower parathyroid gland was removed. Histopathology showed parathyroid adenoma with other biopsied glands normal. In immediate post-op period serum PTH-3.28 pg/ml; Trousseau’s sign positive; serum calcium 7.3 mg/dl; phosphorus 1.4 mg/ dl & ALP 1761 U/L.Patient. was given calcium replacement 3g/d & 60,000 U of 25(OH)vitamin D.Post-operative day 5- calcium rose to 7.5 mg/dl. After 3 weeks patient asymptomatic, serum calcium 8.4 mg/dl; phosphorus 3.5 mg/dl; ALP 1699 U/L; PTH 56.5 pg/ml; 25(OH)vitamin D 46.85 ng/ml; BMD after 4 mth В showed improvement in bone density, yet in osteoporotic range. At 8 mth, pt could walk without support, climb stairs with В no aches & pains. Serum calcium 8.6 mg/dl; phosphorus 3.6 mg/dl; ALP 506 U/L; 24 hr. urinary calcium 172.4mg/day.Due to high prevalence of vitamin D deficiency in India, normocalcemic hyperparathyroidism is not uncommon. This association leads to moreВ В severe bone disease than what is seen in primary hyperparathyroidism without vitamin D deficiency. Conclusion: Our patient is a case of primary hyperparathyroidism due to Parathyroid adenoma of left lower gland with Vitamin D deficiency, presenting with normocalcemia. Abstract #502 NORMOCALCEMIC PRIMARY HYPERPARATHYROIDISM Sachin Kumar Jain, MBBS, MD, DM, FACE, Niti Agarwal, and Ajay Ajamani Objective: To present a case of Primary Hyperparathyroidism with coexisting В vitamin-D deficiency. Case Presentation: 44 yr old postmenopausal lady presented with generalized bodyache & backache for 1year,had been wheel chair bound for last 6 months. History of В myalgia, generalized weakness & difficulty in getting up from lying or sitting position for more than one year. There is no history of В polyuria, flank pain or renal stone. В Examination was normal except bone tenderness & proximal muscle weakness,much more marked in both lower limbs. Investigations revealed-normal hemogram, liver & kidney functions; Serum calcium10.10 mg/dl (8.410.2); Albumin 4.9 g/dl (3.4-4.8); phosphorous 1.5 mg/dl (2.7-4.5); Serum Alkaline phosphatase 4154 U/l(95-240); PTH 1447 pg/ml(10-69); ionized calcium 1.39 mmol/l (1.10-1.38); 24 hr urinary volume-1710ml (800-2500) & calcium-290.70 mg (100-300); 25(OH) vitamin D was 5 ng/ml (9-37.6); vitamin D challenge given with 60,000 U weekly and after 4 weeks serum В calcium rose from 10.10 to 10.80 with ionized calcium being 1.51mmol/l; X-ray spine В showed osteoporotic changes resulting in multiple vertebral compressions; BMD evaluation revealed severe osteoporosis; CT- Neck & 99Tc Sesta MIBI В scan showed adenoma left lower Parathyroid gland. Abstract #503 HYPERCALCEMIA RESULTING FROM COMBINED USE OF TERIPARATIDE AND HYDROCHLOROTHIAZIDE Arun Kumar Movva, MD, and Arnold M. Moses, MD Objective: To report a case of substantial hypercalcemia in a patient who was on treatment with teriparatide and hydrochlorothiazide (HCTZ). Case Presentation: The patient is a 75yr old female with history of severe osteoporosis. She could not tolerate oral bisphosphonates or IV pamidronate because of the side effects. She failed to respond with Miacalcin. Her bone density continued to get worse based on the DEXA scans. The pretreatment serum calcium and Vitamin D levels were within normal range. Her bone turnover markers, phosphorus and PTH were also within normal range. She was treated with teriparatide after which she developed a substantial asymptomatic hypercalcemia. The hypercalcemia resolved once the hydrochlorothiazide was substituted – 56 – ABSTRACTS – Metabolic Bone Disease with aВ nonthiazideВ antihypertensive medication. В Serum calcium (8.4-10.2mg/dl), Baseline on HCTZ:В 9.3, 4-6hrs after Teriparatide:В 12.5, 20hrs after Teriparatide: 11.8, Off Teriparatide and off HCTZ:В 9.6, 5hrs after Teriparatide and off HCTZ: 10.0. Discussion: Teriparatide (Forteo) causes hypercalcemia to a modest degree by elevation of the bone turnover markers. The effect is usually transient.В Thiazide diuretics are known to increase renal calcium reabsorption. They cause hypercalcemia infrequently because of the compensatory mechanisms. Our case illustrates that patients canВ be at risk of developingВ substantial hypercalcemia when they are on both medications. To the best of our knowledge such an association has never been reported before. Further studies delineating the association are needed to be done. Conclusion: We recommend careful monitoring of serum calcium levels in patients on thiazide diuretics who are being treated with Teriparatide. (4.8%) reported drinking >14 alcoholic/week vs 3.4% of Eur and 2.5% of US (p<0.0001); women with a fracture were 0.7, 3.5, 1.8% (p=0.7). Smoking was higher in women with a fracture (Aus/Can 25%, US 13%, Eur 16%, p=0.03) vs those without (8.9, 11, 6.9%, p<=0.0001). Those with a fracture were more likely to use their arms to assist from sitting (Aus/Can 81%, US 59%, Eur 48%, p=0.6) vs those without (35, 29, 32%, p<0.0001). Rheumatoid arthritis was more common in women with a fracture (Aus/Can 26%, USA 21%, Eur 7.3%, p=0.04) vs those without (10, 12, 7.8%, p<=0.0001). Conclusion: In this international real-world cohort, self-reported fracture risk factors varied by region and fracture history. Abstract #505 VITAMIN D DEFICIENCY: EFFECTIVENESS OF WEEKLY ADMINISTRATION OF ORAL 50,000 IU ERGOCALCIFEROL Abstract #504 DISTRIBUTION OF RISK FACTORS FOR FRACTURE IN WOMEN WITH AND WITHOUT A FRACTURE HISTORY: A REGIONAL COMPARISON. THE GLOBAL LONGITUDINAL REGISTRY OF OSTEOPOROSIS IN WOMEN Donald Bodenner, MD, PhD, and Carolyn Redman Objective: The aim of the present study was to evaluate the response of vitamin D (vit D) deficient patients (<30 ng/ml) to treatment with weekly doses of 50,000 IU of vit D2. Methods: The records of patients with complete data available who had been treated weekly with 50,000 IU of vit D for variable amounts of time were retrospectively reviewed. Clinical variables abstracted from each patient’s record included: race, sex, age, diagnosis of malabsorption, vit D levels, and number of vit D treatments. Results: 48 patients were treated with 50,000 IU vit D2.В The mean age was 70.8 (+/-10.1) years, 45 were female, and there were 6 African Americans. All patients were taking greater than 1,000 mg of calcium.В In 11 patients (23 %), the treatment course failed to raise the vit D level more than 6 ng/ml. None of the patients carried the diagnosis of malabsorption, so these treatment failures were considered to be secondary to noncompliance.В Of the 37 patients that appeared to take the vit D as prescribed, one treatment course normalized vit D levels (>30 ng/ml) in 29 patients (78% success rate) and two courses were required in 4 patients for an overall success rate of 89%.В True treatment failures where the vit D level increased by more than 6 ng/ml but did not normalize occurred 6 times, however only in patients severely deficient (2 of 6, 8.0 avg doses of 50,000 IU) or moderately deficient (4 of 6, 8.0 avg doses). Of the 31 patients successfully treated, the average number of weekly 50,000 IU doses prescribed for the severely deficient (1-10 ng/dl), deficient (11-20 ng/dl) and insufficient Nelson B. Watts, MD, FACP, MACE, Susan L Greenspan, MD, Andrea LaCroix, PhD, Kenneth Saag, MD, Stuart Silverman, MD, Ethel Siris, MD, Rebecca Dedrick, MPH, and Robert Lindsay, MD, PhD Objective: To compare factors for fragility fracture in 3 regions. Methods & results: GLOW (Global Longitudinal registry of Osteoporosis in Women) is a study of women >=55 recruited by 540 primary physicians in 17 sites in 10 countries. All women in the practice in the prior 2 yr were eligible. Self-administered questionnaires were used. Prevalence of risk factors (maternal hip fracture, weight <125lb/57kg, smoker, armsВ to assist from sitting, parental fracture, cortisone, >14 alcoholic units/week, rheumatoid arthritis) was age-adjusted. In women with a fracture after 45 (n=353, 18%), 17% said their mother had a hip fracture vs 12% in those without (n=19,767, p<0.01). 29% of women with fracture reported weight <125lb/57kg vs 16% in those without (p<0.0001). In women with a fracture, Australians/ Canadians (Aus/Can;19%) and Americans (US;18%) more often reported maternal fracture vs Europeans (Eur;11%, p=NS); rates were similar in those without fracture (12, 13, 11%, p<0.001). More Aus/Can without a fracture history – 57 – ABSTRACTS – Metabolic Bone Disease (21-30 ng/dl) patients were 9.3 (+/- 1.6), 9.3 ( +/- 3.5), and 7.2 (+/- 2.7). В Vit D levels were elevated outside the normal range (20 to 57 ng/ml) in two patients (91 ng/ml and 61 ng/ml) who remained normocalcemic and asymptomatic. Discussion: Although vit D deficiency is extremely common, there are few guidelines for replenishment. This retrospective review demonstrated that a weekly dosage regimen with 50,000 IU of vit D successfully treated the vast majority of compliant patients without toxicity.В We recommend 50,000 IU vit D2 for 9 weeks in patients with vit D levels less than 21 ng/ml, and 7 weeks for patients with levels from 21 to 30 ng/ml. This should be followed by a repeat vit D level and maintenance with at least 800 IU D3 daily. Conclusion: Weekly 50,000 IU doses of vit D were safe and effective in treating vit D deficiency, but noncompliance was a major problem. A prospective study will be required to determine the specific duration required to adequately treat all patients. vitamin D supplements. В Many of the patients with vitamin D deficiency were also on low-dose supplements.В Only 1 of 18 AA’s had a 25VitD >32 ng/ml. В Vitamin D deficiency and secondary hyperparathyroidism are associated with metabolic bone disease, myopathy, cardiomyopathy, vasculopathy, and carcinogenesis.В Therefore, this high incidence of deficit could have wide-spread clinical consequences. Conclusions: These data indicate that vitamin D deficiency is extremely common in older, relatively healthy, affluent patients being seen in a sunbelt location for generally unrelated problems. Abstract #507 PARATHYROID STORM Lisa Young, MD Abstract #506 VITAMIN D DEFICIENCY IN AN ENDOCRINOLOGY-LIPID PRACTICE IN THE SUNBELT Syeda Sadia Zaidi, MD, and Thomas A. Hughes, MD Objective: In order to assess the frequency of vitamin D deficiency, we reviewed the charts of all patients seen in the previous 6 years in the University of Tennessee, Endo-Lipid private practice office of one of the co-authors in Germantown, TN (a relatively affluent population).В Patients with primary or tertiary hyperparathyroidism (Ca >11.0 mg/dl), a serum creatinine >2.0 mg/dl, and those on high-dose vitamin D supplementation (>5000 U/day) were excluded.В A total of 262 patients were included in this analysis. Demographics: Average age: 59.9+12.8 (+SD) years (range: 21-88); 89% Caucasian, 7% African-American; 46% male; serum Ca 9.6+0.5 mg/dl (range 7.8-11.0); serum creatinine 1.0+0.3 mg/dl (range 0.5-2.0).В Twenty-five percent of patients are known to have osteopenia or osteoporosis.В The most common diagnoses were: Type 2 Diabetes (60%), hyperlipidemia (92%), and thyroid disease (28%). Results & Discussion: Six percent of these 262 patients had severe 25-hydroxy vitamin D (25VitD) deficiency (<10 ng/ml), 32% moderate (10-20 ng/ml), and 35% mild (20-32 ng/ml) deficiency, while 16% were in the low-normal range (32-40 ng/ml).В Only 11% of these patients had satisfactory 25VitD levels (>40 ng/ml) and these patients were typically younger and/or on low-dose – 58 – Objective: To describe a case of acute renal failure precipitating a parathyroid storm in a patient with previously diagnosed primary hyperparathyroidism. Case: A 73 year old African American male was admitted to the hospital with altered mental status and abdominal pain. At the time of this admission he had a serum calcium 21.4mg/dl and a serum iPTH 2872pg/ml. Past medical history was significant for a 6-year history of primary hyperparathyroidism and peptic ulcer disease. Ten days prior, he was admitted with acute renal failure, his creatinine had increased from a baseline of 1.4mg/dl to 9.4 mg/dl and his serum calcium increased from 12.2mg/dl to 12.7mg.dl. A presumptive diagnosis of NSAID associated interstitial nephritis was made based on a history of recent Ibuprofen use and the presence of white blood cells in sterile urine. His creatinine improved to 3.4mg/dl with hydration but his calcium continued to rise. Physical exam revealed an afebrile, elderly black male with normal vital signs. There was a 2cm by 1.5 cm firm, mobile left sided neck mass. Serum iPTh which was 875 pg/ml 2 months prior, increased t0 2872 pg/ml. A prior ultrasound showed a 1.7 by 1.7 by 1.6 cm possible thyroid adenoma in the left cervical area and a sestambi scan was also positive in this area. The patient was aggressively hydrated and furosemide and calcitonin were added to his regimen. Bisphosphonates were not used due to his significant renal impairment. The patient was taken to surgery and a left sided parathyroid adenoma and a normal left hemi-thyroid was removed. His iPTH decreased to 49pg/ml and his serum calcium to 9.9mg/dl immediately after the surgery. His postoperative course was complicated by hypocalcemia, with a nadir ionized calcium of 0.80mmol/l at post op day 5. He responded to calcium and activated vitamin D supplementation and is currently normocalcemic off of supplementation. ABSTRACTS – Metabolic Bone Disease Discussion: Parathyroid Storm was first described by Dawson in 19321. It has also been called parathyroid crisis and parathyroid intoxication. These terms refer to a condition with a very elevated iPTH and serum calcium leading to clinical complications. The last clinical review suggests that there have been less than 200 cases reported2. It is typically caused by sporadic primary hyperparathyroidism or parathyroid carcinoma. In primary hyperparathyroidism, it is not clear what triggers the rapid increase in iPTH. Prior case reports have noted an association with a preceding viral illness and dehydration. Renal insufficiency has been associated with parathyroid storm in 9% of cases3 but often it is not clear if it is a precipitating event or a complication of the severe hypercalcemia. In this case, the renal failure preceded any significant changes in his serum calcium or osmolarity. Therefore, it more likely represented a triggering factor. The mechanism for the rapidly increasing iPTH is unclear. The liver and kidneys degrade iPTH. In the kidneys, a small amount is degraded after binding to physiologic PTH receptors. The majority of iPTH degradation occurs after the hormone is filtered through the glomerulus and metabolized internally by the tubules4. It is possible that the decreased glomerular filtration lead to an accumulation of iPTH. The hypercalcemia may also have been exacerbated by biologically active fragments of PTH. Conclusion: This is a case of acute renal failure precipitating a parathyroid crisis. cose), and a generalized aminoaciduria. Knee radiographs revealed rickets. The data was consistent with RFS. He was treated with bicarbonate, calcitriol, and phosphorus supplementation. Despite hypoparathyroidism and subsequent renal failure, he continued to require phosphorus supplementation. Hypoparathyroidism and hypophosphatemia persisted after his renal transplantation, but his rickets resolved. He developed multiple endocrine, renal, neurologic, and hematologic disorders. Discussion: Pearson Syndrome (PS), Kearns Sayre Syndrome (KSS) and Progressive External Ophthalmoplegia (PEO) are three syndromes associated with a deletion of mtDNA. Clinical expression of these disorders is broad and can include anemia, heart disease, pigmentary retinopathy, cerebellar ataxia, and endocrinopathies such as diabetes mellitus, growth hormone deficiency, hypoparathyroidism, and RFS. HypoparathyroidismВ and congenital heart defects in the newborn merits an evaluation for DiGeorge Syndrome. Our patient had a normal chromosome 22q11 analysis. He developed several disorders that have been previously associated with deletion of mtDNA. As in our patient, clear delineation between PS and KSS is difficult since clinical features can overlap or change over time.В RFS is caused by a proximal tubulopathy associated with multiple inherited or acquired disorders. In the context of mtDNA deletion, it would seem that an intrinsic renal defect would cause the tubulopathy and renal phosphate wasting.В It is striking that the renal phosphate wasting has persisted despite his renal transplantation and hypoparathyroidism suggesting that a circulating factor may play a role. Conclusion: Mitochondrial DNA deletion syndromes are rare and can result in significant endocrine abnormalities including concurrent RFS and hypoparathyroidism. Abstract #508 FANCONI SYNDROME AND HYPOPARATHYROIDISM ASSOCIATED WITH A MITOCHONDRIAL DNA DELETION SYNDROME Abstract #509 Remberto Cuenca Paulo, Jr, MD, and Peter J. Tebben, MD PAGET’S DISEASE PRESENTING AS CAUDA EQUINA SYNDROME MIMICKING A SPINAL TUMOR Objective: To describe a boy with a mitochondrial DNA (mtDNA) deletion syndrome associated with hypoparathyroidism and renal Fanconi syndrome (RFS). We present his clinical, biochemical, radiographic, and genetic data. Case Presentation: The patient is a 7 year old boy with congenital heart defects, pancytopenia, and hypocalcemia discovered shortly after birth.В He has had persistent inappropriately normal or low PTH levels despite hypocalcemia. Physical exam and genetic analysis did not support a diagnosis of DiGeorge Syndrome. Mitochondrial studies revealed mtDNA deletion. He subsequently developed short stature, hypophosphatemia, hyperphosphaturia, metabolic acidosis, glucosuria (with normal serum glu- Daniel Rubin, MD, and Robert Levin, MD Objective: To describe a case ofВ cauda equina syndrome in a patient with Paget’s disease of bone mimicking a spinal tumor. Case Presentation: A 67 year-old man with a history of Paget’s disease of bone presented with 3 weeks of low back pain radiating down the left leg and left thigh weakness.В CT and MRI revealed diffuse osteolytic and sclerotic lesions of the spine and pelvis.В Additionally, a 6 x 5 x 7 cm bony mass arising from the L3-L5 vertebrae was causing neuroforaminal narrowing and spinal canal stenosis. – 59 – ABSTRACTS – Metabolic Bone Disease SPECT bone scan showed increased radiotracer uptake at multiple sites including the L3-L5 vertebrae.В Serum alkaline phosphatase was 1287 U/L (normal 25-100) and serum calcium was 9.1 mg/dL.В CT-guided biopsy of the mass revealed increased osteoclastic activity and irregular bone trabeculae consistent with Paget’s disease.В Pamidronate 60 mg IV monthly and 2 weeks of high dose corticosteroids were administered, which temporarily relieved the patient’s symptoms.В One month after corticosteroids were discontinued, the pain and weakness worsened.В Electrodiagnostic testing revealed active denervation of the L3-S1 innervated muscles.В The patient underwent lumbar laminectomy and partial corpectomy, resulting in modest improvement.В Despite a decrease in alkaline phosphatase to 416 U/L after 180mg total of pamidronate, his symptoms again recurred and the patient underwent a second laminectomy 7 weeks later. В В В He was given zoledronic acid 4 mg IV when his alkaline phosphatase climbed to 1068 U/L 5 weeks after the second surgery. Discussion: Cauda equina syndrome is a rare complication of Paget’s disease of bone.В Multiple mechanisms have been implicated, including compression of the neural elements by overgrowth of pagetic bone, compression by pagetic intraspinal soft tissue, and neural ischemia produced by blood diversion or arterial compression.В Symptoms typically progress over months or years before coming to medical attention.В Treatment options include calcitonin, mithramycin, bisphosphonates, corticosteroids, and surgery.В Recognition of Paget’s disease as the etiology of neurologic dysfunction is important because medical therapy alone has been shown to be effective in some cases.В Furthermore, bisphosphonate therapy prior to surgery is critical for reducing bone vascularity and bleeding complications. Conclusion: Given his unusually rapid progression of symptoms, this patient underwent two laminectomies.В It is unclear if more aggressive medical therapy would have enabled delay or avoidance of surgery.В Patients must be followed closely because recurrence is common. Abstract #510 OSTEODYSTROPHY – A RARE PRESENTATION IN WILSON’S DISEASE Simmi Dube, MD, VK Sharma, and TN Dubey Objective: To report a case of osteodystrophy which is an uncommon but well documented feature of the Wilson’s disease. – 60 – Case Presentation: A 14 year old male child, was admitted with the history of difficulty in walking and painful movements of the limbs for 2 years which had progressively worsened and was bedridden for last 2 months. He had jaundice 3 years back, which recovered in 6 months. Then, he noticed difficulty in going up and coming down a staircase and in getting up from the squatting position with no weakness in distal part of upper and lower limbs. He had generalized aches and pains, which were aggravated by palpation. Physical examination revealed anemia, knock knees and mild icterus, firm, non-tender liver 2.5 cm and firm spleen 3 cm. Nervous system examination revealed tremor and symmetrical wasting with spasticity, muscle power was grade 2, exaggerated deep jerks of all the four limbs and flexor planter reflex. Slit lamp examination of eyes showed Kayser-Fleischer ringВ on both sides. Complete haemogram and renal functions were normal. Prothrombin time was 40 seconds. Liver function studies revealed total serum bilirubin 3.4 mg/dl, SGPT 150 IU/L, SGOT 100 IU/L, alkaline phosphatase 204 IU/L, serum total protein 5.5 mg/dl of which albumin and globulin were 3 gm/dl and 2.5 gm/dl respectively. Serum calcium level was 8 mg/dl. A skeletal survey showed generalized demineralization Serum ceruloplasmin level was 34 mg/dl. The level of 24 hours urinary copper excretion before and after 750 mg of oral penicillamine were 30 mmol. and 68 mmol in 24 hrs.respectively. CT scan of brain showed hypodense area over caudate nucleus extending to the subcortical area. Discussion: Neurological features and hepatic involvement are the presenting manifestations of Wilson’s disease. The osseomuscular syndrome of Wilson’s disease is uncommon but well documented presentation and seems to be peculiar to the Indian subcontinent as maximum cases so far reported come from India. Several mechanisms have been implicated in the pathogenesis of osseomuscular manifestations of Wilson’s disease. They are: a) A genetic variant of Wilson’s disease b) Secondary to renal tubular acidosis, renal tubular phosphate leak c) Exhibit hepatic dysfunction d) Copper-mediated oxidative damage to collagen probably underlies the arthritis Conclusion: We reported a case of osseomuscular dystrophy that is a rare presentation in Wilson’s disease. It highlights that Wilson’s disease should be considered in the differential diagnosis of rickets and osteomalacia particularly when rachitic manifestations appear after first decade. ABSTRACTS – Metabolic Bone Disease Conclusion: Risedronate 75 mg for 2 consecutive days each month appears as effective as the 5 mg daily dose in reducing the risk of new vertebral fractures in the first year of treatment. Abstract #511 REDUCTION OF VERTEBRAL FRACTURE RISK AT ONE YEAR WITH TWO-CONSECUTIVE DAYS-A-MONTH RISEDRONATE 75 MG (2CD) Abstract #512 Nelson B. Watts, MD, FACP, MACE, J. Brown, MD, G. Kline, PhD, and P.D. Delmas, MD, PhD A CASE OF HYPERCALCEMIA OF MALIGNANCY WITH UNIQUE FEATURES Objective: To use historical control data to investigate the anti-fracture efficacy of a less frequent dosing form of risedronate. The antifracture efficacy of new osteoporosis therapies is usually based on placebo-controlled trials, but inclusion of a placebo arm in subsequent clinical trials may be limited by practical or ethical considerations. In these cases, use of historical controls can be explored as an interesting alternative. A recent active-controlled study of risedronate 75 mg for 2 consecutive days per month (2CD) demonstrated that this regimen increases bone mineral density (BMD) comparable to what is seen with risedronate 5 mg daily, which has proven anti-fracture efficacy. Methods: To assess the anti-fracture efficacy of this new regimen, we analyzed fracture data in an active-controlled study of risedronate dosing regimens (the 2CD study) using matched historical controls from previous placebo-controlled trials. Women in the 2CD study were matched for age, years since menopause, BMD and prevalent vertebral fractures, with placebo patients in the Vertebral Efficacy of Risedronate Therapy (VERT) trials, forming an historical placebo group. We also constructed an historical active-treatment group from the risedronate 5 mg daily arm of the VERT trials for comparison with the 5 mg daily (n=613) and 2CD (n=616) treatment groups in the 2CD study; historical control groups consisted of daily placebo patients (n=99, matched from 993) and risedronate 5 mg daily patients (n=96; matched from 990) in the VERT studies. Results: Over 1 year of treatment, risk of new vertebral fractures in the 2CD group (1.1%) was reduced by 79% relative to the historical placebo group (5.1%) (OR 0.21; 95% CI, 0.05 to 0.88, P=0.016), similar to the 1-year risk reduction observed in the VERT trials of risedronate 5 mg daily (61-65%). The incidence of new vertebral fractures, assessed for internal validation, was similar in the three treatment groups: 1.0% in the historical risedronate 5 mg group, 1.5% in the risedronate 5 mg daily group from the 2CD study, and 1.1% in the 2CD group. Discussion: The use of appropriate historical control data provides an approach to the assessment of fracture effects in osteoporosis trials for which placebo-controlled data are not available. Fadi Adel Nabhan, MD, and Alaleh Mazhari Objective: To report a case of mild and intermittent hypercalcemia that has lead to the diagnosis of lung cancer.В В We will also discuss the unique features that are present in this case. Case Presentation: A 64 y/o female initially noted to have mildly elevated calcium at 10.4 mg/dL (8.9-10.3) in November 2006.В Patient’s past medical history was significant for cirrhosis and osteoporosis. She has a smoking history of 25 pack year.В Osteoporosis was being treated with Risedronate, calcium and Vitamin D2.В В The patient was also taking calcitriol but the reason is not known to us.В В In Jan 2007 she was evaluated by the liver service and instructed to stop vitamin D2, calcium and calcitriol due to her hypercalcemia. She was seen by our service in April 2007 shortly after she had a repeat calcium measurement that was still elevated at 11.8 mg/dL with an intact parathyroid hormone (PTH) that was suppressed at 9 (10-65).В В In reviewing her medications, she was noted to be still taking calcitriol as she misunderstood the recommendation to stop it.В Calcitriol was thought to be the cause of her hypercalcemia and she was therefore instructed again to stop it and careful verification was done to ensure that.В В Repeat calcium level in May and June showed elevated (at 10.6 mg/ dL) and high normal (at 10.2 mg/dL) levels respectively.В В Given the persistent hypercalcemia even after stopping calcitriol,В The patient had a repeat intact PTH which was at 21 pg/mL (10-65) and PTH related protein which was elevated at 2.4 pmol/L (<1.9).В В 25 hydroxy vitamin D, 1, 25 dihydroxy vitamin D and phosphorus were within normal range.В В Due to the elevation in PTH r P and especially with her smoking history, a CT scan of chest was done and it revealed a 3.2 cm X 3.3 cm left upper lobe mass with extension into the chest wall and hilum and hilar/ mediastinal lymphadenopathy, multiple liver lesions and lytic lesion at L3 compatible with metastatic disease.В The patient underwent a CT guided biopsy of lung mass, which revealed squamous cell carcinoma.В The patient continues to have mild intermittent hypercalcemia with the highest level being at 10.8 mg/dL. – 61 – ABSTRACTS – Metabolic Bone Disease Discussion: The prevalence of hypercalcemia in patients with cancer has been reported to be between 20 and 30% and it signifies a poor prognosis. Tumors present in this disease are generally large and readily apparent. This case has several unique features: the calcium elevation was mild and intermittent, the parathyroid hormone therefore was not consistently and fully suppressed, and the hypercalcemia preceded the diagnosis of cancer for several months.В The case was also confounded by the use of calcitriol which was considered to be the main culprit of the hypercalcemia and the use of Bisphosphonate which might have been a factor in attenuating the severity of hypercalcemia. Conclusion: It is essential to recognize that in patients with hypercalcemia of malignancy, the level of hypercalcemia can be mild and intermittent and therefore the level of intact PTH may vary. Measuring PTH r P could be useful in making the diagnosis in these patients and this should be considered especially in patients with high risk for malignancy. Month 6, with significant absolute risk reduction of 1.0% (95% CI: 0.3%, 1.6%).Discussion:В The magnitude of the difference in fracture risk between the placebo and risedronate 5 mg groups increased over time. Relative to placebo, RIS significantly reduced the risk for radiographic vertebral fracture starting from the first scheduled radiographic visit at one year. In general, the mean magnitude of the difference in the fracture risk between the placebo and risedronate 5 mg groups increased over time (from 5.3 % at 12 months up to 8.6%, (95% CI: 5.5%, 11.6%). Conclusion: The results confirmed reduced risk of clinical vertebral fracture as early as Month 6 in the risedronate treatment group. Further, risedronate anti-vertebral fracture efficacy, as reflected in absolute fracture risk reduction, increased over 3 years for both clinical and radiographic vertebral fractures. Abstract #514 A CASE OF PAGET’S DISEASE OF THE BONE WITH A POOR RESPONSE TO VARIOUS BISPHOSPHATES FOLLOWED BY A SUBSTANTIAL IMPROVEMENT IN BONE TURNOVER MARKERS INTO THE MID NORMAL RANGE AFTER TREATMENT WITH ZOLEDRONATE Abstract #513 VERTEBRAL FRACTURE EFFICACY IS APPARENT EARLY AND IS SUSTAINED WITH Nelson B. Watts, MD, FACP, MACE, Christian Roux, MD, PhD, and Xiaojie Zhou Andreas Grauer Brijmohan Sarabu, MD, and Arnold M. Moses, MD Objective: To show the effectiveness of Zoledronate in a patient with Paget’s disease with a poor response to other bisphosphonates Case Presentation: We describe a case of polyostotic Paget’s disease of the pelvis bilaterally, femur and right humerus who was referred to our metabolic bone clinic for further evaluation in 1997. She was diagnosed with Paget’s disease in 1970 and was subsequently treated with etidronate for four years and then alendronate10mg daily for several years. She did quite well with this treatment until 1997 when she complained of progressive pain in her right leg, right hip, low back and both knees. At that time a bone scan confirmed increased uptake in all her known areas of Pagetic bone. Bone turnover markers at the time showed alkaline phosphatase of 852 U/L (ULN 126). She subsequently received four courses of IV pamidronate (each course 60 mg three times) with some improvement in her alkaline phosphatase, but never below 239 U/L. She subsequently received risedronate which eventually lowered her alkaline phosphatase to 89 U/L. She was then lost to follow up for five years. In 2006 she was referred back to our clinic with worsening left hip pain and was found to have an alkaline phosphatase of 720 U/L. She was again treated Objective: To examine the absolute vertebral fracture risk reduction in the Vertebral Efficacy with Risedronate Trials (VERT).Treatment with an agent that provides both early and sustained fracture protection can benefit patients. Superficial examination of published studies suggests that the early effect of treatment on vertebral fracture (as reflected in relative risk reduction) may lessen over time. Methods: The population included 2442 patients from VERT-NA and VERT-MN who were treated with at least 1 dose of either placebo or risedronate (RIS) 5 mg daily. The mean age was 69 and the mean spine T-score was 2.5. Treatment groups were balanced with respect to key baseline characteristics. Fracture endpoints included clinical vertebral fracture and radiographic vertebral fractures. Difference in risk of vertebral fractures between placebo and RIS 5 mg groups was estimated using the difference of the Kaplan-Meier (KM) estimators at months 3, 6, … and 36. Results: The findings for clinical vertebral fracture were consistent with the rapid onset of risk reduction with risedronate treatment; relative to placebo, RIS significantly reduced the risk for clinical vertebral fracture starting from – 62 – ABSTRACTS – Metabolic Bone Disease with risedronate for four months, but did not normalize her alkaline phosphatase. She was then infused with 4mg of zoledronate which resulted in a decrease of bone turnover markers to the mid normal range along with an improvement in her bone pain. Discussion: Various bisphosphonates have been used to treat Paget’s disease of the bone. In patients with a poor response to these agents, Zoledronate may be effective in normalizing bone turnover markers and improving bone pain. Conclusion: This abstract describes a case of Paget’s disease that was refractory to various bisphosphonates except for zoledronate which decreased bone turnover markers into the mid normal range. failure or anterior pituitary dysfunction were noted. Five patients had more than one endocrinopathy. Both patients with adrenal infiltration also had hypothyroidism. Three patients with diabetes insipidus also had at least one additional gland involved, one with Hashimoto’s thyroiditis, one with impaired fasting glucose and one with both hypogonadism and diabetes mellitus. Conclusion: We conclude that ECD may be associated with infiltrative disease of endocrine organs, including the posterior pituitary gland, testes, or adrenal glands. Thyroid hypofunction and diabetes mellitus may occur, although these may not be directly related to ECD. Abstract #515 EFFECTS OF RESIDRONATE AND PROSTAGLANDIN E2 ON CANCELLOUS AND CORTICAL BONE IN HYPOPHYSECTOMIZED RATS Abstract #516 ERDHEIM-CHESTER DISEASE: ASSOCIATION WITH ENDOCRINE DISORDERS Kimberly Ann Placzkowski, MD, and Bart L. Clarke, MD Mauricio Ernesto Flores, MD, James Yeh, PhD, and Mariano Castro-Magana, MD Objective: Erdheim-Chester Disease (ECD) is a rare systemic disorder characterized by tissue infiltration with lipid-laden histiocytes. The phenotype is variable, ranging from benign appendicular bony sclerosis to more diffuse organ involvement with granulomas and fibrosis. Although bony involvement is almost universal, solid organ infiltration portends a poorer prognosis. Methods: We evaluated associated endocrine disorders after reviewing all patients with ECD seen at Mayo Clinic between 1980 and 2006. A total of 24 patients were included in our analysis, 92% of whom had biopsy-proven ECD. The remainder of our patients had clinical findings consistent with the disease. We have previously shown decreased bone density (63%) and increased fracture risk in ECD1. Twelve patients (48%) were identified as having other associated endocrine disorders. Results: The most common abnormality was hypothyroidism, with six patients (25%) on L-thyroxine replacement or with an elevated TSH. Two patients had ultrasound appearance of or antibody-confirmed Hashimoto’s thyroiditis, while the remainder did not have further assessment of their thyroid disease during their evaluation. В Diabetes insipidus was present in 5 patients (21%), and was diagnosed prior to ECD in all cases. Two patients (8%) had hyperglycemia, one receiving therapy for diabetes mellitus and one followed for impaired fasting glucose. One patient (4%) had adrenal insufficiency, while another was found to have unilateral adrenal enlargement on imaging with normal adrenal function. Hypogonadism was documented in 3 of 15 men (21%), but no cases of premature ovarian Objective: Whether Risedronate (Ris) as anti-resorptive drug and Prostaglandin E2 (PGE2) as anabolic drug haveВ an additive effect on bone metabolism in hypophysectomized (HX) rats. Methods: Fifty female Sprague-Dawley rats were randomly divided into groups of 10 animals each as follows: Intact, HX, HX+PGE2, HX+Ris, HX+ PGE2+Ris. All HX rats were supplemented 5 days a week for 4 weeks with hydrocortisone succinate 100 ug/100gm, thyroxine 2ug/100gm SQ. PGE2 was administered IMВ atВ 0.83 mg/kg (low dose)В andВ Ris was administered SQ at 2.5ug/0.1 ml. IGF-1 in serum was measured upon sacrifice to assess the completeness of HX. Results: HX rats resulted in a significant reduction of final body weight, tibial and femoral length, femoral bone area, bone mineral content (BMC), bone mineral density (BMD), cancellous bone mass of the proximal tibia, total tissue and cortical area of the tibial diaphysis and IGF-1 when compared with the intact group. Administration of Ris attenuated HX-induced loss of trabecular bone mass, femoral BMC and BMD when compared o HX-rats. A low dose of PGE2 significantly improved cortical and marrow area of the tibial shaft, trabecular, periosteal and endosteal bone formation rate when compared to intact, HX and HX+Ris groups. Discussion: The combination of Ris and a low dose of PGE2 had an important additive effect on cancellous/ cortical bone when compared to the HX group. However it was statistically insignificant with intact group. IGF-1 – 63 – ABSTRACTS – Metabolic Bone Disease levels remained low throughout the administration of both drugs. Conclusion: Further studies using Ris and a high dose of PGE2 will be necessary to establish additional benefits on bone metabolism. Conclusion: These results confirmed the rapid reduction of non-vertebral fracture risk as early as Month 6 with risedronate. Further, the risedronate anti-fracture efficacy was sustained through out the remaining study period. Abstract #518 Abstract #517 THE IMPACT OF RISEDRONATE ON CLINICAL FRACTURE RISK IN PATIENTS WITH A PRIOR HIP FRACTURE EARLY AND SUSTAINED NON-VERTEBRAL FRACTURE RISK REDUCTION WITH RISEDRONATE Andreas Grauer, MD, PhD, Xiaojie Zhou, PhD, Paul D. Miller, MD, Steven Boonen, MD, PhD, and Michael R. McClung, MD Andreas Grauer, MD, PhD, Christian Roux, MD, PhD, Jonathan D. Adachi, MD, Xiaojie Zhou, PhD, Nelson B. Watts, MD, and Robert Lindsay, MD Objective: To evaluate the antifracture efficacy of risedronate among patients from the HIP Trial who had one hip fracture at baseline.В A hip fracture is a risk factor for subsequent fractures. Methods: The analysis population included 5445 subjects from the HIP trial (McClung,MR et al. 2001 NEJM), aged 70-79 years, with low BMD ( FN T-score <=-2.5 SD). В Among these subjects, 339 had experienced a traumatic or an atraumatic hip fracture at some time prior to the entry into the study (determined via lifetime medical history). These subjects were treated with either placebo (PLC) or risedronate (RIS) 2.5mg or 5 mg daily. The incidence of osteoporosis-related clinical fracture, defined by the occurrence of the radiographically confirmed clinical vertebral fracture or radiographically confirmed non-traumatic non-vertebral fracture was calculated using KaplanMeier survival estimates over a 3 year period and was compared between PLC- and RIS-treated subjects. Treatments were compared using log rank test, and the risk ratio and its 95% confidence interval were obtained using a Cox regression model stratified for study. Results: Subjects’ mean age was 75 years, and their mean femoral neck (FN) and lumbar spine (LS) T-scores were -3.1 and -3.2 SD, respectively. Baseline characteristics were well balanced between the 3 treatment groups. Over the 0-3 year period, the clinical fracture incidences were 28.4%, 14.9% and 13% for the PLC, RIS 2.5mg and RIS 5mg groups, respectively. Discussion: Relative to theВ PLC group, RIS 5mg and 2.5 mg statistically significantly reduced the risk for clinical fracture over 0-3 year period (p<0.05). The risk ratio of clinical fracture was 0.5 for both theВ RIS 5mg and 2.5 daily groups relative to the placebo group. RIS treatment was well tolerated in HIP trial. Conclusion: Risedronate significantly reduced the risk of clinical fracture among women with postmenopausal osteoporosis who had a prior hip fracture. Objective: To investigate whether the non-vertebral fracture risk reduction with risedronate is early and sustained. Previous analyses have shown non-vertebral fractures account for 77% of the osteoporosis-related fractures and over 90% of costs. Predicting an osteoporosis-related fracture is not possible. Therefore, treating with an agent that provides both early and sustained fracture protection will provide maximum patient benefit. Methods: The analysis population included 1169 postmenopausal women from VERT andВ BMD trials with low BMD (LS T-score <-2.5 SD), who were treated with at least one dose of either placebo or risedronate 5mg daily. The mean age of the population was 67 years and 58% of the patients had at least one prevalent vertebral fracture at baseline. The fracture endpoint was radiographically confirmed osteoporosis related non-vertebral fracture. Risk difference of osteoporosis-related non-vertebral fracture between the placebo and risedronate 5mg groups was estimated using the difference of the Kaplan Meier (KM) estimators from month 3 through 36. The standard error of the risk difference was approximated by the square root of the sum of the variance of the KM estimators of the placebo and risedronate 5mg groups. The upper and lower bound of the 95% confidence intervals were calculated as the mean plus and minus 1.96 times the standard error of the estimated risk difference. Results: Relative to placebo, risedronate significantly reduced the risk for non-vertebral fracture starting from Month 6 with an absolute risk reduction of 1.8% (95% CI: 0.4%, 3.3%). The magnitude of the difference in the risk for non-vertebral fracture between the placebo and risedronate 5mg groups increased during the first 2 years and remained constant during the 3rd year of the trial with an absolute risk reduction of approximately 4%. Discussion: The findings are consistent with the rapid onset of fracture risk reduction with risedronate treatment. – 64 – ABSTRACTS – Metabolic Bone Disease Abstract #519 Abstract #520 PREDICTORS OF BONE MINERAL DENSITY IN MEN WITH PRIMARY HYPERPARATHYROIDISM VITAMIN D DEFICIENCY IN PATIENTS WITH OSTEOPOROSIS Giorgio Borretta, MD, Laura Gianotti, Francesco Tassone, Flora Cesario, and Giampaolo Magro Harinder Singh, MD, Satish Karmegan, Aswatharayan Manandhi, Jyothi Ratti, Kenneth Grant, Swamy Venkatesh, and Ambika Rao Objective: In primary hyperparathyroidism (PHPT) bone involvement is frequent. In women with PHPT it has been previously reported that menopausal status together with PTH, calcium levels and renal function are independent predictors of bone density. In male subjects, the impact of PHPT on bone status is less defined.В Aim of the study was to investigate possible predictors of bone mineral density (BMD) in a series of male subjects affected by PHPT. Methods: Sixty male patients with PHPT were consecutively studied (age, mean В± SD: 57.9В± 14.1 yrs; Symptomatic /Asymptomatic 32/28; PTH, median and interquartile levels: 119 and 95.0-228 pg/ml, calciumВ 11.1В±1.0 mg/dl). In all subjects BMI, levels of calcium, PTH, 25 hydroxy-vitamin D, creatinine and creatinine clearance and bone mineral density (BMD) at lumbar spine, femur and distal radius by DXA were evaluated. Results: A positive association between BMI and DXA measurement at femoral levels was found (BMIBMD: R=0.52, p<0.004; BMI-T score : R=0.53, p<0.002; BMI-Z score : R=0.55, p<0.002). On the contrary, neither PTH, calcium, renal function nor 25-hydroxy-vitamin D showed significative correlation with BMD levels. Discussion: BMI resulted a good predictor of BMD in male patients with PHPT as found in women with PHPT, confirming the important role of BMI as risk factor for bone damage in osteoporosis of both primary and secondary origin.В On the contrary, biochemical indices of PHPT as well as renal function did not associate with DXA measures in male patients, differently from female. These findings could indicate gender-dependent differences in the clinical expression of PHPT, particularly at bone level. A peculiar resistance of male bone to PTH excess in PHPT could be also hypothesized. Conclusion: These findings suggest that the clinical management of the modern form of PHPT should be differently by gender. Objective: Vitamin D facilitates intestinal absorption of Calcium, Phosphate, and maintains normal serum calcium and mineralization of bone. Vitamin D deficiency is not uncommon and may contribute to the development of osteomalacia and fractures. Purpose of this study was to find the prevalence of Vitamin D deficiency in osteoporotic patients who were already on the recommended dose of Vitamin D and calcium. Our observations suggest that Vitamin D deficiency in patients diagnosed with osteoporosis by DEXA scanning is underdiagnosed. We suggest Vitamin D levels as part of initial evaluation of patients with osteoporosis. Methods: This retrospective chart review study was conducted at the outpatient endocrinology clinic in Las Vegas. Study inclusion criteria were as follows; any patient with osteoporosis diagnosed on DEXA scan who had documented vitamin D levels, irrespective of race, gender, and age or other underlying diagnoses. 328 charts with diagnosis of osteoporosis were reviewed, of which 71 had documented 25-hydroxyvitamin D levels and were included in the study.В Patients were on Vitamin D 800 IU and calcium 1200 milligrams daily. 25-hydroxyvitamin D level was checked while patients were assumed to be taking Vitamin D 800 IU. We also reviewed other risk factors including family history of osteoporosis, tobacco use, steroid use and other major pre-existing medical diagnoses. Results: The average age was 62.2 years and 89% were females. 60 (84.5%) were Caucasians and 11 (15.5 %) were smokers. Five (7%) had family history of osteoporosis and 2 (2.81%) had osteoporotic fractures in the past. Thirteen (18.3%) were taking steroids for various medical reasons. Thirteen (18.3%) subjects were found to be Vitamin D deficient (<20ng/ml) and 16 (22.5%) were Vitamin D insufficient (20-30 ng/ml). Seven (9.86%) patients were hypocalcemic (<9 mg/dL). Conclusion: Our study demonstrates that many patients with osteoporosis who were on Vitamin D and calcium had low vitamin D levels, which in turn contributes to increased risk of fractures. Therefore, all patients with osteoporosis should have vitamin D levels measured, and replaced adequately. – 65 – ABSTRACTS – Metabolic Bone Disease compression fracture when an obvious cause such as osteoporosis is not found, even when antecedent trauma can potentially account for the fracture. Plasmacytomas do not have the typical manifestations of multiple myeloma and may not be evident on routine labs and imaging. Therefore SPEP should be obtained in all cases of suspected pathological fracture. Abstract #521 VERTEBRAL COMPRESSION FRACTURE CAUSED BY A PLASMACYTOMA Sreevidya Kannoorpatti Subbarayan, MD, and Thomas Moraghan Objective: To present a case of solitary plasmacytoma causing vertebral compression fracture. Case: A 54-year-old-woman developed severe back pain that radiated along the T10 dermatome, while attempting to lift a 50 lb bag at work. X-rays showed severe compression fracture of the T10 vertebra with marked anterior wedging and mild osteopenia. MRI of the spine demonstrated a new/non healing T10 compression fracture with 80% loss of anterior height and spinal cord compromise. The patient was referred to Endocrinology for evaluation regarding metabolic bone disease. She denied steroid use, nephrolithiasis, family history of osteoporosis or prior fractures. She was menopausal and had a 20 pack-year history of smoking. There was no history of sustained weight loss, night sweats, rash or anemia. Physical exam was unremarkable except for mild kyphosis.В DEXA scan performed a year ago was normal. CBC, 25 hydroxyvitamin D, intact PTH, calcium, Phosphorus, Alkaline phosphatase, Albumin, Creatinine, LFTs and urine calcium levels were normal.В Repeat DEXA scan showed T-score of -0.5 at the spine andВ -0.1 at the hip.В SPEP showed a minimal monoclonal IgG spike. Skeletal survey was negative for lytic lesions. CT of the chest through pelvis demonstrated no adenopathy or organomegaly. Bone marrow biopsy showed 1% mature plasma cells. Repeat MRI showed progression of the vertebral lesion with radiological features worrisome for malignancy. Biopsy of T10 vertebra demonstrated a plasmacytoma. Discussion: Plasmacytomas are tumors arising from malignant plasma cells that are histologically identical to those seen in multiple myeloma. They can occur in bone or soft tissue as solitary or multiple lesions. Plasmacytoma is characterized by the absence of osteolytic lesions, anemia, hypercalcemia or renal involvement that is associated with multiple myeloma. Solitary plasmacytomas of the bone account for 5% of all patients with plasma cell disorders and commonly involve the thoracic spine. Median age at diagnosis is 55. Patients usually present with skeletal pain, pathological fractures or cord compression. Plasmacytomas have a 54% chance of eventual conversion to multiple myeloma. Tumoricidal radiation is the treatment of choice. Conclusion: Our case underscores the importance of considering plasmacytoma as an etiology for vertebral Abstract #522 HYPERPARATHYROIDISM-JAW TUMOR SYNDROME Amanda Reagan Schiefer, MD, and Vahab Fatourechi, MD Objective: Discuss the clinical aspects of the rare genetic disease, HPT-Jaw Tumor Syndrome, and, in particular, report case series with the presenting clinical aspects seen at Mayo Clinic from 1997 to 2007. Case Presentation: In 1982, 13 yo female was diagnosed with benign jaw tumor (JT) requiring surgery.В In 1988 (age 18), she underwent a right nephrectomy for a malignant Wilms’ tumor (WT) and multiple hemartomas with concurrent chemoradiation.В In 1993 (age 22), a second jaw tumor was removed.В Both jaw tumors were benign ossifying fibromas.В In 9/1993, she was diagnosed with hyperparathyroidism (HPT).В A left superior parathyroid gland was resected.В No evidence of parathyroid carcinoma (CA) was seen on pathology.В Her hypercalcemia resolved.В In 1995 (age 26), she underwent hysterectomy for Mullerian adenofibroma.В Her family history was positive for jaw tumors and HPT.В In 5/2005, she was seen at our institution for second opinion with recurrent HPT in the setting of HPT-JT syndrome.В Her calcium was normal (9.4mg/dL) with low PO4 (2.0 mg/dL) and elevated PTH 167 pg/mL.В She underwent cervical re-exploration and excision of right superior parathyroid adenoma per pathology.В Panoramic x-ray revealed multiple mandibular tumors that were not clinically relevant.В In 12/06, repeat biopsy of right posterior mandibulur tumor revealed benign ossifying fibroma.В In 6/07, a screening MRI of left remaining kidney revealed solid enhancing mass.В She underwent left partial nephrectomy and was found to have 2 renal mass: oncocytoma and metanephric adenoma.В This case prompted a retrospective review of cases with this diagnosis seen at Mayo Clinic from 1997 to 2007.В The case series consists of 3 patients (2’s and 1) aged 33-38.В All 3 patients have tested positive for the HRPT-2 mutation.В AllВ 3 patients hadВ HPT with ages at diagnosis of 17, 22, and 28.В Only 1 of the 3 cases had JTs and the full blown syndrome. – 66 – ABSTRACTS – Metabolic Bone Disease Discussion: HPT-JT syndrome is a rare genetic syndrome with clinical features that include ossifying jaw fibromas, HPT, kidney tumors, and uterine tumors.В HPTJT was initially identified by Jackson et al in 1958.В In 2002, the gene responsible was linked to HRPT2 on the long arm of chromosome 1.В It is inherited in an autosomal dominant fashion with high but incomplete penetrance.В In HPT-JT syndrome, 90% of patients develop HPT, 3035% of patients have JTs, and 10% of patients have renal cysts with solid renal tumors less common.В Parathyroid carcinoma is seen in 15% of patients.В The frequency of other cancers such as uterine cancer and Wilms’ tumor are unknown.В There are no published surveillance guidelines for HPT-JT. Conclusion: Unlike other familial HPT syndromes, HPT-JT has solitary parathyroid adenomas that recur, not pluriglandular disease or parathyroid hyperplasia.В Also, unlike “brown tumors” associated with severe HPT, jaw tumors in HPT-JT are restricted to the maxilla and mandible, lack multinucleated giant cells on pathology, occur asynchronously with HPT, and do not heal after parathyroidectomy. Renal manifestations can be bilateral renal cyst or, as in 1 of 3 cases presented here, Wilms’ tumor with hamartomas followed by benign solid tumors.В In 2005, uterine tumors were added to the spectrum.В HPT-JT is a complex syndrome with diverse clinical aspects spanning over a long time with various manifestations.В This can lead to an under recognized syndrome with multiple medical professionals focusing on only one aspect of the syndrome at a time without putting the entire spectrum together as HPT-JT syndrome.В Given the increased risk of tumors, in particular parathyroid carcinomas and renal tumors (such as Wilms’ tumor), it is important to recognize those families at risk and perform appropriate screening surveillance. MANAGEMENT OF RECURRENT TERTIARY HYPERPARATHYROIDISM IN A PATIENT WITH HYPOPHOSPHATEMIC RICKETS temic rickets at 18 months and started on phosphate and calcitriol therapy. There is no history of nephrolithiasis, renal failure, fractures or family history of hypophosphatemia. She developed tertiary hyperparathyroidism at age 30, treated with subtotal parathyroidectomy. Fifteen years later she presents with fatigue and worsening bone pain. On physical exam, height of 4’10”. Laboratory values showed calcium of 10.8 mg/dl, phosphorus 3.9 mg/dl, PTH 286 pg/ml and Cr 1.5 mg/dl. Kidney ultrasound with medullary calcinosis. Calcitriol and calcium were discontinued. It was decided that a second neck exploration should be undertaken to remove the remaining gland to prevent further nephrocalcinosis. Operative notes from the surgery were not readily available so efforts to localize the remaining parathyroid gland were undertaken. Sestamibi parathyroid scan demonstrated a focal uptake of tracer overlying the right thyroid gland. Thyroid ultrasound showed a hypoechoic cystic nodule in the posterior right lobe. В Fine needle aspirate of this nodule was obtained to differentiate it from thyroid origin. PTH levels of the fluid were reported > 2500 pg/ml. At the time of referral for surgery, operative notes were found, confirming the remaining gland in the right neck. Removal of the adenoma was performed with peri-operative auto-transplant to forearm. Cryopreservation also requested. Patient seen 3 months after surgery with clinical evidence of graft function, normal serum calcium levels and stable renal function with decreasing doses of calcitriol and calcium. Discussion: X-linked hypophosphatemic rickets (XLH) is the most common inherited form. Tertiary hyperparathyroidism in patients with hereditary hypophosphatemic rickets is rare, reported in the literature in 23 patients. The treatment is subtotal parathyroidectomy but recurrence of hypercalcemia has been reported. Treatment with cinacalcet can be considered, but in patients with nephrocalcinosis the treatment should be definitive. Autotransplant and cryopreservation can be done in efforts to prevent complications of hypoparathyroidism. Conclusion: Patients with recurrent hyperparathyroidism in hypophosphatemic rickets should be treated definitively in those with nephrocalcinosis. Ana Mendoza, MD, and Mira S. Torres, MD Abstract #524 Abstract #523 Objective: Tertiary hyperparathyroidism is though to be a rare complication of patients with hypophosphatemic rickets treated with lifelong oral phosphate therapy. We describe a case of a patient with hereditary hypophosphatemic rickets with recurrent hypercalcemia, nephrocalcinosis and worsening renal function Case Presentation: A 45 year old female was referred for hypercalcemia. She was diagnosed with hypophospha- ACUTE RENAL FAILURE PRECIPITATING PARATHYROID STORM Lisa Young, MD, and Anup Sabharwal Objective: To describe a case of acute renal failure precipitating parathyroid storm. – 67 – ABSTRACTS – Metabolic Bone Disease responded to calcium and vitamin D supplementation and is currently normocalcemic off supplementation. Discussion: Parathyroid Storm was first described by Dawson in 19321. It refers to a very elevated iPTH and serum calcium leading to clinical manifestations. It is rare. It is caused by primary hyperparathyroidism or parathyroid carcinoma. In primary hyperparathyroidism, the trigger for the rapid increase in iPTH is not known. Renal insufficiency has been associated with parathyroid storm in 9% of cases3 but often it is not clear if it is a precipitating event or a complication of the severe hypercalcemia. In this case, renal failure preceded any significant changes in his serum calcium or osmolarity. Therefore, it more likely represented a triggering factor. The mechanism for the rapidly increasing iPTH is unknown. In the kidneys, the hormone is degraded after binding to physiologic PTH receptors. The majority of iPTH degradation occurs after the hormone is filtered through the glomerulus and metabolized internally by the tubules4. The decreased glomerular filtration may have lead to an accumulation of iPTH and elevated serum calcium. Conclusion: This is a case of acute renal failure precipitating a parathyroid crisis. Case: A 73 year old man was admitted with altered mental status and abdominal pain. He had a serum calcium of 21.4mg/dl, phosphorus 5.5mg/dl and serum intact parathyroid hormone (iPTH) 2872pg/ml. Past medical history included a 6-year history of primary hyperparathyroidism and peptic ulcer disease. Ten days prior, he was admitted with acute renal failure, his creatinine had increased from a baseline of 1.4mg/dl to 9.4 mg/dl and his serum calcium increased from 12.2mg/dl to 12.7mg/dl. A presumptive diagnosis of NSAID associated interstitial nephritis was made based on a history of recent ibuprofen use and the presence of white blood cells in sterile urine. His creatinine improved to 3.4mg/dl with hydration but his calcium continued to rise. Physical exam revealed a 2 cm by 1.5 cm firm, mobile left sided neck mass. Serum iPTH which was 875 pg/ml 2 months prior, increased to 2872 pg/ml. An ultrasound showed a 1.7 by 1.7 by 1.6 cm left cervical mass and a s sestamibi scan was positive in this area. The patient was treated with hydration, furosemide and calcitonin. The patient was taken to surgery and a left sided parathyroid adenoma was removed. His iPTH decreased to 49pg/ml and his serum calcium to 9.9mg/dl immediately after surgery. His postoperative course was complicated by hypocalcemia, with an ionized calcium nadir of 0.80mmol/l. He – 68 – ABSTRACTS – Obesity ing waist circumference and blood pressure measurements was obtained. Using the International Diabetes Federation (IDF) 2005 definition, central obesity was defined as waist circumference of > 90cm (men) or > 80cm (women). Hypertension was considered to be present if blood pressure was >130/85 mmHg at two different visits or on antihypertensive medications. Results: 90/120 subjects were male with a mean age of 22 (21-24) years. None of the medical students had any known history of hypertension nor were they taking any antihypertensive medications. 14% (17/120) of the medical students had systolic blood pressure >130 mmHg and diastolic blood pressure >85 mmHg. 22% (26/120) medical students had central obesity. Conclusions: Our study shows an alarmingly high prevalence of obesity and hypertension amongst otherwise healthy young adults. This study clearly highlights the need for primary preventative measures to reduce development of obesity, hypertension and eventually metabolic syndrome and diabetes among young adults in Pakistan. The results are disturbing and warrant further comprehensive studies. LEAP COHORT KEMU is an ongoing study and we plan to follow these medical students throughout their undergraduate medical career till they graduate. We plan to perform fasting blood glucose, HDL cholesterol and Serum triglycerides levels to identify metabolic syndrome amongst them. OBESITY Abstract #600 PREVALENCE OF CENTRAL OBESITY AND HYPERTENSION IN YOUNG MEDICAL STUDENTS: PRELIMINARY RESULTS OF LAHORE EPIDEMIOLOGICAL ADULT POPULATION COHORT KING EDWARD MEDICAL UNIVERSITY (LEAP COHORT KEMU) STUDY Ali Asghar Jawa, MD, MPH, Jawad Zaheer Mumtaz Hasan (S.I.), Muhammad Shahid Jamil, Umair Javaid Chaudhary, Syed Ali Imran, and Ghazanfar Ali Jawa Objective: Obesity and hypertension is on the rise especially in adolescents and young adults. Anecdotal evidence suggests that awareness amongst medical students and young health professionals is lacking at best. We systematically screened medical students studying at King Edward Medical University, Lahore for frequency of central obesity and hypertension. Methods: 120 medical students were enrolled in the study. Their willingness to participate in this study was construed as a verbal consent. Anthropometric data includ- – 69 – ABSTRACTS – Other wise) is associated with pachydermoperiostosis. Treatment is usually conservative with NSAIDS, and treatment of complications of arthritis. OTHER Abstract #700 Abstract #701 PACHYDERMOPERIOSTOSIS: AN UNUSUAL CAUSE OF ACREMEGALOIDISM MALE HYPOGONADISM Svetlana Fomin, MD, and Sunil Asnani, MD, FACE Adefunke Omosefe Lipede, MBBS, and Anthonia Ogbera, MBBS, MPH, MWCP, FACE Objective: To describe an unusual case of acromegaloidism secondary to pachydermoperiostosis. Case presentation: A 32 year-old hispanic male was admitted to the trauma service after a motor vehicle accident. Endocrinology consultation was requested for questionable acromegaloid appearance. Patient was essentially asymptomatic prior to admission. On direct questioning, he did state that his hands and feet had gotten bigger over last 5 years requiring different shoe sizes. His forehead had also become more prominent. The patient denied any significant past medical or surgical history; his social and family history was noncontributory. Physical examination revealed a normotensive male with BMI 23 kg/m2; he had coarse facial features with seborrheic dermatitis of his scalp and face. He also had enlarged, protruding jaw, enlarged hands and feet with skin thickening, and mild clubbing. There was no evidence of congestive heart failure or valvular dysfunction, or joint abnormalities. Initial laboratory workup including a comprehensive metabolic panel, IGF-1 (127 [106-255] ng/ml), prolactin, testosterone, LH, FSH, TSH, free T4 was within normal limits. Repeat set of labs specifically assessing growth hormone overproduction were within reference range as well: IGF-1 122(106-255) ng/ml, IGFPB-3 2710(2500-5806) ng/ml, GH 0.26(0.011.0) ng/ml and Insulin 4(3.5-30) ВµU/ml. MRI of the pituitary to rule out a вЂ�burnt-out’ tumor was negative for any abnormality. X-rays of the hand and distal ulna revealed hyperostotic bone dysplasia and cortical thickening. Discussion: This typical radiographic abnormality with acgromegaloid features is consistent with a rare condition called pachydermoperiostosis or primary hypertrophic osteoarthropathy. This disease is a rare genetic disorder, and can lead to significant disability with musculoskeletal morbidity with advancing polyarthritis. It is more common in African American males; our case is unusual given his Hispanic origin. Conclusion: We present a case of pachydermoperiostosis, one of the differential diagnoses of acromegaloidism, and often confused with acromegaly. Diagnosis is based on characteristic phenotypical and radiological abnormality and ruling out other diseases.В It is important to recognize this condition as a differential in workup of acromegaly since no hormonal abnormality (growth hormone or other- Background: Male hypogonadism is a condition in which the body fails to produce enough testosterone or a deficiency in spermatozoa production or both. It may result from a disorder of the testes (primary hypogonadism) or of the hypothalamic-pituitary axis (secondary hypogonadism). It is oft encountered in clinical practice. This case report serves to describe the clinical features and cause of hypogonadism occurring in a young man. Case Report: A 39-year-old man presenting with a 5year history of erectile dysfunction and infertility. Further questioning revealed a history of reduced libido, increase in breast size and reduced body hair. He also complained of easy fatigability and weight gain. He admitted to loss of early morning erections and a history of reduction in penile and testicular size. He noticed these adverse bodily changes progressively over a period of 5 years preceded by a history of torsion of both testes. (He had torsion of his left testis and refused surgical intervention. He subsequently had torsion of the right testis a year later). He had no history suggestive of a thyroidal disorder. There is no family history of delayed sexual maturation. He is the first male in a family of six children and his younger brothers have no history of sexual dysfunction. Examination revealed a young man with a feminine body pattern (absence of beard, and body hair, gynaecomastia–Tanner Stage 4). He had eunuchoidal bodily proportions. Weight was 120Kg, height 1.62m and a BMI of 46Kg/m2. He also had centripetal obesity with a waist circumference of 115cm. The cardiovascular system examination was essentially normal. Genital examination revealed bilateral pea sized testes. An assessment of the testicular size using an orchidometer was 2ml. Investigation results showed normal thyroid function test, low testosterone levels and elevated gonadotrophin levels. Discussion: Hypogonadism can affect males at any age and present with clinical features which differ according to the timing of disease onset in relation to puberty. In post-pubertal onset, the established secondary sexual characteristics regress slowly, and the effects can occur at different rates. Energy and libido diminish within days to weeks and the hematocrit decline within a few months. Decreases in sexual hair, muscle mass, and bone – 70 – ABSTRACTS – Other over decades. The condition is relatively common among Finns, Sardinians, and Iranian Jews. This is the first study of APECED in the Saudi population. Conclusions: APCED manifested at an early life in all, majority of cases were familial, & it was relatively common in females. The rank order distribution of the organ system exhibited the following pattern: HP was most frequently present, followed by MC, alopecia, KCJ, AI, hepatitis. T1 DM, hypothyroidism & PA were least frequent. Sequential involvement of different organ system did not manifest a predictable pattern. Early age HP/MC should trigger the possibility of APCED & longitudinal FU should be undertaken at uncovering other organs involvement. mineral density are usually not recognized until years later. Testicular torsion causes permanent damage especially if not treated promptly. Conclusion: Testicular torsion, a surgical emergency could lead to primary hypogonadism. Abstract #702 AUTOIMMUNE POLYENDOCRINOPATHYCANDIDIASIS- ECTODERMAL DYSTROPHY (APECED) Mohammed Ahmed, MD, FACP, FACE, Saud Al-Harthi, MD, and Bassam Bin-Abbas MD Abstract #703 Objectives: To study the natural history of Autoimmune Polyendocrinopathy-Candidiasis-Ectodermal Dystrophy (APECED) in the Saudi population, with a special emphasis regarding the variability of the syndrome. Specifically, our objective was to explore the age of onset, the sequence in which the clinical features unfold with advancing age, constellation of the affected organ system, relative frequency of each affected organs,& the presence or absence of malignancy. Case Presentation: It was a retrospective study of clinical, biochemical, & hormonal data for 13 pts. They were first diagnosed with APCED at ages ranging 1 ВЅ 8 yrs; there were 8 females & 5 males. Familial cases accounted for 10 cases. The frequency distribution of the organ system involved were: Hypoparathyroidism (HP) was the commonest endocrinopathy (12: 92%), followed by mucocutaneous candidiasis (MC) (10:77%), alopecia (7: 54%), keratoconjunctivitis (KCJ: 5:38%), adrenal insufficiency (AI: 4:31%), hepatitis 3 (23%). Type 1 diabetes mellitus (DM) & primary hypothyroidism each was present in 2 pts.(15%). One pt. had Pernicious anemia (PA). HP was the presenting feature in 6(46%) & MC in 4 (31%). Pts. were followed for a median of 77 months. There was no orderly sequence of the evolution of organ involvement. For example HP was followed by either DM or hepatitis, or dystrophic nail changes; alternatively HP followed MC. Synchronous involvement of various organs consisting of MC, HP, KCJ, hepatitis occurred in one, MC & alopecia in another, & MC & AI in a third pt. Liver Cirrhosis complicated hepatitis in one pt. None had kidney involvement, celiac disease nor cancer. Discussion: APECED is a rare autosomal recessive disorder with protean clinical manifestations. The cardinal features consist of classical triad of chronic MC, HP, and AI. Two of these, the dyad, are required for the diagnosis. However, the disorder is much more complex and variable with several other clinical features unfolding THE ENDOCRINOPATHIES OF END STAGE ANOREXIA NERVOSA Lisa S. Usdan, MD, Lalita Khaodhiar, MD, and Caroline M. Apovian, MD Objective: To discuss the endocrine abnormalities which develop in end stage anorexia nervosa (AN). Case Presentation: A 20 year old woman was admitted with malnutrition, dizziness, weakness, electrolyte instability, profound bradycardia, and hypothermia.В She had struggled with AN for five years.В Prior to admission she consumed 200 calories a day. She weighed 68 pounds, and her body mass index was 11.7.В Physical exam revealed an extremely cachexic, restless female with cool skin, bradycardia, and profound muscle atrophy.В Admission labs revealed thrombocytopenia, neutropenia, hypoglycemia, and transaminitis. She had a complicated hospital course involving resistance to refeeding, transient hepatic failure, severe edema, and urgent neurosurgical intervention following a fall.В Refeeding was initiated and maintained in the postoperative period.В A 10% weight gain was achieved at discharge. Discussion: AN is a life-threatening psychiatric illness associated with significant morbidity and mortality.В Severe malnutrition precipitates hormonal aberrancies which help preserve energy in times of inadequate nutrition. All hormonal axes appear to be affected by starvation. Amenorrhea is a diagnostic criteria for AN, and is noted early in the disease course.В Although amenorrhea impairs ovulation and fertility, the lack of estrogen also leads to significant and sometimes irreversible bone loss.В Growth hormone and glucocorticoid resistance are well described findings in AN.В The thyroid dysfunction seen in AN is akin to sick euthyroid syndrome.В Osteoporosis is very common in patients with AN due to a variety of hormonal and activity factors. – 71 – ABSTRACTS – Other Treating the AN patient involves a multidisciplinary approach to maximize caloric intake while preventing the medical complications of refeeding syndrome.В Behavioral therapy and social support must also be available to address the psychiatric needs of these patients.В Maintaining a healthy weight is crucial for resolving the hormonal aberrancies of AN, as well as for achieving a cure of this devastating illness. Conclusion: AN is a severe psychiatric disorder which can lead to extreme malnutrition and starvation.В AN provides a model for the body’s hormonal response to starvation.В Alterations in the hormonal axes are initially adaptive, mitigating the devastating consequences of starvation.В Those who recover from AN face long term complications from prolonged malnutrition, such as osteoporosis and infertility.В AN patients require close monitoring as interventions geared toward achieving a healthy weight are aggressively pursued. Abstract #704 POST-OPERATIVE ADJUVANT RADIATION THERAPY FOR PARATHYROID CARCINOMA CAN BE ASSOCIATED WITH PROLONGED DISEASE-FREE SURVIVAL John T. Chow, MD, Robert L. Foote, MD, Haitham S. Abu-Lebdeh, MD, and Robert A. Wermers, MD fractions (range, 30-35) over 50 days (range, 42-63).В At the time of last follow-up, none of the 5 patients who had undergone adjuvant RT had evidence of recurrence (mean follow-up duration, 95 months).В Recurrence occurred in 9 of 22 patients (41%) who underwent surgery alone and returned for follow-up at our institution. Discussion: Parathyroid carcinoma is a rare cause of hyperparathyroidism, and can have a variable clinical course.В En bloc surgical resection is the standard method of treatment, but cure is often not possible due to tumor burden or microscopic disease.В In a previous retrospective review of patients at the Mayo Clinic, the 5-year rate of locoregional disease progression was 44% in patients treated with surgery alone.В Although there is controversy as to whether adjuvant RT changes the outcome of patients with parathyroid carcinoma, there is evidence that the disease-free interval can be increased.В Our study supports this notion in a small subset of patients seen at a large referral center, at especially high risk for recurrence.В Although there are no clear guidelines for the use of adjuvant RT, it is reasonable to consider this measure in patients at high risk for post-operative locoregional progression. В Data from larger cohorts is needed to identify patients most suitedВ for adjuvant RT. Conclusion: In patients with parathyroid carcinoma at high risk for recurrence following en bloc resection, adjuvant RT may provide prolonged disease-free survival. Abstract #705 Objective: To assess long-term outcome in patients with parathyroid carcinoma treated with post-operative adjuvant radiation therapy (RT). Methods: All cases of parathyroid carcinoma from January 1, 1991 to December 31, 2006, were identified through the diagnostic code index and tumor registry of the Mayo Clinic (Rochester, MN) and reviewed through the medical record.В Patients included in the analysis required confirmation of surgical pathology at our institution, if the initial operation was performed elsewhere. Result: Thirty-four confirmed diagnoses of parathyroid carcinoma were identified, of which 25 patients (74%) had at least one operation performed at our institution.В The mean age at the time of surgery was 52 years, and the male: female ratio was 1:1.В The mean pre-operative serum calcium was 13.7 mg/dL.В Adjuvant RT was administered to 5 patients due to concerns of residual microscopic disease following surgery (including 3 with evidence of tumor invasion into soft tissue).В The mean pre-operative calcium and post-radiation calcium levels in this subset were 14.1 mg/dL and 9.5 mg/dL, respectively.В The median radiation dose was 70 Gy (range, 60-70), administered in 35 CHROMIUM INFUSION REVERSES EXTREME INSULIN RESISTANCE IN THE CARDIOTHORACIC ICU Michael Via, MD, Jayashree Raikhelkar, MD, Corey Scurlock, MD, Gabriele Di Luozzo, MD, and Jeffrey I. Mechanick, MD, FACP, FACE, FACN Objective: To report a case of a thoracic surgery patient who developed extreme insulin resistance postoperatively. The resistance to insulin was apparently attenuated by intravenous chromium, a trace metal micronutrient. Methods: We present a case report, including hourly blood glucose, insulin and chromium infusion data in a critically ill patient. A summary of the related literature is also provided. Result: Insulin resistance is common and often multifactorial in acutely critically ill patients. The patient presented required 2,110 units of insulin over 40 hours following surgical repair of a thoracic aorta aneurysm. After the administration of intravenous chromium, the blood sugar normalized and insulin therapy was discontinued. – 72 – ABSTRACTS – Other Discussion: This case represents an example of extreme insulin resistance, which poses a significant obstacle to successful intensive insulin therapy in the ICU. The administration of intravenous chromium coincides with this patients decline in insulin requirements and improved glycemic control. Conclusion: We utilized a unique approach toward the achievement of glycemic control in acute critical illness. Therapeutic intravenous chromium reduced insulin resistance. calcium excretion. Our patient presented with hypocalcaemia secondary to vitamin D deficiency and decreased calcium consumption. As a 44-year-old adult, he should have been consuming about 1000mg/day of dietary calcium and 200 IU of vitamin D.В By following the Ital diet, our patient believed that his healthy eating habits would protect him from obesity, diabetes and dyslipidemia, which are common to the typical Western diet. Conclusion: Approximately 2.5% of adults in the United States follow vegan diet, and if well-balanced, that diet can provide an adequate source of the necessary vitamins and minerals. Clinicians should emphasize the importance of a well-balanced diet to their vegan patients, educate them about diet supplementation and vegetablebased sources of calcium and vitamin D, and provide early screening for osteoporosis. Abstract #706 UNHEALTHY OUTCOME FROM A “HEALTHY” DIET Kateryna Komarovskiy, MD, and Nathaniel Winer, MD, FACP, FACE Abstract #707 Objective: To describe hypocalcemia caused by dietary modifications in patient from Grenada who was following vegan diet. Case presentations: A 44 year old male without significant past medical history presented with generalized weakness and bone pain for 2 to 3 months. He was practicing Rastafarian culture, including strict vegan (Ital) diet (all food was consumed unprocessed) and was working night shifts. His laboratory tests were significant for calcium, corrected by albumin of 6,6 mg/dl, phosphorus 2.8 mg/dl, intact PTH (parathyroid hormone) 214 pg/ml, creatinine 0.4 mg/dl, magnesium 2.0 mg/dl, vitamin D 25 level less than 4 (20-100) ng/ml, vitamin D1-25 8 (19-67) pg/ml, no evidence of malabsorption. Due to bone pain X-Ray was done and showed poorly healed old fractures of multiple ribs and pelvic bones with evidence of severe osteopenia.В The patient was diagnosed with secondary hyperparathyroidism, hypocalcaemia due to vitamin D deficiency caused by combination of his diet, minimal exposure to sunlight and race (hyperpigmented skin). After dietary counseling, calcium and vitamin D supplementation, his calcium level normalized, and his generalized weakness and bone pain improved. Discussion: In the United States dairy products are major contributors of calcium in the typical diet. Boiling vegetables reduces their calcium content by 25%. Most of commonly accessible products consumed by Ital dieters are poor source of calcium: most vegetables provide less than 5% daily calcium value. Vegetarians consume food rich in oxalic (chives, parsley, spinach) and phytic acids (flaxseed, whole grains, nuts), compounds which interfere with calcium absorption from vegetable sources. In addition, typical vegetarian diets contain less protein, which may reduce – 73 – VITAMIN D DEFICIENCY AND INSULIN RESISTANCE Marjan Vahedi, MD, Gail Nunlee-Bland, MD, Wolali Odonkor, MD, Mariama Semega-Janneh, MD, James T. Williams, MD, Kanwal Gambhir, PhD, and Cynthia Abrams, PhD Objective / Introduction: Vitamin D deficiency has a negative effect on beta cell function and has been linked to metabolic syndrome and insulin resistance. Recent studies have shown that decreased vitamin D level is associated with increased age, body mass index (BMI), systolic blood pressure and decreased HDL-C. Vitamin D supplementation might be an element in the treatment and prevention of diabetes mellitus (DM) type-2.We sought to compare the 25-hydroxyvitamin D (25OHD) levels in a group of obese adolescents with lean controls, and examine its relationship with insulin resistance, body mass index (BMI) and adiponectin. Adiponectin is a protein hormone produced by adipose tissue and low level adiponectin is associated with obesity, diabetes, and cardiovascular disease. Methods: 19 obese African American adolescents with BMI >В 85% for age, with first or second degree relatives with DM, ages 10-21 years, were studied. The control group consisted of 15 normal weight African American adolescents with a family history of DM, of the same age. Parameters compared between the two groups were 25OHD levels, BMI, adiponectin, and insulin resistance measured by Homeostatic Model Assessment (HOMA). Results: The 25OHD level was 13.48 ng/ml +3.97 in the study group vs 20.77 ng /ml +7.45 in the control group (p <0.003). BMI (percentile) was 98.84+ 0.50 in the study ABSTRACTS – Other group, compared to 64.80 +19.25 in the control group (pВ В = 0.000). HOMA was 3.96 +1.84 in the study group vs 2.34+ 0.94 in the control groupВ (p < 0.002). Adiponectin was 6.79 +4.55 in the study group vs 17.28+ 6.89 in the control group (pВ = 0.000). Calcium intake was 46% of the recommended daily allowance in the obese group and 45% in the control group. Vitamin D intake was 67% of the recommended daily allowance in the obese group and 52% in the control group. The difference of the calcium and vitamin D intake was not significantly different between the two groups (p = 0.74 and p = 0.45 respectively). The 25OHD level correlated negatively with HOMA and BMI (p <0.042 and p < 0.002, respectively) but correlated positively with adiponectin level (p <0.001). Conclusion: In these African American adolescent patients, vitamin D levels appear to be related directly to adiponectin and inversely to body mass index and insulin resistance. stopped on Day 5. After stopping levofloxacin the patient did not experience any further hypoglycemic episodes. However despite the continued normolycemia over the next 36 hours there was no improvement in the neurological status. Medical efforts were withdrawn on Day 8 at the request of the family and the patient went home were he expired. Discussion: At the time of the first episode of hypoglycemia the possibilities which were considered in this patient were hypoglycemia due to renal failure and/or because of systemic sepsis. However over the next 48 hours the continued hypoglycemia despite increasing infusions of Dextrose fluids and the elevated serum insulin levels despite low blood sugar values make the above etiologies unlikely. In addition to levofloxacin the patient was receiving piperacillin/ tazobactum, clindamycin, pantoprazole, deltaparin, diclofenac sodium and tramadol. Among the drugs the patient was receiving the most likely cause of the adverse event was levofloxacin. A score of four was obtained on the Naranjo probability scale with levofloxacin which denoted the possibility of hypoglycemia being a levofloxacin related adverse event. Similar to other reports with levofloxacin the hypoglycemia was documented within 24 hours of starting levofloxacin. Our patient was elderly, had underlying renal impairment as seen in other reports. The mechanisms of development of hypoglycemia are related to abnormalities in insulin secretion from the beta cells. Flouroquinolones increase insulin release from rat isolated beta cells. The molecular mechanism of insulin release is similar to sulfonylurea drugs which are by inhibiting the K ATP channels. Conclusion: Hypoglycemia with the use of levofloxacin is an uncommon occurrence but failure to recognize the cause could lead to disastrous results. Abstract #708 FATAL HYPOGLYCEMIA WITH LEVOFLOXACIN USE IN AN ELDERLY PATIENT Jubbin Jagan Jacob, MD, Madhurita Singh, and Navjot Singh Objective: To report a case of Fatal Hypoglycemia with the use of Levofloxacin in an elderly surgical patient. Case Presentation: A 65 year old non diabetic Asian gentleman was admitted with complaints of acute onset severe periumblical pain with a provisional diagnosis of a duodenal ulcer perforation. On admission the patient’s renal function determined by the creatinine clearance was 12ml/ min/1.73m2. After the patient was stabilized with intravenous fluids and dialysis he was taken up for an exploratory laparotomy. Intraoperatively, over two litres of pus was drained from the peritoneal cavity. In the immediate post operative period he was empirically started on piperacillin- tazobactum 4.5 gm three times daily, clindamycin 600 mg three times daily and levofloxacin 200mg once a day. Twenty four hours after the first dose of levofloxacin the patient was noticed to have low blood sugar values with autonomic and neuroglycopenic symptoms. For the next 72 hours patient received multiple infusions of 50% Dextrose and Dextrose containing fluids but continued to have recurrent hypoglycemic episodes with progressively worsening neuroglycopenic symptoms. In the later part of this period the patient developed seizures and decerebrate posturing. Serum insulin levels sent during an episode of hypoglycemia revealed unsuppressed values (57microIU/ml) suggesting hyperinsulinemic hypoglycemia. Levofloxacin was Abstract #709 SURVEY OF THE USE OF LEVOFLOXACIN AND GATIFLOXACIN AND AWARENESS ABOUT ITS POTENTIAL HYPOGLYCEMIC SIDE EFFECTS Jubbin Jagan Jacob, MD, and Navjot Singh MD Objective: Hypoglycemia has been reported with all flouroquinilone antibiotics. Dysglycemic episodes with Gatifloxacin (GTX) are well reported in literature but potential hypoglycemia with Levofloxacin (LFX) is less well reported. This questionnaire survey attempts to quantify prescription practices with respect to LFX and GTX and the awareness of these antibiotics to potentially cause hypoglycemia. – 74 – ABSTRACTS – Other Methods: Questionnaire survey was conducted among doctors in the clinical services of a University affiliated teaching hospital regarding prescription practices with LFX and GTX and about the awareness of its hypoglycemic side effects. Results: About 64 completed questionnaires were obtained out of a 134 doctors approached. Majority of them were from internal medicine or its allied specialties (IMAS) 34 (53%). The rest were from surgery and allied specialties (SAS); 14 (22%), Otolaryngology; 4 (6%), Orthopedics; 4 (6%), Ob/Gyn; 4 (6%) and Critical Care; 4 (6%). Eighteen of 64 doctors (28%) and 19/64 (30%) prescribed LFX more than 3 times a week among Outpatients (OP) & Inpatients (IP) respectively. While 3/64(5%) & 4/64 (7%) prescribed GTX >3/week in IP & OP respectively. 22% and 48% of physicians were aware that LFX & GTX causes hypoglycemia respectively. Five (8%) of doctors recalled having observed a hypoglycemic episode with LFX while 7 (11%) recalled a hypoglycemic episode with GTX. The majority of doctors prescribing LFX (52% &56%) & GTX (9% & 9%) > 3/week in OP & IP were from IMAS. Awareness that LFX and GTX cause hypoglycemia was 9% and 30% respectively among doctors in IMAS. In the SAS awareness was 21% and 2% about hypoglycemia and LFX & GTX respectively. Specifically among those doctors prescribing LFX > 3/week in OP the awareness that it causes hypoglycemia was only 5% and with GTX >3/week in OP it was 50%. Discussion: LFX is more widely prescribed flouroquinilone than GTX in our Hospital. While a little less than half of doctors are aware of the hypoglycemic side effect of GTX only a little over a fifth of the doctors were aware of similar side effects with LFX. There was a higher awareness of LFX induced hypoglycemia among doctors in surgical specialties probably because of an unfortunate death of a surgical patient with LFX induced hypoglycemia. Doctors from Internal medicine and specialties, who were among the most frequent prescribers of LFX, were least aware of the hypoglycemic side effect of LFX. There seemed to be similar number of recalled episodes of Hypoglycemia with both drugs. Conclusion: Despite widespread use of LFX and GTX in medicine and Surgical specialties the awareness about its hypoglycemic side effect is less than satisfactory. There appears to be a prescription bias in favour of LFX as fewer doctors are aware of its potential hypoglycemic side effects though the recalled hypoglycemic episodes with both agents appear to be similar. Abstract #710 THE CHALLENGES OF ENDOCRINOLOGY PRACTICE IN NIGERIA: FOUR ILLUSTRATIVE CASES Felicia Ohunene Anumah, MBBS, MWCP, FMCP Objective: In Nigeria endocrine disorders are on the increase and constitute a significant cause of morbidity and mortality. They have not had much attention because of the enormous burden posed by infectious diseases. This presentation attempts to highlight a few management challenges in our setting using 4 case illustrations in our endocrine practice in Nigeria. Case Presentation: Case 1: A 56year old male motor mechanic who has had diabetes mellitus and hypertension for 20 years, He could not afford proper control of his diabetes and developed bilateral amputation, diabetic retinopathy and nephropathy. He therefore lost the source of income and was eventually dependent on goodwill for his medicare. He died from acute complications of diabetes. This is an illustration of the vicious cycle of poverty and disease which led to fatality. Case 2: A 17 year old female school student from the low socio-economic class. She presented with florid features of Graves disease and Graves ophthalmopathy. She defaulted while on treatment and opted for alternative medical therapy. She unfortunately reappeared a year later to our center with bilateral blindness due to corneal opacity. This patient should have benefited from corneal graft but the facility was not readily available. She has been lost to follow up. Case3: A 20 year old younger brother of a medical doctor who was diagnosed diabetic for 5 years and was placed on insulin therapy. He, however, despite adequate counseling, preferred alternative medical care. He eventually presented in our center with short stature, pancreatic diabetes and malabsorption syndrome. He has since been lost to follow up. Case 4: A 45 year old house wife who presented with features of acromagly and congestive cardiac failure secondary to acromegalic cardiomyopthy. She could not have a complete hormonal assessment because of poverty. She could only afford bromocriptin erratically but was not able to afford other treatment modalities such asВ surgery and radiotherapy. She was eventually lost to follow up. – 75 – ABSTRACTS – Other Conclusion: The four cases illustrated a few of the challenges of endocrine practice such as ignorance, poverty, the menace of untrained alternative caregivers, affordabilty and availability of dequate treatment facilities in our setting. TheВ cases also illustratedВ the impact of disease on morbidity and mortality due to these challenges. hip and spine BMD over time were independent of baseline CrCl (interaction P-values=0.10–0.63). Discussion: Both subgroups showed highly significant relative risk reductions greater than 60%. However, there was a marginally significant treatment-by-baseline CrCl interaction for the reduction in morphometric vertebral fractures, with patients with renal impairment showing a lesser response (P=0.0504). For hip fractures, there was no significant interaction with baseline CrCl (P=0.58), with risk reduction of 34% in the <60 mL/min group and 46% in the ≥60 mL/min group. Conclusion: In conclusion, the 30–40% increase in bone exposure to ZOL in patients with mild-to-moderate renal failure has no significant impact on the skeletal response to ZOL, as assessed by histomorphometry, biomarkers of bone turnover, BMD or antifracture efficacy. Abstract #711 THE SKELETAL RESPONSE TO ZOLEDRONIC ACID IS NOT AFFECTED BY RENAL IMPAIRMENT Paul D. Miller, MD, Steve Boonen, Dennis Black, Deborah Sellmeyer, Henry Bone, Arne Skag, S Giannini, K Lippuner, Peter Mesenbrink, and Erik Fink Eriksen Objective: To test whether or not skeletal response is affected by zoledronic acid in patients with renal impairment. Methods: In patients with mild-to-moderate renal impairment [creatinine clearance (CrCl) >20 mL/min and <60 mL/min], pharmacokinetic studies show a moderate 30–40% increase in serum levels of zoledronic acid (ZOL). To test whether this difference had any impact on the tissue level response to ZOL infusion, we compared skeletal responses to ZOL in patients with a baseline CrCl ≥60 mL/min (n=4222) to the responses observed in patients with a baseline CrCl <60 mL/min (n=3514) in the 3-year HORIZON-Pivotal Fracture Study (n=7736). Patients with a baseline CrCl <30 mL/min were excluded from the study. The analysis comprised bone histomorphometric parameters, bone mineral density (BMD), biomarkers of bone turnover, and morphometric and clinical fractures in the two groups. Result: Comparison of histomorphometry results showed that the reduction of bone turnover, as shown by activation frequency and mineralizing surface, was similar in the two groups (63% in patients with CrCl <60 mL/min vs. 56% in patients with CrCl ≥60 mL/min, and 88% in patients with CrCl <60 mL/min vs. 91% in patients with CrCl ≥60 mL/min, respectively). Microcomputed tomography indices related to bone structure were also unaffected by baseline CrCl. There was no association between treatment and baseline CrCl in the reduction of biochemical markers of bone formation (serum bone-specific alkaline phosphatase and serum procollagen type I intact N-terminal propeptide) and bone resorption (serum C-telopeptides) over time (6–36 months) after treatment with ZOL (interaction P-values=0.09–0.67). Also, increases in total Abstract #712 A FAMILY WITH MEN 2 DUE TO A NOVEL MUTATION Sumedha Ram Pathak, MD, and Ram D. Pathak, MD Objective: To report aВ family withВ MEN 2 with rare mutationВ where phenylalanine (TTC)В replaced cystein (TGC) at codon 618. Case Presentation: A 53 year old male was noted to have thyromegaly. Ultrasound of thyroid revealed a 5 cm nodule in the left lobe. Fine needle aspiration biopsy revealed medullary thyroid cancer (MTC). Serum calcitonin was markedly elevated at 22000. He underwent total thyroidectomy with modified neck dissection on left side. Histopathology revealed invasive medullary carcinoma in both lobes with extension to lymph nodes. There was no family history of MTC. Genetic testing revealed a mutation in RET proto-oncogene at codon 618 where cystein was replaced with phenylalanine and patient was diagnosed with MEN 2. Evaluation for pheochromocytoma was negative. Genetic screening done for this mutation is positive for 6 out of 8 family members, all of whom except a 3 year old grandson underwent total thyroidectomies. All the specimens were positive for medullary thyroid cancer on histopathology. The patient and the affected family members are being serially monitored for pheochromocytoma. Discussion: MTC is a rare calcitonin producing tumor. Familial variety is seen in 3 distinct forms- MEN 2A where it is associated with pheochromocytoma and parathyroid adenoma; MEN 2B where it is associated with pheochromocytoma, marfanoid habitus, mucosal neuromas – 76 – ABSTRACTS – Other and intestinal ganglioneuromas. In third form or familial MTC (FMTC), it is not associated with other manifestations. All 3 forms are inherited as autosomal dominant. Genetic defect involves mutation of RET proto-oncogene on chromosome 10. The majority of mutations in MEN 2A and most in FMTC kindreds involve cystein residue in RET protein’s extracellular domain encoded in exon 10 (codons 609,611, 618 and 620) or 11 (codons 630 or 634). There is a clear genotype-phenotype correlation between specific mutation, component of MEN 2 and course of the disease. We hereby report a novel mutation on codon 618 where cystein residue was changed to phenylalanine. Because FMTC is the most limited variant of MEN 2A, making wrong diagnosis of FMTC could result in missing a pheochromocytoma in a patient with MEN 2. The clinical distinction of FMTC from MEN 2A may be difficult, the designation of FMTC has been changed to MEN 2A in some families. Therefore FMTC kindreds should be defined using more rigorous criteria. Conclusion: Early diagnosis by screening of вЂ�at risk’ family members is essential because MTC is a life threatening disease that can be prevented by early thyroidectomies. Close monitoring for pheochromocytoma is also mandatory. with inappropriately raised proinsulin of 64.1 pmol/L, CPeptide 3.8ng/mL and beta-hydroxybutyric acid of 1.0 mg/ dL. An endoscopic ultrasound guided biopsy of the mass confirmed insulinoma. This was subsequently removed along with another satellite lesion on pancreatectomy and splenectomy. Discussion: This rare case has many interesting learning points. First, Insulinoma is a rare tumor affecting only 1 in 100,000 people in the general population, and less than 10% of the cases are malignant. Secondly, in contrast to our patient’s presentation, islet cell tumors arise most frequently in the fifth to seventh decades. T he history is often lengthy involving neuropsychiatric symptoms and weight gain from increased food ingestion. Third, even though far less is known about the pathogenesis of hypoglycemia induced peripheral neuropathy; it is nearly always symmetrical, predominantly distal, and usually sensori-motor. Conclusion: Juvenile onset Insulinoma with sensori-motor neuropathy is uncommon and rarely described. Unusual manifestations such as those in our patient make the diagnosis even more challenging. An early diagnosis may lead to definitive cure, like surgery in our patient. Abstract #713 METASTATIC GASTRINOMA WITHOUT TYPICAL ZE IN THE STOMACH – NORMALIZATION OF GASTRIN WITH SANDOSTATIN THERAPY Abstract #714 HYPOGLYCEMIC POLYNEUROPATHY IN A JUVENILE: A RARE CASE OF INSULINOMA Deepa Taneja, MBBS, Ralph Miller, Lisa Tannock, and L.R. Reynolds Silvia Velinova, MD, and Rasa Kazlauskaite, MD Objective: To present a rare case of a young patient with asymptomatic metastic gastrinoma. Case Presentation: 27- years-old female was diagnosed with prolactinoma in 1997, after presenting with amenorrhea and galactorrhea. The size of the prolactinoma remained stable at 14 mm for 10 years, while treated with dopamine agonists. The patient was diagnosed with multiple duodenal ulcers in 2003, when she presented with gastric outlet obstruction. Her symptoms resolved with proton pump inhibitor (PPI) treatment. Due to the prolactinoma, fasting gastrin levels were measured (330 pg/ml). Secretin test was also positive, but CT scan, PET and Octreotide scans remained negative. Genetic testing confirmed the diagnosis of multiple endocrine neoplasia (MEN) type 1. She has had mild hypercalcemia periodically. Prior to exploratory laparotomy in 2005, the CT scan of the abdomen revealed 10 mm tumor of the pancreatic head. Laparoscopic wedge resection of the duodenum and lymph node excision, confirmed well-differentiated neuroendocrine tumor with positive gastrin stains (T1N1MX). Background: Insulinoma in children and adolescents is extremely rare. Peripheral neuropathy associated with hypoglycemia is even rarer. We report an unusual case of malignant insulinoma with peripheral neuropathy associated with hypoglycemia in a 16 year old male. Case: A 16 year male was admitted to the ER following motor vehicle collision. CT scan of the abdomen and pelvis demonstrated a presumptive pancreatic tail hematoma that was found to be a 2.5 cm mobile nodular mass on exploratory laparotomy. Resection of this pancreatic mass was deferred due to multiple traumatic injuries. Approximately one year later, the patient was found to be unresponsive at home and his blood glucose was documented to be 25mg/ dL. His symptoms resolved after administration of intravenous glucose. In concurrence with several subsequent hypoglycemic episodes, the patient developed paresthesias in both upper extremities, that later progressed to proximal and distal arm muscle weakness. An overnight fasting test showed plasma glucose of 40 mg/dL associated – 77 – ABSTRACTS – Other Case Report: A 78 year old woman was referred for evaluation of hypercalcemia which was noted several months prior to referral. She did not report any history of anorexia, difficulty in swallowing, weight loss or history of kidney stones. Blood investigation shown high serum calcium, high PTH intact, with normal 24-hour urinary calcium. Thyroid profile was unremarkable. Bone density study shown severe osteoporosis. Tc-99m Sestamibi imaging revealed suggestive of parathyroid adenoma on the lower pole of the right thyroid lobe. Primary hyperparathyroidism possibly due to parathyroid adenoma was confirmed biochemically and radiologically.В Based on the above findings, our patient underwent exploratory neck operation. The location of the adenoma at the inferior part of right thyroid lobe was confirmed by using a navigator probe prior to the procedure. Right thyroid lobectomy was performed because it was believed that the parathyroids are intrathyroidal. The specimen was sent for the histology study. After the operation, the complete disappearance of radioactive activity was confirmed with the probe. Intraoperative parathyroid assay was not carried out due to mechanical failure of machine on that day.В Postoperative serum calcium level shown high level raised the suspicious of possible persistent hyperparathyroidism. Interestingly, the microscopic examination revealed the thyroid lobe containing the Hurthle cell neoplasm with encapsulated angioinvasion with a focus of angioinvasion beyond the level of tumor capsule. Our patient declined for further work up and treatment providing her advanced age and asymptotic for years. Both serum calcium level and PTH intact level are found to be still high in postoperative interval follow up. Four months after surgery, repeat Tc-99m Sestamibi scan also revealed an area of retained activity on lower pole of right side of the neck compatible with a parathyroid adenoma. Discussion: While Tc-99 m Sestamibi scan is now the imaging procedure of choice particularly for localization of parathyroid tumors, the specificity of Sestamibi scans has been questioned because some reports in the literature shown that uptake has been demonstrated in coexisting thyroid carcinoma, metastatic thyroid carcinoma and adenoma.В The presence of Hurthle cell carcinoma obscure the presence of the parathyroid adenoma byВ first Sestamibi scan in our patient. Our report illustrates the importance of awareness of rare coexisting of HCC with primary hyperparathyroidism and it is always prudent to confirm the removal of adenoma by measuring serum PTH in the operating room before withdrawal of anesthesia. Whipple’s procedure was deferred at that time. The abdominal scan in 2006 showed stable size of the pancreatic mass, identified as gastrinoma and a liver mass 15 x 14 mm, confirmed to be a liver metastasis with Octreotide scan.The patient remained completely asymptomatic on PPI with gastrin levels 300 - 500 pg/ml and refused surgical treatment. As Octreotide scan has been positive, she has been treated with Somatostatin with normalization of serum gastrin levels (24 pg/ ml). Discussion: The patient had primary duodenal gastrinoma as part of MEN 1 with lymph node metastasis and residual disease in the head of the pancreas with metastasis to the liver. The size of the pancreatic tumor of less than 3 cm favored less aggressive course. However, a combination of other aggressive growth predictors was present: age younger than 35 years at diagnosis, liver metastasis and duodenal tumor equal or more than 1 cm. The literature suggests surgical debulking of the pancreatic mass and cryoablation of the liver metastasis could potentially improve symptoms and survival, when cure cannot be ascertained. Octreotide, similarly to Lanreotide (known to reduce gastrin level and tumor size) has high affinity for Somatostatin receptor subtype 2 (sst2), but higher for sst5. Sst2 predominance is found in more than 80% of the pancreatic endocrine tumors. However, majority of them express multiple receptor subtypes. Conclusions: Even though we still suggest surgical debulking, adjuvant therapy with PPI and Somatostatinanalog preparations makes plausible sense in this young patient with asymptomatic metastatic gastrinoma. Abstract #715 INCIDENTAL FINDING OF HURTHLE CELL CARCINOMA BY Tc-99 M SESTAMIBI IMAGING IN A PATIENT WITH PRIMARY HYPERPARATHYROIDISM. Hla Win, MD Introduction: Hurthle cell carcinoma, considered as a variant of follicular cell carcinoma of thyroid, accounts < 5% of all differentiated thyroid malignancies.В It may represent as a low-grade tumor or as a more aggressive type. The pathological association of thyroid and parathyroid diseases are not uncommon, but the presence of both thyroid cancer and parathyroid adenoma is rare.В We report a case of incidental finding of Hurthle cell carcinoma by Tc-99m Sestamibi scan in a patient with primary hyperparathyroidism. – 78 – ABSTRACTS – Other tablets along with erythropoietin should be the mainstay of therapy.В Weight gain has been reported to alleviate this condition. Conclusion: Physicians should be aware about possible cardiovascular and neurological complications of rapid weight loss after GBS. Abstract #716 DYSAUTONOMIA, A SIDE EFFECT OF GASTRIC BYPASS SURGERY? Mikhail Signalov, DO, Pratik R. Shukla, DO, and Bankim Bhatt, MD Abstract #717 Objective: Gastric bypass surgery (GBS) has become a common treatment modality in the management of morbid obesity.В The relationship between hypertension, diabetes and obesity is well-established. In most cases, the weight loss after GBS has been associated with significant improvement in diabetes and blood pressure control, but in some cases it can be associated with dysautonomia.В Here, we report a case of 34-year-old woman who developed severe dysautonomia after rapid weight loss as a result of GBS. Case: A 34-year-old woman with past medical history of morbid obesity (BMI 44), status-post GBS thirteen months ago, was admitted with near syncope and dizziness. During recent hospitalization at another institution, an echocardiogram and 24 hour Holter monitoring were normal, while an MRI showed an empty sella with compressed pituitary.В On admission to our institution, she complained of severe dizziness, improving only with supine position, as well as generalized fatigue that has been worsening over the last 5 to 6 months.В She had lost over 175 pounds since her GBS (current BMI 18).В On physical exam, she had significant orthostasis without reflex tachycardia (supine BP 102/64 and upright BP 70/52 with HR 50).В The rest of the physical exam was remarkable only for decreased sensation in lower extremities, left more than right, and absent patellar reflexes. The evaluation of adrenal function showed low morning cortisol level (1.4 mcg/dl) and a brisk response to an ACTH (250 mcg) stimulation test (ACTH = 6 pg/ml, baseline cortisol 2.4mcg/dl, 30 min and 60 min cortisol levels 14.0 and 17.3 respectively). The rest of the work-up (TFT, LH, FSH, Estradiol, Free T4, TSH, T3, B12 CBC, CMP) was normal.В Treatment with steroids did not improve the orthostasis. Abdominal wall fat biopsy was negative for amyloid, while SPEP and UPEP did not show any monoclonal bands.В She was placed on fludrocortisone, salt tablets, and erythropoietin with slow improvement in the dizziness and blood pressure. Discussion: Orthostasis following rapid weight loss after GBS has been reported.В A possible explanation for the orthostasis is a direct effect of the quick change in BMI on the sympathetic nervous system.В It is unlikely that adrenal insufficiency is the primary cause of the hypotension in this case since the patient did not improve with steroid therapy.В Volume expansion with fludrocortisone and salt AN UNUSUAL CASE OF GYNECOMASTIA Jorge Ivan Martinez Osorio, MD, and Jack E. Lewi, MD Objective: Describe an infrequent cause of gynecomastia and increase in level of estradiol and estrone in a patient due to increase ingestion of soymilk. Case Presentation: A 60 year-old Caucasian male presented with bilateral gynecomastia of 6 months of duration, decreased libido and erectile dysfunction. LFT, TSH, LH, FSH, beta HCG, testosterone, prolactin, PSA, androstenodione, and DHEAS levels were normal.В However, serum estradiol and estrone levels were four-times the upper limit of normal. A testicular ultrasound, CT of the chest, abdomen and pelvis and a PET scan were unremarkable.В The patient later reported a daily intake of over three quarts of soymilk due to lactose intolerance.В After discontinuation of the soymilk, his estradiol and estrone levels gradually returned to normal and his gynecomastia slowly improved. Discussion: Gynecomastia has been reported with herbal supplements containing phytoestrogen. Soymilk and soy protein have been extensively studied for the last fifteen years for possible beneficial effects in human health which include: decreased levels of cholesterol, decreased incidence of prostate cancer and breast cancer, decreased menopausal symptoms, and increased bone density. It is very well documented that soymilk has phytoestrogens. More specifically, the soymilk phytoestrogens are known as the isoflavones genistein and daidzein which are structurally and functionally similar to 17 beta-estradiol but with weaker bioactivity than estradiol. Ingested isoflavones undergo biotransformation by the intestinal microflora followed by absorption and enterohepatic recycling which can result in high circulating concentrations. This is one reason why the estradiol levels were delayed in returning to normal. There is much variability in absorption of isoflavones from one individual to another. Soy isoflavones likely interfere with the CYP enzymes that assist in the metabolism of estrogen. It is possible that isoflavones in large amounts could explain the increase in estradiol and estrone levels and caused the gynecomastia in our patient. The normal amount of phytoestrogen in a cup of soymilk – 79 – ABSTRACTS – Other Discussion: Fortunately, symptomatic hypercalcemia that presents during pregnancy is a very rare occurrence, with fewer than 200 cases reported. Asymptomatic hypercalcemia is usually detected incidentally on laboratory tests and can usually be watched, with instructions to increase PO fluid intake. If symptomatic, hypercalcemia usually causes nephrolithiasis, but pancreatitis and hyperemesis gravidarum are known complications. Further investigation poses a problem as sestimibi scans are contraindicated in pregnancy. Ultrasounds can be done in an attempt to localize an adenoma. Surgical parathyroidectomy would ideally be performed in the second trimester, when risks to the mother and fetus are minimized. In the third trimester, options for treatment are surgery or fluid hydration and close monitoring, until the patient is considered safe for induction of delivery and a follow up parathyroidectomy. The presence of 4 gland hyperplasia versus adenoma, as expected in MEN 1 or 2, would not alter treatment in this circumstance. Conclusions: The standard treatments of primary hyperparathyroidism with symptomatic hypercalcemia include medications that are all unsafe in the pregnant patient. In the third trimester of pregnancy, close consultation with the obstetrics team, induction and delivery, and subsequent surgical parathyroidectomy is an effective management for this rare presentation. is 25 mg. Our patient was taking three quarts a day of soy milk which is the equivalent of taking 361mg of isoflavones a day.В His breast tenderness resolved and his estradiol and estrone levels normalized with discontinuation of use of soy products. Conclusion: Soymilk is not considered an herbal or a supplemental medicine. With a myriad of dietary supplements and choices, it is important for health care providers thoroughly review patient’s habits as the review can reveal the etiology of unusual medical conditions. Abstract #718 A CASE OF HYPERCALCEMIA IN A PREGNANT PATIENT Supna Bhagat Lowery, MD, Elizabeth Mason, Donald Richardson, John O’Brian, and Ann Colle Objective: This report demonstrates the therapeutic challenge in the manage-ment of a patient in her third trimester of pregnancy with hypercalcemia and pancreatitis. Case Presentation: We present the unusual case of a 33 week pregnant G2P0 26 year old female with a remote history of prolactinoma, treated intermittently with bromocriptine, and hyperemesis gravidarum earlier in her pregnancy, who now presented with symptoms of abdominal pain, nausea, and vomiting. Amylase and lipase were elevated, and clinical signs were consistent with pancreatitis. In her evalauation, the patient was noted to be hypercalcemic with an ionized calcium of 6.9 mg/dL, elevated PTHs of 60.2 and 90 pg/mL, and a 24 hour urinary calcium level of 767 mg/24 hours, all consistent with primary hyperparathyroidism. The combination of a history of a prolactin-secreting pituitary adenoma and primary hyperparathyroidism suggested MEN1 Syndrome. The routine treatments for hypercalcemia (e.g., calcitonin, bisphosphonates, sensipar) could not be employed as they are all pregnancy category C. As she was in her third trimester, neck exploration surgery was not preferred. The patient was maintained on intravenous hydration and underwent induction at 34 weeks with a successful delivery. She then received intravenous pamidronate as a temporizing measure. A subsequent neck exploration resulted in the removal of a 417 mg adenomatous-appearing parathyroid gland. Intraoperative PTH fell from 182 to 22 (consistent with curative adenomectomy as opposed to a reduction of hyperplastic parathyroid mass). Her Prolactin was 167 at the time of presentation, consistent with physiologic hyperprolactinemia of pregnancy. A MENIN gene test has been ordered. Abstract #719 TURNER SYNDROME ASSOCIATED WITH AORTIC INSUFFICIENCY AGGRAVATED UNDER GROWTH HORMONE AND ESTROPROGESTATIVE THERAPY Cristina Iuliana Bejnariu, MD, and Pavel Suciu, MD Objective: To estimate the evolution of cardiovascular disorders, stature, secondary sexual characteristics, bone density with adequate endocrinologic treatment. Case presentation: We are presenting a 21 year old female with Turner Syndrome (diagnosticated from the age of three years old) associated with aortic insufficiency (second degree), hypertension, polycystic left kidney, youthful glaucoma, chronic lymphedema at the left shank. In the last three years the patient received growth hormone therapy and in the last year it was associated with estroprogestative therapy. Under this therapy the height range was between 139-148 cm. The estroprogestative treatment permitted the maturation of breasts and of genitals. WeВ also administered beta blockers, diuretic and venolymphatic trophic treatment. Her physical examination was remarkable for turnerian fenotype. Systemic examination indi– 80 – ABSTRACTS – Other rhea. Physical examination revealed high blood pressure, facial plethora, moon face, buffalo hump, truncal obesity, branched reddish purple abdominal striae extending to the chest and tights and bilateral lower extremity edema. Laboratories revealed high cortisol levels after low and high doseВ dexamethasone suppression tests, high ACTH levels, metabolic alkalosis, and hypokalemia. That correlates with ectopic ACTH secretion. Abdominopelvic CT scanВ and Thorax CT scan revealed a right pericardial mass. Head MRI suggested a pituitary microadenoma. Patient was referred to cardiothoracic surgery for removal of mediastinal mass.В Pathology reported a carcinoid tumor. Removal of the tumor lead to marked clinical improvement. Four years after tumor resection she presented with recurrence of symptoms clinically and biochemically. No mediastinal masses detected in thorax CT scan. Whole body PET/CT scan showed hypermetabolic left mediastinal tumor. Mass was resected and phenotype study was consistent with a neuroendocrine carcinoma with cytoplasmic expression of ACTH. Patient persisted with evidence of ectopic ACTH secretion after second thoracic surgery. Imaging studies did not reveal evidence of any mass.В Octreotide scintigraphic showed evidence of residual disease. The optimal therapy is surgical excision. Patient is currently on an adrenal enzyme inhibitor, pending radioguided surgery, using a hand-held probe after IV administration of radiolabeled octetreotide. This procedure has allowed detection and removal of residual multiple tumor foci and previous incomplete removal of the tumor in previous case reports. Discussion: Carcinoid Tumor consists of a neuroendocrine carcinoma that can have cytoplasmic expression of ACTH. There is not a single endocrine test or imaging procedure accurate enough to diagnose and localize occult ectopic ACTH-secreting carcinoids, which make them a formidable diagnostic challenge. Recurrences have been previously demonstrated in medical literature years after surgical treatment. These recurrent tumors can be difficult to localize with modalities like CT or MRI. Some ectopic ACTH-secreting tumors can be detected by scintigraphy with 111-In-octreotide or an analog of octreotide В because, like other neuroendocrine tumors, their cells have cellsurface receptors for somatostatin, which illustrate the relevance of octreotide scan as a diagnostic tool to detect carcinoid tumors. Conclusion: We can take advantage of the presence of cell-surface receptors for somatostatin in recurrent carcinoid syndrome, when usualВ imaging modalities fail to localize the tumor.В In this case we identify the tumor using scintigraphy with 111-In-octreotide. This can also help in it’s intraoperative localization using radioguided surgery with IV administration of radiolabeled octreotide. cated aortic regurgitation spill IV/VI. Under this treatment laboratory evaluation showed: subclinical hypotyroidism, hypercholesterolemia, IGF 1 normal range. Radiology exam: osteoporosis,В the presence of growth cartilages. E chocardiography: В bicuspid aortic valve with severe aortic insufficiency (third degree). Pelvic ultrasound: polycystic left kidney. Discussion: Hypotyroidism is often associated with Turner Syndrome but it could appear during growth hormone therapy. SoВ we started to administrate thyroid replacement therapy. В It is known that thyroid hormone have a permissible effect for growth hormone and this increases the growth. It is important to evaluate bone density and how much the estroprogestative treatment in association with growth hormone therapy influences its recovery. We observed that aortic insufficiency had an accelerating evolution in the last year, probably influenced by the highest doses of growth hormone and estroprogestative therapy. At the moment theВ patient needs surgical treatment. Conclusions: Even ifВ the treatment with growth hormone is useful for increase of bone density it is possible that the high doses are aggresive for aortic insufficiency. For that reason the growth hormone therapy should be stopped after the growth cartilages are closed and the estroprogestative therapy remains as of long standing treatment for a good bone density. It is known that patients with Turner syndrome appear to have a decreased life expectancy as a result of complications of heart disease. For a good quality of life the patient needs a variety of follow-up controls which can be obtained through a multidisciplinary approach. Abstract #720 RECURRENCE OF CUSHING’S SYNDROME SECONDARY TO NEUROENDOCRINE TUMOR DETECTED BY OCTREOTIDE SCINTIGRAPHY AFTER A SECOND MEDIASTINAL MASS RESECTION Meliza Martinez, MD, Myriam Allende, MD, Margarita Ramirez, MD, and Vilma Rabell, MD Objective: To report a case of recurrent carcinoid syndrome and the diagnostic usefulness of octreotide scintigraphy for tumor localization. Case presentation: This is a 29 y/o female referred to endocrinology clinics with a two years history of 29 kg weight gain associated with abdominal and facial obesity. В She also presented increase in facial hair, easy bruising, acne, proximal muscle weakness and amenor– 81 – ABSTRACTS – Other Discussion: Metabolic Clinic is ideal for Chronic CAD management with excellent results. What isВ the explanation of these important findings? First let us start from our understanding of the pathogenesis of ischemia in acute vs. chronic CAD. The Atheroma in Acute Coronary Syndrome (ACS) is unstable, vulnerable, has thin surface, few smooth muscles, less supporting collagen fibers, large lipid core, many inflammatory cells, ready to rupture leading to acute MI or unstable angina, often with minor obstructive feature which may not even be recognized on catheterization, thus not treated by stenting until the acute clot phase. On the other hand; Atheroma in chronic Coronary Artery Disease is stable, has thick surface, more smooth muscle cells, more supporting collagen fibers, lesser lipid core, less inflammatory cells, resistant to rupture but produce more obstruction, seen large often at catheterization, and but associated with more symptoms in the pattern of chronic stable Angina and less risk of rupture in acute form. But which one today is treated more by stenting? The numbers speak: 85%В of stenting are done inВ chronic stable disease.В The reverse should be true. Conclusion: Optimum medical therapy in MetabolicВ ClinicВ is recommended to All patients with stable CAD. it is effective in 85% of cases. Stint is reserved to 15% with acute presentations. Optimum medical therapy includes: Aspirin, Statin, B blocker, Ace or ARB, with the intensive management of diabetes, hypertension, obesity, lifestyle changes (diet, exercise and smoking). This is exactly what a good internist or an endocrinologist will do. This is exactly why I believe it is important you stop sending every CAD patients to cardiac catheterization laboratory. Treat in optimum fashion “The deadly quartet”: diabetes, hypertension, obesity, hyperlipedemia, and help your patients modify their lifestyle (smoking, exercise, and diet). This is what our patients deserve because they deserve the best evidence medicine. This is what we are all about in our professional life. This is the future of CAD management. Abstract #721 EDOCRINOLOGISTS SHOULD TREAT MAJOR RISK FACTORS, NOT INVASIVE CARDIOLOGISTS Saad Sakal, MD, FACE Objective: Endocrinologists had a long interest inВ Atherosclerosis as physicians who treat cardiovascular risk factors (diabetes, obesity, hyperlipedemia, hypertension and lifestyles). The question is then who should deal with CAD in their own patients: is the issue of atherosclerosis an issue of biologic vascular integrity for the endocrinologist or just an obstruction for the cardiologist? The question should beВ asked today, not ignored. Methods/Case series: We compared the medical therapy given to ourВ Metabolic clinic patients toВ Optimum medical therapyВ (OMT)В as we know it described in the Courage Trial: 1) Antiplatelets aggregation with small dose of Aspirin or clopidogrel 2) Antianginal therapy with nitrates,В Beta blocker or calcium channel blocker 3) Anti lipids therapy: to lower cholesterol a Statin alone or with ezitimib, To lower triglycerides a fibrate alone or with niacin to raise HDL.В 4) Anti rennin/angiotensin system: an ACE or an ARB. Results: 1) In Courage Trial 70% had LDL cholesterol below 85 mg/dl. (67% in our clinic) 2)94% had diastolic BP below 85, 65%had systolic BP below 130. (ours: 90% and 77% respectively) 3)45% of diabetics had HgA1C below 7%. (ours: 65%) 4)77% followed diet, 40% exercise. (ours: 66% and 55% respectively) 5) Compliance with therapy was very good: 85% received B blocker, 40% nitrate or calcium channel blocker. (ours: 80%and 40%) 95%used Aspirin daily. (ours: 89%) 93%used a statin, 40% used fibrate or ezitimib. (ours: 84%and 64%) 60% used ACE inhibitor, 11% used ARB.( ours : 70% and 20% ) In general a good compliance rate with a reasonable success in therapy end points of similar or better than OMT in the lttreture. At 5 years the CV events were equal. – 82 – ABSTRACTS – Pituitary Disorders can be effective in treating approximately 50% of these adenomas. Therefore, octreotide therapy was initiated in our patient in order to facilitate a more optimal surgical outcome. The nodule in the thyroid, and subsequent histological and Tc99m characteristics were concerning for a concurrent follicular neoplasm. Conclusion: This case demonstrates the importance of complete evaluation of any thyroid abnormality, since, in the setting of a TSH-secreting pituitary adenoma, a goiter or nodule might be attributed to hypertrophy of normal gland, missing a thyroid malignancy. PITUITARY DISORDERS Abstract #800 A PAIN IN THE HEAD AND NECK: A CASE OF A THYROTROPIN/SOMATOTROPIN-SECRETING PITUITARY MACROADNEOMA PRESENTING AS THYROID GOITER Robert J Carpenter, DO, Christopher J. Warner, MD, Nicole M. Dankert-Hsu, William L. Falls, Jeffery S. LaRochelle, MD, and K.M. Shakir, MD Abstract #801 Objective: There are fewer than 350 cases of TSHsecreting pituitary adenomas reported in the medical literature. In order to emphasize the importance of thorough evaluation of any thyroid abnormality, we present a case of a TSH/GH-secreting pituitary macroadenoma that presented with symptoms of hyperthyroidism and thyroid nodule subsequently found to have characteristics of a follicular neoplasm. Case presentation: A 55-year-old Caucasian female with hypertension (treated with atenolol), macular degeneration, and migraines presented with 3-week history of left neck mass. She noted a 20lb weight loss over 3-month period coincident with diet and exercise, and new headache over the prior 3 weeks associated with nausea, emesis, and olfactory hypersensitivity. She reported mild palpitations and denied insomnia, diarrhea, anxiety and heat intolerance. PE was remarkable for blood pressure 197/118, pulse rate 77, fine postural tremor, a 5cm thyroid nodule and normal DTRs. Serum free T4, total T3, and TSH concentrations were all elevated prompting subsequent MRI examination of the sella, which revealed a 2.6x1.5cm enhancing intrasellar mass. Thyroid ultrasound revealed a 5.6x4.1cm nodule in the left lobe. In addition to inappropriately elevated TSH, complete evaluation of anterior pituitary hormone metabolism revealed only elevated serum IGF-1. In addition, oral glucose tolerance testing failed to suppress GH suggesting unregulated secretion of GH by the intrasellar mass. In-111-Octreotide concentrated in both the intrasellar mass and the left thyroid nodule. A 5.0 mCi Tc99m pertechnetate thyroid scan showed decreased activity in the nodule and FNA revealed abundant follicular cells with no definite colloid. Discussion: TSH-secreting adenomas represent a small percentage of pituitary adenomas. Those that also secrete GH are even more rare and account for approximately 16% of TSH-secreting tumors (with fewer than 55 reported in the medical literature). While surgical resection remains the treatment of choice for pituitary adenomas, studies have demonstrated that somatostatin analogs DETECTION OF PITUITARY ADENOMA FOLLOWING USE OF LEUPROLIDE Jasleen Kaur Duggal, MD, Poonam Beniwal, Kanwal Mallhi, Sarabjeet Singh, Navneet Attri, Eshraq Al-Jaghbeer, Paula Butler, and Earl Smith Objective: To report a rare presentation of the pituitary adenoma. Case presentation: A 60 year old African American man was diagnosed with prostate adenocarcinoma via an ultrasound guided transrectal biopsy in June of 2007.В В Pt had a Gleason score ofВ В 6(3+3).Shortly after diagnosis, patient began prostate cancer therapy consisting of daily subcutaneous leuprolide (Gonadotropin Releasing Hormone agonist-GnRH) injections. Approximately fourteen days after initiating this therapy, the patient experienced gradual onset of bilateral diplopia, dizziness, headache (8/10 intensity) and vomiting.В Patient presented to the hospital because of worsening of these symptoms. Examination revealed left eye mydriasis, ptosis, absence of direct and consensual pupil responses, restricted adduction, elevation, and depression motion, consistent with left cranial nerve III and IV deficit. Fundus exam revealed bilateral normal fundi. MRI of the brain revealed a 2x2 cm pituitary adenoma occupying an enlarged sella turcica and extension into the left sphenoid sinus. No hemorrhage observed. Endocrine evaluation were-TSH: 0.65 uIU/mL (0.34-5.60), free T4: 0.85ng/mL (0.58-1.64), FSH: 8.2 mIU/ mL (1.3-19.3), prolactin: 4.0 ng/mL (<15), ACTH: 8.0 pg/ mL (7-50), IGF-1: 77 ng/mL (87-255), IGF BP3: 2.0mg/L (3.4-6.9),Testosterone 0.2 ng/mL(1.75-7.81), urine osmolality: 357Osm (250-1200). This evidence supports the diagnosis of a non-functioning pituitary macroadenoma. A trans-sphenoidal surgical resection was performed. Histopathological examination showed non-functioning pituitary adenoma with hemorrhagic component. – 83 – ABSTRACTS – Pituitary Disorders octreotide(SandostatinTM )30 mg I.M.once monthly.MRI scan obtained six months after initiation of this treatment showed significant reduction of tumor size compared to the pre-treatment images( from 14x12x11 mm to 11x8x7 mm )as well as less mass effect on the optic chiasm. Thus, surgery involving craniotomy to remove the pituitary tumor has been postponed due to the decrease in tumor size in response to medical therapy. Discussion: NFMA of the pituitary gland are generally treated surgically; however, the results are often disappointing. Most studies have found a very limited or no effect of octreotide and/or cabergoline therapy on shrinking the NFMA. Anderson et al demonstrated that combination therapy with cabergoline and octreotide in 6 patients with NFMA resulted in a reduction of tumor size. These investigators selected patients based on elevated levels of serum alpha subunit; somatostatin receptor status of the tumors were not evaluated. We are the first to evaluate the somatostatin receptor status of the pituitary tumor by scan and to then assess the response to combination therapy with cabergoline and octreotide. Although OctreoScan demonstrated somatostatin receptors in the pituitary gland, cabergoline was added based on the evidence of previous study reported by Anderson et al. Conclusion: In summary, this case demonstrates that combination treatment with cabergoline and octreotide may be effective in treating somatostatin receptor-positive NFMA. Additional prospective controlled studies are needed to confirm this finding. Discussion: Pituitary adenomas arise from epithelial pituitary cells and account for 10-15% of all intracranial tumors. GnRH agonist given for prostate cancer interacts with LH and FSH receptors and can lead to pituitary tumor growth and apoplexy as in this patient. The symptom complex produced is characterized by its endocrine effects and mass effects. The mass effects manifest as headache, nausea, vomiting, visual impairment and opthalmoplegia which if present acutely denotes a pituitary apoplexy. Our patient exhibited symptoms consistent В with this. Of note was normal hormonal work up indicating non functioning tumor. There was no sequela of pituitary hypofunction that can occur from the pressure effects by the mass. Incidental detection of the adenoma subsequent to the use of GnRH analogues as a rare presentation made this case worth reporting. Conclusion: GnRH analogs may occasionally lead to rapid growth of a silent pituitary adenoma & present acutely as pituitary apoplexy. Clinicians should be aware of this rare complication of GnRH analog therapy. Abstract #802 COMBINATION TREATMENT WITH OCTREOTIDE AND CABERGOLINE REDUCES TUMOR SIZE IN A PATIENT WITH NONFUNCTIONING PITUITARY MACROADENOMA Thaslim Ahamed Kassim, MBBS, William M Yudt, MD, Patrick W Clyde, MD, and K.M. Mohamed Shakir MD Abstract #803 Objective: To demonstrate therapeutic effect of treating somatostatin receptor positive non functioning pituitary macroadenomas (NFMA) with combination therapy of octreotide and cabergoline. Case Presentation: A 42 year old male, 12 years status post transsphenoidal surgery(TSS)of the pituitary gland for NFMA, presented to our hospital for followup. Because of tumor recurrence, he underwent TSS four additional times since his initial surgery 12 years ago. The surgeries resulted in central hypogonadism and diabetes insipidus, for which he takes testosterone gel and desmopressin, respectively. There were no symptoms or signs of other hormonal imbalances. His visual fields were normal. Serum TFT’s,prolactin,IGF-1and alpha subunit levels were normal. A recent MRI of the pituitary revealed a macroadenoma abutting the optic chiasm and nerve. An OctreoScanR (In-111 pentetreotide)spect imaging performed to evaluate whether the patient may respond to somatostatin analogue confirmed the presence of somatostatin receptors in the tumor. After discussing the possible treatment options, he began cabergoline 0.5 mg twice weekly and long-acting PITUITARY APOPLEXY IN AN ELDERLY ANTICOAGULATED GENTLEMAN N Teresa Allison Nimmo, MD, Jonathan Stringer, MD, and Vitaly Kantorovich, MD W A R Objective: To describe a case of pituitary apoplexy in an elderly gentleman on anticoagulation. His presentation and management of this acute insult resulted in a variety of challenging management issues. Case Presentation: A 76 year old previously independent man with multiple chronic medical problems developed progressive lethary and confusion.В He initially presented to his primary care provider with a severe headache and was found to have pituitary apoplexy. Initial imaging studies did not reveal a source for his confusion on chemistry and endocrine lab data indicated he may have an issue with his pituitary function. Discussion: Pituitary apoplexy is a rare cause of pituitary dysfunction. Its onset is described by a classic “thun- W – 84 – IT D H ABSTRACTS – Pituitary Disorders derclap headache” that occurs with sudden onset. There are many risk factors for pituitary apoplexy including trauma, tumors and It is important to assess pituitary function with a suspected pituitary apoplexy. Water and electrolyte balance may also pose a challenge with am acute insult to the pituitary. A patient on antcoagulation may present a unique management dilemma when determining whether on not to discontinue anticoagulation or to proceed with surgical intervention. child with congenital HIV infection and precocious puberty has been described. There is need to establish whether is one of the HIV-related endocrinopathies Abstract #805 ENDOCRINOLOGIC ABNORMALITIES IN SELLAR MENINGIOMAS Airani Sathananthan, MD, John Atkinson, MD, Bernd Scheithauer, MD, and Dana Erickson MD Abstract #804 Objective: Review of Endocrinologic Abnormalities in a case series of sellar meningioma. Case Series: Patients were selected from a Mayo Clinic, Rochester MN neurosurgical registry with diagnosis of sellar meningioma between 1987 and 2003. Records were retrospectively reviewed for initial presentation, preand post-operative endocrine status, operative results, and pathology.В The study group consisted of 7 patients (3 male and 5 female), age 31-74 years. Discussion: Initial Presentation: Five patients had visual complaints, one had galactorrhea, and one presented with confusion secondary to hyponatremia. Two additionally had headaches and one had vertigo. Preoperative formal visual field testing was abnormal in 6 out of the 7 patients. Pre-operative Endocrinopathies: Three patients were on dopamine agonist treatment for hyperprolactinemia. The patient with hyponatremia had secondary hypothyroidism and secondary adrenal insufficiency. One patient had pre-existing primary hypothyroidism. 3 patients had no endocrinopathies. Surgical Treatment: Primary surgical approach with goal of tumor debulking was done in 6 patients, and one had primary external radiation followed by surgery. Four had transsphenoidal surgery (3 transnasal endoscopic and 1 sublabial), 1 right orbitofrontal craniotomy, and 1 right pterional craniotomy. One had transphenoidal biopsy only. Post-operative Endocrinopathies: Three patients developed new secondary hypothyroidism, 3 patients had new secondary adrenal insufficiency, one patient had hypogonadism and one had low IGF-1. Two patients had normal pituitary function. No preoperative endocrinopathies reversed. Pathology: Various forms of meningioma were seen including 2 with meningeal meningioma, 1 with psammomatous meningioma, and 1 transitional meningioma. One patient had meningioma with bony infiltration, while one had no further specification of their meningioma Post-operative course: Six patients had residual tumor following surgery. One patient underwent repeat surgery PRECOCIOUS PUBERTY AND HIV INFECTION: A POSSIBLE EMERGING ENDOCRINOPATHY? Sandra Omozehio Iwuala, MBBS, Adekunle Adeyemi – Doro, MBBS, Anas Sabir, MBBS, Ife Odeniyi, MBBS, and Femi Fasanmade, MBBS Objective: To report a case of precocious puberty associated with HIV infection and review the possible association between precocious puberty and HIV infection. Case presentation: The patient presented at age six years with an 11- month history of appearance of features of puberty but denied history of ejaculations or sexual relationship. He had tested positive to HIV five months prior to presentation after his mother was found to be seropositive. There was no history of blood transfusion. Pregnancy and early childhood were unremarkable. There was no family history of precocity. Physical examination revealed a healthy looking, big for age boy, without cafГ©-au-lait spots, visual field defects, or palpable organ enlargement intraabdominally. He was 1.48 m tall and weighed 39 kg. The B.P. was 80/60 mmHg. He had pubic hair of Tanner stage 4.The testes and phallus were of adult size. Basal plasma hormone assays showed testosterone of 0.8ng/ml, LH of 13mIU/ml, FSH of 10mIU/ml, Cortisol 170ng/ml(A.M), DHEA-S of 550ng/ml. His bone age was between 9 to 14 years. Abdominal USS and skull X rays were normal. A diagnosis of central precocious puberty(CPP) was made. He was placed on medroxyprogesterone acetate. Pubertal development has since not progressed. Discussion: HIV infection and/or its treatment are associated with a variety of endocrinopathies. However, precocious puberty ascribable to HIV infection appears to be very rare. The diagnosis of CPP is not in doubt in this patient. He was unable to do further investigations required or get the treatment of choice due to financial constraints as patients still pay out of pocket in our country. Conclusion: It is conjectural that the HIV could have induced the precocious puberty in this boy but such association appears very rare. One case of an African American – 85 – ABSTRACTS – Pituitary Disorders tumors is meningioma and glioma.В Only one previous publication reports a patient with concurrent prolactinoma and vestibular schwannoma.В Although there was no histological confirmation of the prolactinoma, the high prolactin level and the positive response to bromocriptine support the diagnosis.В Coexisting primary brain tumors occur in those with a history of brain irradiation or hereditary neurocutaneous syndromes such as neurofibromatosis types 1 and 2, tuberous sclerosis, and Von Hippel-Lindau disease.В This patient has no personal history of brain irradiation, and no family history of brain, neurocutaneous, or neuroendocrine tumors.В The prevalence of pituitary adenoma has been reported to be 1 in 1000, and that of vestibular schwannoma 1 in 100,000.В Given these statistics, the likelihood of having both of these brain tumors concurrently is very low. Conclusion: The simultaneous presentation of primary brain tumors of different histologies is rare.В Prolactinomas may coexist with other types of brain tumors and each may need a separate therapeutic approach. with near complete resection. Of the other 5 patients, 1 underwent external radiation, 3 were observed and the biopsied patient was treated with external radiation. Five patients had post-operative visual field testing and all had improvement in their vision. Follow-up duration ranged from 4 to 59 months (mean 34). Conclusion: Patients with sellar meningiomas have a heterogeneous presentation, in this series predominately complaints of mass effect. Hyperprolactinemia is present likely due to stalk effect as one of the initial endocrine abnormalities. The majority of patients had residual disease after surgery and five of the seven (71 %) developed partial hypopituitarism. Abstract #806 SIMULTANEOUS PRESENTATION OF PROLACTINOMA AND VESTIBULAR SCHWANNOMA Leo Tchong, MD, Colleen Veloski, MD, and Elias Siraj, MD Abstract #807 Objective: To report a case of prolactinoma presenting as one of two concurrent primary brain tumors with different histologies. Case Presentation: A 45-year-old man presented with headaches, decreased libido, and erectile dysfunction of 5 years duration.В A total testosterone level was low at 24 ng/dL.В The prolactin level was elevated at 2179 ng/mL.В An MRI showed a 3.2 x 2.7 x 2.6 cm sellar mass suggestive of pituitary macroadenoma, and a 3.1 x 4.2 x 3.4 cm mass in the left cerebellopontine angle (CPA) consistent with schwannoma.В Surgical debulking of the latter mass was performed, and the diagnosis of schwannoma was confirmed.В Postoperatively, the prolactin level continued to be high.В Since a pituitary prolactinoma was suspected, bromocriptine therapy was started.В Levothyroxine, hydrocortisone, and a testosterone patch were started for panhypopituitarism confirmed by biochemical testing.В Six weeks after the initiation of bromocriptine therapy, the prolactin level decreased to 172 ng/mL, and was near normal after 9 months of therapy.В Repeat MRI showed an interval decrease in size of the CPA mass consistent with resection, and an interval decrease in size of the sellar mass by approximately 50% after 9 months of dopamine agonist therapy. Discussion: The coexistence of multiple primary brain tumors of different histologies is rare, with the incidence reported to be 0.3% of all brain tumors.В The most common combination of histologically different brain – 86 – PITUITARY MACROADENOMA PRESENTING AS PROGRESSIVE REFRACTORY WEIGHT GAIN DUE TO ADULT GROWTH HORMONE DEFICIENCY Alla Khalfin, DO, and Harriette Mogul, MD Objective: To describe two cases of pituitary macroadenoma presenting as a dramatic weight gain due to occult adult Growth Hormone Deficiency (GHD). Case Presentation: Case 1 is a 63 year old female presented with the complaint of not being able to loose weight despite extensive physical exercise and diet. Her weight was 166.5 lbs and height was 61 inches. She had abdominal girth with waist circumference of 35.5 inches. Glucose tolerance test revealed insulin resistance and impaired glucose tolerance. The patient was started on Metformin, but still remained in the same weight range one year later. IGF1, measured at that time, was 204, BP-1 was 52. Repeat IGF-1 was 90. Growth hormone stimulation test with LDopa confirmed GHD. All other pituitary hormones were normal. MRI of the brain showed pituitary tumor, with an area of central necrosis, displacing infundibular stalk. Case 2 is a 51 year old female, with past medical history of polycystic ovarian syndrome and gestational diabetes requiring insulin, presented for evaluation of obesity. The patient gained 40 lbs in the last 2 years. On physical exam her weight was 202 lbs, height 62 inches. She had truncal ABSTRACTS – Pituitary Disorders obesity, waist measurement was 46 inches. The patient was diagnosed with hyperlipidemia, impaired glucose tolerance and insulin resistance and was also started on Metformin and diet modifications. The patient’s total cholesterol and triglycerides improved significantly from 232 to 187 and from 558 to 97 respectively. However, she achieved minimal weight loss. The measurement of IGF-1 was 65, BP-1 was <5.0. Growth Hormone failed to stimulate with L-Dopa and GHD was confirmed. MRI of the brain was performed demonstrating pituitary macroadenoma involving sell and suprasellar region extending into the sphenoidal sinus. Both patients underwent transphenoidal surgery for the removal of pituitary mass without complications. Discussion: Adult GHD is the most common hormone deficiency among patients with pituitary macroadenomas. It is associated with marked increase in total fat mass, reduction in lean body mass, reduced exercise capacity, disturbed lipoprotein pattern, and reduced quality of life. GHD has been linked to obesity and insulin resistance in numerous investigations. One of the main clinical features of insulin resistance includes central obesity with an increase in intraabdominal adiposity being also a frequent characteristic seen in adults with GHD, including both of our patients. The study by Iton, E etc. found that insulin resistance values in patients with GHD were significantly higher than in normal individuals. It has been proposed that severe insulin resistance in GHD adults is mainly due to inhibition of glucose storage pathway and glycogen synthase activity in peripheral tissues. These metabolic defects seem to be related to the duration of GHD and are associated with alterations in triglyceride levels, abdominal obesity, and fasting insulin. Given that our patients were at increased risk for prevalence of cardiovascular complications accompanying the illustrated metabolic defects and insulin resistance we referred both of them for the removal pituitary tumor. Both patients were able to loose weight after the surgery and had negative glucose tolerance test. Conclusion: The cases presented highlight the importance of testing for GHD in people with new onset of obesity and diagnosed insulin resistance failing the conventional therapy as GHD may be the only manifestation of pituitary macroadenoma. Abstract #808 RESULTS FROM A PHASE II STUDY OF PASIREOTIDE (SOM230) IN PATIENTS WITH ACROMEGALY: EFFECTS ON GLUCOSE METABOLISM AND GROWTH HORMONE NADIR DURING THE ORAL GLUCOSE TOLERANCE TEST Joan Glusman, MD, Nicole Unger, Klaus Mann, Stephan Petersenn, MD, and The Pasireotide Acromegaly Study Group Objective: Pasireotide (SOM230), the novel multireceptor ligand somatostatin analogue, has high binding affinity for four of the five somatostatin receptor subtypes (sst1,2,3 and sst5). In a randomized Phase II study of 59 patients with de novo, persistent or recurrent acromegaly, pasireotide effectively controlled GH and IGF-I levels and reduced pituitary tumor volume. Here we report the impact of pasireotide on glucose metabolism and GH levels during glucose suppression in 12 patients enrolled in the Phase II study. Methods: Patients in this study had a GH level >5 Вµg/L, an elevated IGF-I level and a lack of suppression of GH to <1 Вµg/L post-OGTT. After treatment with octreotide 100 Вµg sc tid for 28 days, patients received pasireotide 200, 400 and 600 Вµg sc bid in random order for 28 days each. Glucose and GH levels were measured during the OGTT in 12 patients prior to treatment, after octreotide treatment and after each pasireotide treatment phase. Results: During glucose suppression, four of the 12 patients had a similar GH nadir (<10% difference) after pasireotide or octreotide treatment (-71.0% vs -72.3%), and eight patients had a stronger GH suppression with pasireotide than with octreotide (-75.1% vs -22.8%). Under fasting conditions prior to therapy, seven patients had normal glucose tolerance, two patients had impaired glucose tolerance, and three patients had diabetes mellitus. At the last assessment during treatment with pasireotide, nine patients remained in the same category, one patient improved, and two patients had increased glucose levels. Similar results were seen for glucose metabolism 120 minutes post-OGTT; after treatment with pasireotide, eight patients remained in the same category they were in prior to therapy, two patients improved, and two patients had increased glucose levels. – 87 – ABSTRACTS – Pituitary Disorders Conclusions: Compared with octreotide, pasireotide suppressed GH levels during the OGTT to a similar extent in four of 12 patients and to a significantly greater extent in eight of 12 patients, indicating that pasireotide may be effective in patients with octreotide-resistant acromegaly. Furthermore, using stringent criteria for glucose tolerance, the majority of patients did not demonstrate relevant changes in glucose metabolism by the end of the pasireotide treatment period. patients had normal IGF-1 levels (56%). With the assumption that an arginine/GHRH test correctly identifies the presence or absence of GHD, these results suggest that the sensitivity of a normal IGF-1 test may be as low as 70% for ruling out GHD in patients where GHD is highly suspected and that the specificity of a low IGF-1 test may be as poor as 56% for correctly diagnosing GHD in this same population. Conclusions: We found that the IGF-1 test had 56% specificity and 70% sensitivity for correctly identifying the status of the GH axis in a population highly likely to have GHD due to underling pituitary disease.В We conclude that although IGF-1 remains a valuable test to screen for GHD, dynamic stimulation tests such as ITT or arginine/GHRH test should still be done in the context of a normal IGF-1 when clinical suspicion for GHD is high. Abstract #809 IGF-1 LEVEL MAYBE NORMAL IN SOME PATIENTS WITH GROWTH HORMONE DEFICIENCY William Henry Ludlam, MD, Jaimie M. Augustine, and Marc R. Mayberg Abstract #810 Objective: To determine the sensitivity and specificity of the IGF-1 level in correctly identifying the status of the GH axis in patients with known pituitary pathology. Case Presentation: Adult GHD is characterized by fatigue, memory loss, central obesity, hyperlipidemia and bone loss. It is typically seen in the context of pituitary pathology caused by tumors, surgery, radiation or other diseases.В Although the arginine/GHRH stimulation test is considered to be a very sensitive (95%) and specific (91%) means of evaluating the GH axis, the measurement of IGF1 (with age specific normal range) is commonly used as a screening test before this or other dynamic GH stimulation tests are performed. Despite its common use as a screening test, it is not clear how sensitive a normal IGF-1 is for ruling out GHD when the clinical suspicion for GHD is high. We reviewed 286 patients evaluated for pituitary disorders at Swedish Medical Center over a 1-year period (12/1/06 to 11/30/07). IGF-1 levels were measured in 194 patients and 57 were noted to be low. 22 of the patients with low IGF1 were further evaluated with arginine/GHRH testing.В 22 additional patients with normal IGF-1 were also evaluated with arginine/GHRH testing due to high clinical suspicion of GHD. Discussion: Of the 22 arginine/GHRH tests performed in patients with low IGF-1, 7 had positive arginine/GHRH tests confirming GHD (GH level < 4.1 ng/dl at five time points over 2h after stimulation with arginine and GHRH) and 15 had negative tests. Of the 22 arginine/GHRH tests performed in patients with normal IGF-1, 3 had positive tests confirming GHD and 19 had negative tests.В Stated otherwise, of the 10 patients with positive arginine/GHRH tests, 7 patients had consistently low IGF-1 levels (70%). Of the 34 patients with negative arginine/GHRH tests, 19 NEURODEGENERATIVE LANGERHANS CELL HISTIOCYTOSIS AND PANHYPOPITUITARISM: A CASE REPORT Nicole Stephanie Nader, MD, Aida Lteif, MD, and Marc Patterson, MD Objective: We examine a case of neurodegenerative Langerhans Cell Histiocytosis (LCH) that was diagnosed years after the development of panhypopituitarism in order to illustrate the importance of obtaining serial MRIs in patients with diabetes insipidus. Case Presentation: We present a 15 year old girl diagnosed at the age of 2 years with diabetes insipidus after she presented with polyuria and polydipsia.В Her MRI showed absence of the posterior bright spot.В At the age of 4.5, she was also diagnosed with central hypothyroidism and ACTH deficiency requiring replacement with thyroid hormone and hydrocortisone.В Growth hormone deficiency was diagnosed at the age of 7 and treatment with growth hormone was initiated at the age of 7.5. At around age 6, the patient began developing hand tremors and poor coordination.В A bone survey did not demonstrate any lytic lesions.В Spinal fluid analysis was negative.В Tumor markers were normal.В A series of MRIs demonstrated progressive enlargement of an area of T2 signal abnormality involving the central and medial cerebellar hemispheres bilaterally.В T1 sequences suggested central cavitation of these lesions. There was also slight progression of an area of T1 hyperintensity in the globus pallidus bilaterally.В The small volume pituitary demonstrated no focal lesions, although the infundibular stalk was mildly deviated to the left.В These findings were consistent with the neurodegenerative form of LCH. – 88 – ABSTRACTS – Pituitary Disorders At age 15, the patient is intellectually delayed, with severe dysarthria, ataxia, and spasticity. She is mobile only in a wheelchair. Discussion: LCH is caused by a clonal proliferation of dendritic cells.В В Diabetes insipidus and anterior pituitary hormone deficiencies are the most common CNS manifestations of LCH being seen in 10%-20% of LCH patients.В A neurodegenerative form of LCH has also been described, but is much rarer.В This form is characterized by lesions seen on MRI located in the cerebellum or basal ganglia which lack active LCH cells. Previous research has shown that neurodegeneration is present after 15 years in 10.8% of patients with LCH and pituitary dysfunction, but seen in only 0.4% of LCH patients without pituitary dysfunction. В Therefore, LCH patients who develop endocrinopathies are at risk for neurodegeneration and require long term follow up. Conclusion: Since LCH is sometimes not found until years after the diagnosis of diabetes insipidus or panhypopituitarism, serial MRIs are warranted in children with a diagnosis of diabetes insipidus even in the absence of neurologic symptoms and other features of LCH.В Early recognition of neurodegenerative LCH may lead to better treatment options. increased to only 136 nmol/L following synacthen administration. Serum ACTH: <1 ng/L (RR: 5-60), FT4 6.0 pmol/ L (RR:12-22), TSH 0.59 mU/L (RR: 0.27-4.2), testosterone <0.1 nmol/L (9.9-27.8), free androgen index <0.1% (14.8-94.8), LH <0.1 IU (1.7-8.60, FSH 0.6 IU (1.5-12.4), prolactin 17.1 ug/L (4.1-18.4), GH 0.8 mU/L (0-13), IGF1 <25 ug/l (116-358), serum osmolalityВ 275 mosmol/kg, (275-300), low urine osmolality (182), inappropriately low urine Na+ (61 nmol/L).The Dx of hypopituitarism due to pituitary metastases was entertained; MRI showed a large 38x36x34 mm complex solid, partially multicystic sellar and suprasellar mass. Pt. received hormonal replacement consisting of hydrocortisone followed by LT4 & testosterone replacement. As expected underlying central diabetes requiring DDAVP administration got unmasked following this replacement Rx. At transspenoidal surgery only limited decompression could be achieved. Histopathology: metastatic adenocarcinoma compatible with intestinal origin. At 6 months following Dx of panhypoituitarism pt. is alive. Discussion: Pituitary metastases are an unusual cause of intrasellar/suprasellar mass. Autopsy series have reported an incidence of 3.6% for pituitary metastases. Breast and lung malignancy are the commonest ones to metastasize to pituitary in accordance with the high prevalence of the two cancers. Although colon cancer is a fairly common malignancy, it rarely metastasizes to the pituitary. Conclusions: The clinical & MRI features of pituitary metastasis can closely mimic pituitary adenoma. Although relatively uncommon, pituitary metastasis should be considered in pts. with advanced cancer in whom hypopituitarism develops. With improved survival of cancer pts. the recognition of pituitary metastases may increase; hormonal Rx can improve their quality of life. Abstract #811 DISTURBED CONCIOUSNESS RESULTING FROM HYPONATREMIA AS A PRESENTING FEATURE OF PANHYPOPITUITARISM DUE TO METASTASIS FROM COLON CARCINOMA. Mohammed Ahmed, MD, FACP, FACE, Shakir Bakkari, MD, Mohammed Al-Harathi, MD, Imaduddin Kanaan, MD, and Hindi Al-hindi, MD Abstract #812 Objective: To describe disturbed consciousness resulting from hyponatremia as a presenting feature of panhypopituitarism due to pituitary metastasis from colon carcinoma. Case Presentation: A 55 year-old man, a known case of colon cancer with metastases to lungs, presented with confusion, hallucination, hypotension (BP 84/52), hypothermia (oral temperature 35 Celsius, bradycardia (PR 52/min).His BMI was 24.He was pale, with pronounced facial wrinkles, absence of axillary and pubic hair and had atrophic testicles. Visual acuity had deteriorated to finger counting at 3 feet in both eyes. On admission he had microcytic hypochromic anemia (Hb 114 g/L), hyponatremia (Na+ 120mmol/L).A clinical diagnosis of panhypopituitarism was made that was confirmed with the following lab data: AM serum cortisol 12.7 nmol/L (RR: 171-536), it DIABETES INSIPIDUS AND HYPOPITUITARISM AS INITIAL PRESENTATIONS OF A SUPRASELLAR ANEURYSM Victor Richard Marlar, MD, Razvan F. Buciuc, MD, Benjamin W. Seale, MD, William C. Nicholas, MD, FACE, FACP, and Christian A. Koch, MD, PhD, FACE, FACP Objective: To report diabetes insipidus as a rare presentation of a suprasellar aneurysm causing panhypopituitarism and to speculate on the mechanism of pituitary dysfunction. Case Description: A 32-yo woman developed severe headaches followed by decreased vision in her left eye. She then was hospitalized for dehydration after presenting with – 89 – ABSTRACTS – Pituitary Disorders hypotension and intractable nausea and vomiting. Further history was notable for fatigue, anorexia, hair loss, amenorrhea, polyuria and polydipsia. Physical exam revealed pale skin, scant pubic hair and a left visual field deficit. CT showed a 14 mm suprasellar lesion felt to represent a pituitary adenoma, however MRI and subsequent angiography confirmed the presence of a paraophthalmic aneurysm causing compression anteriorly to the pituitary and superiorly to the optic chiasm. Laboratory testing revealed panhypopituitarism with the following values: cortisol 0.3, ACTH < 10, free T4 0.47, TSH < 0.006, FSH < 0.4, LH < 0.5, and prolactin <1.4. Also notable were serum Na 151, serum osmolality 335 and urine SG <1.005, suggesting diabetes insipidus. Visual field testing revealed a left temporal hemianopsia. DDAVP was administered with immediate resolution of polyuria and polydipsia, confirming the diagnosis of central diabetes insipidus. The patient underwent endovascular coiling of the aneurysm without complications and was discharged home two days later on prednisone and levothyroxine. DDAVP was prescribed on an as needed basis though she had only required one dose at the time of her one week follow-up. Discussion: Aneurysms projecting into the sellar region account for 1% to 2% of all intracranial aneurysms and mimic pituitary adenomas both clinically and radiologically. They are a rare cause of pituitary dysfunction with less than 40 cases reported. Presentations may include headaches, nausea, visual impairment or symptoms related to hypopituitarism. Review of the literature shows that the gonadal axis is deficient in 67.5% of patients, adrenal axis in 48.6% and thyroid axis in 40.5%. Diabetes insipidus upon presentation is very rare, estimated at <10%. Hyperprolactinemia is usually present, suggesting hypothalamic or pituitary stalk compression rather than intrinsic pituitary damage as the mechanism of hormone deficiencies. Conclusion: Suprasellar aneurysm should be considered in patients diagnosed with a pituitary tumor and reliable imaging techniques are important in making the distinction. While diabetes insipidus could be explained by hypothalamic or stalk compression, low prolactin levels as seen in this case suggest pituitary damage as the pathogenesis for endocrine dysfunction. Abstract #813 A MYCOTIC PITUITARY ABCESS PRESENTING AS PANHYPOPITUATARISM Robert M. Lind, MD, and Mary Vouyiouklis, MD Objective: To describe a case of a fungal pituitary abscess presenting as panhypopituitarism. Case Presentation: A 37 year old Hispanic female with a past medical history of systemic lupus erythematosus presented with complaints of fatigue, dry skin, cold intolerance, and amenorrhea of 8 months duration. She also complained of extreme polyuria and polydipsia. She denied any headaches, blurry vision, or fevers. TSH was 0.39mIU/L, free T4 0.2mcg/dL, total T4 1.6mcg/dL, and total T3 0.9ng/mL. LH was <1mIU/L, FSH 3mIU/L, estradiol 7pg/mL. B-HCG was negative. Prolactin was 78.3ng/ mL. AM cortisol was 0.71mcg/dL, and IGF-1 was 40ng/ mL. Serum Na+ was 146meq/L, with plasma osmolality of 306mOSm/kg, and urine osmolality of 215mOsm/Kg. A diagnosis of hypopituitarism was made, and the patient was started on glucocorticoids, thyroid hormone, oral contraceptives, and nasal DDAVP. Pituitary MRI revealed a 2 cm sellar mass without extension into the cavernous sinus or optic chiasm. The patient was referred to neurosurgery, but returned prior to surgical evaluation with complaints of headaches, diplopia, and a new left sixth cranial nerve palsy. The patient was admitted for emergent surgical intervention. Transsphenoidal surgery revealed a grossly necrotic pituitary mass. Pathology and cultures were consistent with a fungal infection (Candida). The headaches and cranial nerve palsy resolved after surgery and antifungal therapy. The patient remains with panhypopituitarism. Discussion: Pituitary abscesses are rare conditions, with only a few hundred cases reported in the literature. These may develop in the gland via hematogenous routes or direct extension of infection in the sphenoid sinus or the CSF. Risk factors include prior pituitary surgery, irradiation, or an immunocompromised state. Many patients present without any risk factors. The most common presenting complaint is headache, and only a minority present with fever and leukocytosis. The literature suggests that 3050% of patients present with anterior pituitary deficiencies, and about 30% present with diabetes insipidus. Surgical removal provides the most effective treatment. Most common organisms found in culture are staphylococcus, but up to 1/3 of cultures isolate no organisms. Fungal infections are an extremely rare form of pituitary abscesses. Recovery of pituitary function has been shown to be very variable in different cases. – 90 – ABSTRACTS – Pituitary Disorders Conclusion: Pituitary abscesses are rare conditions, but should be included in the differential diagnosis of sellar masses. In this case, the patient had a fungal abscess, which is an even rarer condition. Diagnosis can be challenging in absence of surgical pathology and culture. Pituitary function should be checked preoperatively and followed closely in the postoperative period. spite of lifestyle modifications and development of violaceous striae led to persistent biochemical testing and subsequent diagnosis of Cushing’s disease. Conclusion: The diagnosis of early Cushing’s syndrome is a challenge, especially in an environment of increasing obesity. Maintaining a high level of clinical suspicion and repeating biochemical tests periodically is important in such cases. Abstract #814 Abstract #815 A CLINICAL CONUNDRUM IN DIAGNOSING EARLY CUSHING’S SYNDROME IN AN EPIDEMIC OF OBESITY INCIDENTAL PITUITARY ABNORMALITIES IN PREGNANT WOMEN Ashwini Reddy, MD, and Uzma Khan Deepa Sundararajan, MD, Maneet Kaur Narula, and Harmeet Singh Narula, MD Objective: To describe the challenge in diagnosing early Cushing’s syndrome. Clinical Presentation: A 22 year old active, previously non obese woman was evaluated for a 30 lbs weight gain and “stretch marks” developing over a 9 month period.В No other features of Cushing’s syndrome were noted.В Family history was negative for obesity.В A 24 hours urinary free cortisol (UFC) was 51.8 Вµg/d (normal < 60 Вµg/d).В Thyroid function, CBC and CMP were normal.В The patient returned to the clinic 3 months later with an additional 5 lbs weight gain in spite of diet and lifestyle modifications.В A repeat 24 hours UFC was 74 Вµg/d. The patient was reevaluated at 6 months by which time she had developed violaceous striae on the abdomen with a 6 lbs weight gain.В Another 24 hours UFC was 84.38 Вµg/d.В She was then screened with additional tests including an overnight 1 mg dexamethasone suppression test (DST) with the serum cortisol post test being elevated at 10 Вµg /dl.В Two midnight salivary cortisol samples were obtained, which were both elevated at 0.58 and 0.72 Вµg/dl (0.05- 0.17).В Serum ACTH at 8 am was 9 pg/ml. Serum cortisol after a standard 0.5 mg q 6 hourly two day DST was elevated at 3.7 Вµg /dl.В An MRI of the pituitary and CT of the adrenal glands was normal.В The inferior petrosal sinus to peripheral ACTH ratio revealed a three fold elevation on the right side.В In the interim the patient also developed HTN and hyperglycemia.В As the clinical testing was consistent with Cushing’s disease, the patient underwent a transsphenoidal removal of pituitary tissue which was identified as an adenoma on the pathology report. Discussion: Endogenous Cushing’s syndrome is a relatively uncommon condition and resembles many of the phenotypic features of obesity, PCOS and depression.В One of the major manifestations of the obesity epidemic is the increase in the number of patients with Cushing’s phenotype.В As seen in this case, the continued weight gain in Objective: To describe two cases with pituitary abnormalities incidentally noted during pregnancy Case 1: 26 year oldВ woman, 6 months pregnant with no significant past medical history presented toВ ER with headacheВ for 2 days and left facial weakness. On exam, vitals were stable & visual fieldsВ intact. She hadВ Left facial weakness (lower motor neuron). CT head revealed a pituitary abnormality. A dedicated pituitaryВ MRI revealed enlarged pituitary, 2 cm x 1.2 cm slightly elevating optic chiasm withВ T1 Hyper-В & T2 hypo-intensity suggesting a possible hemorrhage. Detailed pituitaryВ function tests were normal for a pregnant woman (AM Cortisol 25,free T4 0.97,Prolactin 206,FSH & LH low). With pain meds, patient felt well. The presentation wasВ felt to be secondary to Bell’s Palsy, unrelated headache & exuberant pituitary hyperplasia related to pregnancy and decision was made to observe the patient clinically.В The patient’s pregnancyВ proceeded uneventfully and she delivered a healthy baby. She breastfed postpartumВ & repeat hormonal testing & MRI of pituitary were bothВ normal (pituitary 8mm in size, no hemorrhage)В 8 months postpartum Case 2: 39 year oldВ woman,В 6 months pregnant, with no significant past medical history, saw an ophthalmologist for floaters. On exam she wasВ found to have unusual hemorrhages in the eyes, and possible papilledema.В She had a MRI of the brain which incidentally revealedВ enlarged of the pituitary, 1.3cm (H) x 1.2 cm (T), homogeneous with elevation of optic chiasm. The patient denied headaches orВ visual field defects and wasВ asymptomatic apart from floaters. HerВ pregnancy had been coming along well. On Exam, vitals were stable & visualВ fields intact. She did not appear acromegalic or cushingoid. Hormonal testing was normal for a pregnant woman with Prolactin 235, AM Cortisol 30, free T4: 1.1 & undetectable LH, FSH. Her pituitary enlargement was felt to be due to exuber– 91 – ABSTRACTS – Pituitary Disorders function. В Involvement of the anterior pituitary can disrupt secretion of gonadotropic and other hormones. Pituitary MRI in these patients shows significant reduction of the T2 signal intensity, which correlates with excess hepatic intracellular iron and severity of pituitary dysfunction. Our patient with hypogonadotropic hypogonadism had the classic MRI picture of iron deposition in the pituitary gland. Conclusion: Hematogenic disorders that require frequent blood transfusions, especially when coupled with ineffective erythropoiesis, can cause iron overload and failure of multiple endocrine organs. We have reported a unique case of myelodysplastic syndrome, secondary hemochromatosis and anterior pituitary dysfunction. It is important to be aware of this complication, with the potential for development of panhypopituitarism.В Further follow up of pituitary functions is critical in patient management. ant pituitary hyperplasia related to pregnancy and she was observed. Her pregnancy went uneventfully and she delivered a healthy baby girl. Patient breastfed postpartum, and repeat hormonal testing and MRI of pituitary were both normal (pituitary 8mm in size)В 4 months postpartum Discussion & Conclusion: In normal pregnancy, pituitary enlargement (due to lactotroph hyperplasia) up to 10mm isВ considered normal. In some women, as in these two cases more exuberant enlargement of pituitary may be seen. In women presenting with neurological symptoms during pregnancy, it is important to remember exuberant pituitary hyperplasia as a cause of pituitary enlargement to prevent unnecessary therapy including surgery Abstract #816 SECONDARY HEMOCHROMATOSIS OF THE PITUITARY Abstract #817 Marina Strizhevsky, DO, Zinoviy Abelev, Prajesh Joshi, Bianca Alfonso, and Adrienne M. Fleckman PANHYPOPITUITARISM AND DIABETES INSIPIDUS COEXISTING WITH EMPTY SELLA SYNDROME STARTING IN CHILDHOOD Objective: To report a case of hypogonadotropic hypogonadism with transfusional hemochromatosis in a patient with myelodysplastic syndrome (MDS). Case Presentation: A 47 year old African American woman with recently diagnosed diabetes mellitus presented with hyperglycemia.В Her history includes systemic lupus erythematosus, non-Hodgkin’s lymphoma and MDS diagnosed 3 years ago, requiring multiple blood transfusions. She became menopausal 2 years ago. The patient reported increased skin pigmentation and elevated blood sugars about 3 months prior to admission. Physical exam was significant for cachexia, non-uniform hyperpigmentation of the legs, abdomen and neck, and hepatosplenomegaly. On admission hemoglobin A1c was 10 % (6.4 % three months ago), and hemoglobin was 5.7 g/dL. Further work up showed ferritin of 6953 ng/mL, iron of 108 mcg/ dL, undetectable level of estradiol, FSH of 1.9 mU/mL, LH of 0.5 mIU/mL, morning cortisol level of 17 mcg/dL, prolactin of 8.5 ng/mL and normal thyroid function tests. CT of the abdomen and pelvis showed hepatosplenomegaly, hyperdensity in the liver and normal pancreas and adrenal glands. MRI of the brain showed diffuse abnormal low T2 signal of the pituitary gland parenchyma, consistent with iron overload/hemochromatosis. Repeated treatments with chelating agents did not improve ferritin levels. Discussion: Secondary hemochromatosis, an acquired form of parenchymal iron overload, results from increased iron intake or multiple blood transfusions. Iron deposits in the liver, heart and endocrine organs impair their normal Esperanza Valentin, MD, Edgar AvendaГ±o, Ma. пїЅпїЅпїЅпїЅпїЅпїЅпїЅпїЅпїЅпїЅпїЅпїЅпїЅпїЅпїЅпїЅпїЅпїЅпїЅпїЅпїЅпїЅпїЅпїЅпїЅпїЅпїЅпїЅпїЅпїЅпїЅпїЅпїЅпїЅпїЅпїЅпїЅпїЅпїЅпїЅпїЅпїЅпїЅпїЅпїЅпїЅ Alejandra Ramos, Francisco J. GГіmez PГ©rez, and Juan Rull Objective: To present a case of panhypopituitarism and diabetes insipidus with empty sella that initiated in childhood. Case presentation: A 20 year old woman consulted with a history of normal childhood development until age 8, when she developed polyuria, polydipsia, fatigue, asthenia, and stunted growth. She dropped out of school due to poor performance and severe polyuria with increased water ingestion, up to 8 liters/day. Two years later she was diagnosed with diabetes insipidus and GH deficiency; no imaging studies were performed. She received a GH analog for 6 months, grew about 16 cms, but discontinued it and received no further treatment. At first consultation she referred water ingestion of 10 lts/day, nicturia, asthenia, dry skin and primary amenorrhea. At physical examination her appearance was that ofВ a 10 year old child with 143cm in height, she weighed 83lbs, had a BP of 120/80 supine position and 100/70 standing with a pulse of 82xВґ that increased by 15 at position change. Her skin was dry, she had no axillary or pubic hair and her breasts were Tanner I. Her lab findings included serum estrogen < 5, LH 0.3, FSH 0.6, GH 0.05, ACTH 17, cortisol 2, T3 2.2 (1.34-2.73), T4 67.5 (78.38-157.4), TSH 3.93, glucose 90, Na 139, K 4.2 and urinary density 1.003. An MRIВ showed absence – 92 – ABSTRACTS – Pituitary Disorders of both, anterior and posterior pituitary tissue. Her bone age is about 12 years. Cortisone 30 mg and fludrocortisone 0.25 mg/day were initiated. One week later her polyuria and polydipsia increased and she was started on oral desmopressin 0.05mg QD and then BID; and levotiroxine first 25 and one week later 50 mcg/d.Estrogen replacement was started. She isn’t on GH replacement due to economical reasons. Discussion: Although panhypopituarism in children is rare, even more unusual is the coexistence of an empty sella and the combination of panhypopituarism and diabetes insipidus. As is unusual for these children to remain untreated until adulthood. It is believed that 50% of cases with multiple hormonal deficiencies are due to mutations in the PROP-1 gene; in fact these patients frequently develop empty sella due disappearance of the hypophisis; nonetheless it’s coexistence with diabetes insipidus has not to our knowledge been reported. Trauma another possible etiology was not reported by the patient. Conclusion: We report a rare case of panhypopituitarism, diabetes insipidus and empty sella in a young woman whose symptoms presented as a child. PM cortisol 1397 (RR:64-340), abnormal 24h urine free cotrisol 2000 nmol/D (RR:100-379), abnormal overnight 1mg& abnormal 8 mg dexa test (post 1 mg value 760 nmol/l: post 8 mg: 500 nmol/l), serum ACTH 151 ng/l (560 ng/l). Pituitary MRI: enhancing 2.3x1.3 cm mass in lt. pituitary fossa invading parasellar/cavernous sinus w/ a lt. dural tail. An inferior petrosal sinus sampling for ACTH with CRH stimulation was done to determine the source of abnormal ACTH. It confirmed the pituitary source of abnormal ACTH secretion with lateralization to the left. (basal ACTH left/right: 4095/764 ng/l: ratio 5.3: post CRH left/right at +10 min: >20,000/1701: ratio11. 7). AT TSS surgery/histopathology: left sided corticotroph adenoma was removed with unexpected finding of purulent material filling up the sphenoid sinus with 4+ pseudomonas aeruginosa & 3+ polymorphs. Adenoma showed atypical features consisting of increased mitosis, & Ki-67 proliferation index. It was positive for bacterial culture. Postoperatively, pt. developed bacteremia & was treated using appropriate antibiotics with eventual recovery. Discussion: ACTH-producing pituitary macroadenoma is unusual for CD in its size, in association with severe signs/symptoms of hypercortisolemia & in mimicking ectopic ACTH-secreting tumor. Conclusions: ACTH-secreting macroadenoma can mimic ectopicACTH-producing tumors. It can manifest unusual radiological feature consisting of a dural tail that was initially thought to be specific for meningiomas. Tumoral proliferative activity can be determined by the detection of Ki-67 antigen, a biological marker that is significantly higher in invasive adenomas, information that can be useful in therapeutic postoperative management. The case highlights the need to avoid inadequate surgery and extreme care in avoiding inadvertent seeding of infection in pituitary bed in the context of severe immunocompromised state that is characteristic of CD. Abstract #818 CUSHING’S DISEASE MIMICKING ECTOPIC ACTH-SECRETING TUMOR BUT DUE TO ACTH-PRODUCING PITUITARY MACROADENOMA EXHIBITING ATYPICAL FEATURES OF INCREASED MITOSIS & ABNORMAL MIB-1(Ki-67) PROLOFERATIVE INDEX Mohammed Ahmed, MD, FACP, FACE, Saud Al-Harthi, MD, Shaheen Marwan, MD, Ahmed Nazmi, MD, Imaduddin Kanaan, MD, and M Dababo, MD Abstract #819 Objective: We report a case of pituitary macroadenoma (PM) that mimicked ectopic ACTH-secreting tumor in clinical presentation. The resected tumor demonstrated atypical histopathological features. Additionally, an unexpected sphenoid sinus abscess was encountered at transphenoidal surgery (TSS). Case presentation: A 62-yr.man w/Cushing’s disease (CD) was referred from В outside hospital following a minimal debulking of a PM. Pt. presented with myopathy & classical signs of CD, BP was 230/110 despite the use ofВ maximal antihypertensive medications, uncontrolled diabetes (FBS 11.5 mmol/l, HbA1C 10.9%), hypokalmic alkalosis (K+ 2.4 mmol/l, CO2 of 32 mmol/l), loss of diurnal serum cortisol (AM value: 1314 nmol/l (RR:171-536), SHEEHAN’S SYNDROME MASQUERADING AS SYMPTOMATIC HYPONATREMIA Hiba Al-Dabagh, MBBS, Wolali Odonkor, MD, Gail Nunlee-Bland, MD, and Mariama Semega-Janneh, MD Objective: Recognize Sheehan’s syndrome (SS) as one of the disorders to be considered in the differential diagnosis of hyponatremia. Case presentation: Four days after initiating appropriate antibiotic treatment for a urine tract infection, this 46 year-old Hispanic lady was admitted to the hospital – 93 – ABSTRACTS – Pituitary Disorders with persistent vomiting, abdominal and flank pain. On examination she was afebrile, hypotensive (BP 98/56), and dehydrated. She was alert and oriented but irritable and agitated. The remainder of her examination was remarkable for absent axillary hair and sparse pubic hair; no hyperpigmentation. Initial labs revealed Na108 meq/l, Cl 80 meq/l non-anion gap metabolic acidosis, K 3.9 meq/l, BUN 8 mg/dl, Cr 0.8 mg/dl, and glucose 75 mg/dl; serum osmolality was 223 mmol/kg. The review of systems was significant for fatigue, nausea and dizziness for 2 wks prior to presentation, amenorrhea since the age of 29, cold intolerance, hair loss and dry skin. Past medical history is significant for postpartum bleeding after her last delivery. She was not onВ any regular medication and denied smoking, drinking alcohol or using illicit drugs. Family history was not contributory. Evaluation of the hyponatremia revealed normal TSH, low T4 and T3; random cortisol level was low at 1.66 Ојg/dl; ACTH stimulation test confirmed the diagnosis of adrenal insufficiency. She was started on hypertonic saline and decadron which resulted in gradual correction of hyponatremia and resolution of symptoms. Further investigations confirmed a pituitary cause of adrenal insufficiency: ACTH level was < 5 pg/ml; FSH, LH, estradiol, IGF-1 and prolactin were low and an MRI of the brain showed empty sella. A diagnosis of panhypopituitarism was made. The patient was discharged home on prednisone and levothyroxine Discussion: SS is one of the causes of pituitary failure; classically it develops following severe post partum hemorrhage. In pregnancy, pituitary gland enlarges due to estrogen stimulation making it hypervascular and susceptible to acute changes in arterial pressure. Although SS is less frequent in the era of current obstetric care it remains an important cause of hypopituitarism that is often missed for a long period of time. Hyponatremia is reported variably in SS (5-35%) however symptomatic hyponatremia as the initial presentation of SS is uncommon. Conclusion: Hyponatremia is a common problem in general medical practice. A detailed history (including reproductive history in childbearing women) and physical examination is essential to make a timely diagnosis and avoid further morbidity and mortality. Abstract #820 HYPOPITUITARISM AND QUALITY OF LIFE FOLLOWING TRAUMATIC BRAIN INJURY AND SUBARACHNOID HEMORRHAGE Lakshmi Srinivasan, MD, Brian Roberts, Gary Steinberg, David A Spain, MD, Tamara Bushnik, PhD, Zahraa Al-Lawati, Henry L Lew, MD, PhD, and Laurence Katznelson, MD Objective: To correlate pituitary function with quality of life and overall performance-function in patients with a recent history of TBI and SAH Methods: 18 subjects with moderate (Glasgow Coma Scale (GCS) 9-13) or severe (GCS <9) TBI including 6 female (F)/ 12 male (M) with mean age 31.9 yr (range 20 – 59) and 17 with SAH of any Hunt and Hess grade, including 12 F / 5 M of mean age 50.3 yr (range 25 – 64) were evaluated in a cross-sectional study 6-12 months following the event. Pituitary hormonal assessment included prolactin, thyroid and gonadal testing; a low dose (1 mcg) cortrosyn stimulation test (normal > 18 mcg/dL at 45 min) to assess adrenal reserve; and growth hormone (GH) reserve via a GHRH-Arginine stimulation test (GH deficiency defined by peak GH < 10 ng/mL). The вЂ�Satisfaction with Life (SWL)’ questionnaire was administered to assess quality of life. Craig Handicap Assessment and Reporting Technique (CHART), Disability Rating Scale (DRS), and Functional Independence Measure (FIM) were administered to assess overall performance-function Results: Hypopituitarism (at least one axis deficient) was present in 22 (63%) subjects, including 17 (49%) with adrenal insufficiency (AI). Hypothyroidism, GHD, and hypogonadism were present in 7 (20%), 9 (26 %), and no subjects, respectively. Ten subjects (29%) were deficient in at least two axes. Subjects with hypopituitarism (= 1 axis deficient) reported a non-significant trend towards lower quality of life compared to subjects with normal pituitary function (24.1 В± 7.2 vs. 27.9 В± 6.4; p = 0.13). The presence of hypothyroidism correlated negatively with SWL (r=-.-4, p=0.02. В Overall performance-function scores did not correlate with presence of hypopituitarism, though there was a trend towards impaired functional measurements compared to subjects with normal pituitary function (CHART: 533 В± 74.5 vs. 562 В± 82.6 p = 0.35; DRS: 1.3 В± 1.8 vs. 0.7 В± 1.7 p=0.34; FIM: 123 В± 3.2 vs. 124 В± 3.8 p=0.4). There was no statistical difference in functional measures between subjects with isolated AI and those with normal pituitary function. – 94 – ABSTRACTS – Pituitary Disorders months postoperatively, he continues to be symptom-free with normal urinary and midnight salivary cortisol values. Discussion: Cyclic CS is a rare disorder with 65 cases reported in the literature since 1960. It is characterized by periodic fluctuation of adrenal cortisol secretion with cycles of hypercortisolism lasting from 12 hours to 86 days alternating with inter-cyclic phases of normal or low cortisol production lasting from days to years. The cyclic nature of the disease often makes the diagnosis challenging. Cyclic CS is associated most commonly with pituitary corticotroph adenomas and less commonly with ectopic ACTH-producing neoplasms or adrenal adenomas. Ectopic pituitary adenomas are rare. These generally occur in anatomic locations along the path of the embryologic development of the anterior pituitary and may be a cause of surgical failure in the treatment of Cushing disease. Conclusion: To our knowledge, this is the first case of cyclic CS due to an ectopic pituitary adenoma. Conclusions: In our series, hypopituitarism was present in 63% of subjects with history of TBI or SAH. The presence of hypothyroidism correlated with worse quality of life. AI assessed with a low dose cortrosyn stimulation test was more prevalent than previously reported using a standard cortrosyn stimulation test, suggesting that a modest degree of AI may be highly prevalent following TBI and SAH. Endocrine function, particularly thyroid and adrenal, should be routinely tested in these subjects. Abstract #821 CYCLIC CUSHING SYNDROME DUE TO AN ECTOPIC PITUITARY ADENOMA: A CASE REPORT Rahfa Kurdi Zerikly, MD, Esin Eray, MD, Charles Faiman, MD, Robert R. Lorenz, MD, Robert J. Weil, MD, and Amir H. Hamrahian, MD Abstract #822 Objective: To describe a case of an ectopic pituitary adenoma as a rare cause of cyclic Cushing syndrome (CS). Case Presentation: A 39 year-old Caucasian male presented with facial plethora, a 45-pound weight gain and easy bruisability. The following lab results were consistent with hypercortisolemia: urinary free cortisol (UFC) 120 Вµg/d (20-100), two consecutive midnight salivary cortisol 1500 and 384 ng/dL (<100), serum cortisol 13.3 Вµg/dL at 15 minutes during a 2-day DEX/CRH test. The ACTH level of 44 pg/mL (6-48) indicated ACTH-dependent CS. Pituitary MRI was normal. At the time of inferior petrosal sinus sampling (IPSS), he was found not to be hypercortisolemic, which triggered further investigation. Weekly 24hr UFC measurements ranged from 7.3 to 789 Вµg/d, consistent with cyclic CS. He underwent a second IPSS after confirming a significantly elevated 24 hr UFC (692 Вµg) the day before the procedure. Once again, he was found not to be hypercortisolemic during the test (cortisol 5.6 Вµg/dL at baseline) indicating a change in ACTH secretion in less than 24 hours. The patient underwent trans-sphenoidal surgery, during which a 5 mm firm, round midline lesion was encountered in the sphenoid sinus, pedicled to the posterior wall byВ a thin bridge of mucosa. The pituitaryВ gland exploration was normal. The sphenoid sinus lesion had been preoperatively interpreted as a mucosal polypВ on imaging. Microscopically, it was found to be a pituitary adenoma which stained diffusely for ACTH. Postoperatively, the patient became hypocortisolemic and had resolution of all his Cushingoid features. He was found to have normal adrenal function at 3 months following surgery. At 12 SILENT PITUITARY APOPLEXY AS A COMPLICATION OF METASTATIC PROSTATE CANCER THERAPY: MULTIPLE ENDOCRINE IMBALANCES AT TWO POINTS IN THE HYPOTHALAMIC-PITUITARY-ADRENAL AXIS Sofronio Cruz Ramirez, Jr., MD, Simonette Soler, MD, and Latha Dulipsingh, MD Objectives: To describe & review the literature on the atypical presentation of silent pituitary apoplexy as a complication of GnRH agonist treatment for patients with prostate cancer. To present the physiologic effects of medications used in prostate cancer therapy on adrenal steroidogenesis. Case Presentation: An 82-year old male was admitted for altered mental status. He was discharged 3 days prior with the diagnosis of metastatic prostate cancer, with obstructive uropathy on presentation. He was sent to a short-term rehab facility on bicalutamide, ketoconazole, tamsulosin, & received an initial dose of intramuscular leuprolide before discharge. Three days later, the patient was found unarousable, and was brought to the ER. He was found to be hypoglycemic. IV glucose was administered with improvement in sensorium. ROS revealed anorexia, constipation, & easy fatigability, without headache, visual changes, nausea or vomiting. Exam revealed a weak-looking, cachectic, elderly male with pale mucous membranes and dry oral mucosa. He had full extraocular movements and no visual field cuts, proptosis, lid lag, or ptosis. Thyroid – 95 – ABSTRACTS – Pituitary Disorders was nonpalpable. Subsequent evaluation for hyponatremia revealed suppressed TSH (0.34uIU/mL), and low FT4 (0.27ng/dL) & total T3 (0.67ng/mL). He had low ACTH (5pg/mL) & low cortisol (0.4ug/mL). Serum FSH, LH, total & free testosterone were decreased (0.5mIU/mL, 0.5mIU/ mL, 2ng/dL, & 0pg/dL, respectively). Prolactin was 6.0ng/ mL. On standard ACTH stimulation test, there was with low baseline, 30-minute, & 60-minute cortisol (0.2ug/mL, 1.5ug/mL, & 3.4ug/mL, respectively). Brain MRI results were consistent with pituitary apoplexy. He was started on corticosteroids & levothyroxine. Ketoconazole was discontinued. Prednisone, levothyroxine, bicalutamide, tamsulosin, & leuprolide were continued on discharge. Discussion: Pituitary apoplexy is an endocrine emergency classically presenting with headache, nausea, vomiting, visual impairment, and meningismus. Pituitary apoplexy after GnRH analog therapy for advanced prostate cancer has been reported in the setting of an underlying pituitary adenoma. GnRH analogs have become a promising treatment for prostate cancer. The few cases of pituitary apoplexy with GnRH analog use were associated with symptomatic pituitary apoplexy. The presentation is peculiar in that typical signs & symptoms of apoplexy were absent. In addition, impaired response to ACTH stimulation test in the setting of a relatively acute event cannot be fully explained by secondary adrenal insufficiency. Ketoconazole has been reported to cause primary adrenal insufficiency by inhibiting the 11?-hydroxylase step in steroidogenesis. Conclusion: Silent pituitary apoplexy in the setting of GnRH therapy for advanced prostate cancer is rarely recognized and likely underreported. The catastrophic sequelae associated with pituitary apoplexy make recognition of this clinical presentation crucial. The multiple influences of pharmacotherapy for advanced prostate cancer on the HPA axis make cautious interpretation of endocrinologic tests equally important. the disease confined in the brain and was characterized of hydrocephalus and diabetes insipidus. Case description: A 31-year-old female who had history of six months of worsening headache, blurred vision and progressive polyuria, polydipsia and nocturia despite well controlled diabetes mellitus. She also reported amenorrhea and weight gain over the past year. Initial investigation revealed hydrocephalus which was treated by mean of a VP shunt. Physical examination revealed a morbidly obese woman. Visual field exam revealed bitemporal defects. Laboratory studies: prolactin 100 ng/dl, FSH and LH <1mIU/ml, estradiol 23.5 pg/ml, progesterone 0.4 ng/ml and TSH 1.84 ОјIU/ml. Serum and urine osmolality were 310 mOsm/kg and 74 mOsm/kg respectively. Serum sodium was 152 mEq/L and urine volume was 8 L/day. Serum ACE was 19 u/L. No hilar adenopathy was seen in a CXR. CSF fluid revealed high protein, low glucose and lymphocytic pleocytosis. VDRL, HIV Ab and ANA were negative. AFB and fungal culture were also negative. A CT of the brain showed hydrocephalus secondary to fourth ventricle blockage. A MRI of the brain revealed numerous patulous areas of enhancement within the ventricular system which obstructed the ventricular outlet. The evidence for central diabetesВ insipidus, hypogonadism and hyperprolactinemia raised the possibility of infiltrative lesion in the hypothalamo-pituitary area. DDAVP was instituted with an improvement of sodium level and urine output to 138 mmol/L and 4 L/day respectively. A brain biopsy was performed to make a definitive diagnosis. Pathologic examination demonstrated non-necrotizing granulomatous inflammation consistent with neurosarcoidosis. High dose intravenous methylprednisone was started and subsequently changed to oral prednisone. Discussion: CNS involvement occurs in only approximately 5 % of patients with sarcoidosis. In particular, hydrocephalus and central diabetes insipidus due to infiltrative lesions in the hypothalamo-hypophyseal region are relatively unusual manifestations of this disease. Our patient illustrates a rare presentation of sarcoidosis because she exhibited CNS involvement without other systemic manifestations of the disease. Abstract #823 DIABETES INSIPIDUS AND HYDROCEPHALUS: ATYPICAL PRESENTATIONS OF SARCOIDOSIS Tasma Harindhanavudhi, MD, Tanyanan Tanawuttiwat, MD, Natasha Akhter, MD, and Stanley Blumenthal, MD, FACE Objective: Sarcoidosis is a chronic multisystem disorder of unknown cause characterized by the presence of non-caseating epithelioid-cell granulomas. The organs most commonly involved are the lungs, skin, eyes and lymph nodes. We describe a case of sarcoidosis in which – 96 – ABSTRACTS – Pituitary Disorders Conclusion: This case highlighted delayed diagnosis and concormitant presence of hyperpituitarism and hypopituitarism. In the short term patient can be controlled medically but long term management poses challenges. Abstract #824 GIGANTISM ASSOCIATED WITH HYPOPITUITARISM Ifedayo Adeola Odeniyi, MBBS, Adekunle Adeyemi-Doro, MBBS, Chuks Ekpebegh, Olufemi Fasanmade, MBBS, FWACP, and Augustin Ohwovoriole, FMCP, FWACP Abstract #825 SEPTO-OPTIC DYSPLASIA: A RARE CAUSE OF CONGENITAL HYPOPITUITARISM Objective: To present an unusual case of gigantism due to pituitary tumour in a patient who was also having features of hypopituitarism. Case Report: A young Nigerian diagnosed as having gigantism secondary to pituitary adenoma is reported in this communication. He was referred from theВ orthopaedic clinic where he was being managed for pathological fracture. He is 18 year old senior secondary school student. He was very tall compared with his peers in the neighborhood and his siblings. Pregnancy and early childhood were uneventful. He had excessive somnolence, sluggishness and weight gain. His weight was 114 kg, height was 2.10m, upper segment was 1.0m, lower segment was 1.10m and arm span was 2.32m. He was dull, anemic, had thick lips, bilateral gynaecomastia with milky nipple discharge, large hands and feet. He had scanty axillary hair, and his pubic hair distribution was Tanner stage 4. He had bitemporal hemianopia, diminished reflexes globally, but no delayed relaxation phase of the ankle reflex. His pulse rate was 86bpm; blood pressure was 90/60mmHg. Basal growth hormone was markedly elevated. Basal Prolactin was also elevated. Thyroid and testicular functions were impaired. Basal cortisol and stimulated cortisol were equivocal. OGTT with serial growth hormone measurement showed no suppression of growth hormone. Imaging studies confirmed enlarged pituitary fossa due to pituitary tumour. The problems with this patient are hyperpituitarism with hyperprolactinaemia, hypothyroidism, hypogonadism and borderline adrenocortical function. He is currently responding to treatment with bromocriptine and hormonal replacement. Discussion: Gigantism is a rare disorder, a major cause of which is hyperpituitarism. Even rarer is hyperpituitarism causing gigantism in the company of pituitary failure. Our patient has a combination of hypopituitarism and hyperpituitarism as shown by the presence of hypothyroidism, hypogonadism and borderline adrenal function with hyperprolactinaemia and excessive growth hormone. He is on hormonal replacement presently and doing well. The challenge in his management is the refusal of the parents to accept surgical intervention as the better option for the management of his case. Deepa Sundararajan, MD, Maneet Kaur Narula, MD, and Harmeet Singh Narula, MD, FACE Case Presentation: A 27 yВ woman with Panhypopituitarism presented for refill of her meds. She had recently moved from California; old records were unavailable. Her prior endocrinologist also did not have her remote records, and had been refilling her meds.В Physical examination revealed a short obese woman with severe visual impairment without any dysmorphic features. Her biochemical testing at the time of presentation to us was consistent with panhypopituitarism, with IGF-1 of 12 ng/mL (normal 114-492); repeat <25 ng/mL; Prolactin 16ng/mL, free T4 normal on T4 175mcg/d, Cortisol low, on hydrocortisone replacement, gonadotropins undetectable on Estrogens (as birth control pill). She had no evidence of DI. She was diagnosedВ with Growth hormone deficiency (GHD) & adrenal insufficiency at age 9. Hypothyroidism was diagnosed at age 15; she had primary amenorrhea and was started on estrogen at age 19.В SheВ was legally blindВ in her Rt eye and had very poor vision in her left eye and had been toldВ of optic nerve hypoplasia;В sheВ also hadВ astigmatism, nystagmus & myopia. Because of theВ optic nerve abnormalities and the panhypopituitarism, a diagnosis of septo-optic dysplasia was considered. An MRI of the pituitary confirmed severe optic nerve hypoplasia, hypoplastic pituitary, ectopic posterior pituitary, but septum pellucidum was present, likely a variant of septo-optic dyplasia.В Further detailed history from the patient revealed prolonged jaundice as newborn, several hospitalizations as a child for febrile illnesses, frequent migraines, growth delay starting early in life, consistent with congenital panhypopituitarism which was not diagnosed until much later in life. Discussion & Conclusion: Septo-Optic Dysplasia (De Morsier syndrome), a rare developmental disorder, can cause congenital hypopituitarism. ItВ is most commonly sporadic, although rare familial forms, with HESX1 mutations have been described.В Patients typically have abnormalities of septum pellucidum, severe optic nerve hypoplasia and other midline abnormalities. Patients with septo-optic dysplasia may have hypopituitarism and may have morphological abnormalities of the pituitary. Adult endocrinolo– 97 – ABSTRACTS – Pituitary Disorders Conclusions: Timely recognition, prompt glucocorticoid Rx & decompression of pituitary bleed results in a satisfactory outcome. Pituitary apoplexy may produce complete or partial tumor destruction of tumor, may result in serious visual deficits, varying degrees of pituitary insufficiency requiring long term hormonal replacement therapy & empty sella (ES).The presence of an enlarged eroded ES in a patient with visual deficit is a reasonable presumptive evidence of an infracted pre-existing pituitary tumor. gists need to be aware of this syndrome as some cases may not be accurately diagnosed earlier in life. Abstract #826 CLASSICAL PITUITARY APOPLEXY: PRESENTATION AND FOLLOW-UP OF THIRTEEN PATIENTS. Mohammed Ahmed, MD, FACP, FACE, Saleh Al-Ahmed, MD, Mohammed Al-Sheef, MD, and Imaduddin Kanaan, MD Abstract #827 LYMPHOCYTIC HYPOPHYSITIS: A RARE CAUSE OF HYPOPITUITARISM Objective: To report presenting features, FU data & outline recommendations for management of patients with classical pituitary apoplexy (CPA). Case Presentation: Thirteen patients (8 males & 5 females, aged 19-60 yrs) with pituitary adenomas presented with CPA. Apoplexy antedated the presentation by several days to weeks in 4. Eight patients had visual disturbances (bitemporal hemianopsia in 4, acute visual acuity decrease in 2, bilateral blindness in one & optic atrophy in one. Four had cranial nerve paralysis:3rd & 6th cranial nerves in 2 & 6th nerve palsy in 2. All had macroadenomas (suprasellar with/withoutВ parasellar extension) on MRI imaging. All had MRI findings consistent with recent pituitary bleed. The tumors were nonfunctioning in 6,GH-producing in 3, prolactinomas in 3 & ACTH-producing in one. All patients had hormonal deficiencies at presentation. These consisted of hypopituitarism in 5,central hypoadrenalism in 3,central hypogonadism in 3, a combination of central hypothyroidism & hypoadrenalism in one & central hypothyroidism in concepts. were treated with stress doses of glucocorticoids after obtaining blood samples for baseline studies. Twelve pts. had transsphenodial decompression & one had transfrontal surgery. They had FU for 3-164 months. External beam therapy was given to 2 patients (with residual GHsecreting and ACTH-secreting tumors). Seven patients developed empty sella (ES) with resolution of the tumors. Tumor recurrence occurred in 2 patients. Aforementioned hormonal deficiencies have persisted in all requiring replacement therapy. Two patients were lost to follow up at 22 & 34 months. The rest were alive with persistent visual deficits in all but one. Discussion: CPA is a rare acute clinical syndrome of an abrupt onset characterized by sudden headache, disturbed consciousness, & visual disturbance caused by the enlargement of a pituitary tumor due to hemorrhage or an extensive infarction. Little is known about the long term outcome of pts. Most of the reported information relates to a limited experience describing initial presentations of isolated cases or small series. Ana Lugaro-Gomez, MD, Margarita Ramirez, MD, Myriam Allende, MD, and Vilma Rabel, MD Objective: To describe the atypical presentation of a rare cause of hypopituitarism reporting a case of lymphocytic hypophysitis. Case Report: 43 y/o woman with past medical history of fibromyalgia and HBP taking naproxen 500mg po bid and enalapril 5mg po daily who came to our clinic referred due to hyperprolactinemia and galactorrhea. Patient had very strong right sided throbbing headaches, amenorrhea since 4 months previous to the evaluation, decreased libido, 15 pounds weight gain, fatigue, cold intolerance, constipation, dry skin, and axillary hair loss. Also refers polyuria, polydypsia, dizziness, nausea, and vomits and states that she noted the symptoms since about 3 months prior to the evaluation one month after her last menstrual period. Her last delivery was on 1989. Physical examination with stable vital signs and remarkable for dry oral mucosa, decreased temporal vision bilaterally, decreased relaxation phase of the DTR’s, and absence of axillary hair. The brain MRI showed a T2 hyperintense mass expanding the sella and causing mass effect upon the optic chiasm and pituitary stalk. It also showed a right CP angle mass of 1.9cm x 1.3cm. Was found to have hypogonadotropic hypogonadism(FSH-4.03MIU/ML), secondary hypocortisolism(ACTH-less than 10.0pg/ml and cortisolless than 0.20ug/dl), secondary hypothyroidism (TSH0.46MIU/ML, free T4-0.77ng/dl), and hyperprolactinemia (prolactin-55.2ng/ml). Diabetes insipidus was confirmed with a water deprivation test. She was started in hormone replacement therapy for cortisol and thyroid deficiencies as well as DDAVP. She underwent a craniotomy with partial resection of the tumor which pathology showed chronic inflammation and lymphocytic infiltration as seen in lymphocytic hypophysitis. IGF-I levels and new prolactin levels are pending to evaluate for GH deficiency and to – 98 – ABSTRACTS – Pituitary Disorders determine if the hypogonadism is secondary to elevated prolactin levels or due to the infiltration itself. Discussion: Lymphocytic hypophysitis is a rare disorder initially characterized by lymphocytic infiltration and enlargement of the pituitary; followed by destruction of the pituitary cells. Most often occurs in late pregnancy or postpartum period. Female:Male ratio is 8:1 and usually coexists with other autoimmune disorders. About 100 cases has been described since the original report in 1962. Final diagnosis is done based on histological examination due to the lack of markers for the disease as antipituitary antibodies have been detected in only a minority of patients. Affected patients typically present with headaches of intensity out of proportion to the size of the lesion and hypopituitarism. Preferential hypofunction of ACTH and TSH secreting cells has been described. However, diabetes insipidus, hyperprolactinemia, growth hormone excess can be present. Conclusion: This case comprises an atypical presentation for this already uncommon disease which made it difficult to diagnose it on clinical bases only. The patient was not in the peripartum period nor had any associated autoimmune disease. The importance of developing new markers would be helpful in order to diagnose and treat patients like this without the need for a surgical intervention. patient admitted to no medication or follow up for over 10 years. Other causes for pericardial tamponade, including tuberculosis, neoplasia, uremia, bacterial, cardiomyopathy and myocardial infarction were ruled out. Following hemodynamic stabilization, he was given hydrocortisone 100mcg TID and later levothyroxine 50 mcg IV daily. He was discharged on hydrocortisone 20mg in AM and 10mg PM, and levothyroxine 100mg daily. Two months later, TSH normalized; MRI showed a small pituitary gland with no masses and testosterone replacement was begun. Discussion: We will discuss the association of CT with untreated hypothyroidism and hypocortisolism. Cardiac symptoms in hypothyroidism include rhythm disturbances, failure, and ischemic disease. Pericardial effusion is the most common cardiac manifestation of primary hypothyroidism; however, due to the decreased metabolic state, florid tamponade with cardiovascular compromise (as in this case) rarely occurs. The low incidence of CT in hypothyroidism is likely due to slow accumulation of fluid in the pericardium and increased distensibility. Hypocortisolism has also been rarely associated with CT. One case of isolated ACTH deficiency with CT and several cases with Addison’s disease and an autoimmune process linked to serositis have been described. Conclusion: Clinicians should be aware of the association of hypothyroidism and hypocortisolism with CT. A diagnosis of exclusion, this rare and life threatening complication may be the presenting manifestation of these endocrine disorders. Abstract #828 HYPOTHYROIDISM AND HYPOCORTISOLISM PRESENTING WITH CARDIAC TAMPONADE Abstract #829 Evana Valenzuela, MD, Paulina Kunecka, MD, Regina Dodis, MD, and Nancy J. Rennert, MD, FACE TSH-SECRETING PITUITARY MICROADENOMA: DIAGNOSIS BY DYNAMIC CONTRAST ENHANCED MR SCAN AND OCTREOSCAN Objective: To report a case of cardiac tamponade (CT) associated with hypothyroidism and hypocortisolism. Case presentation: A 48 year-old male with a history of pituitary adenoma resection (using a cranial approach) 20 years prior presented with chest pain. Initially, the patient had stable vital signs but decompensated with hypotension (BP 40/negligible) and mental status changes. Physical exam was remarkable for tachycardia and faint pulses. EKG had low voltage and CXR was negative. Echocardiogram showed large pericardial effusion, with evidence of increased pressures (right ventricular diastolic collapse and marked respiratory variation in mitral inflow velocities) consistent with CT. Pressor support was initiated and a pericardial window was performed. Laboratory values on admission showed primary hypothyroidism (TSH 75uIU/ mL, total T4 3.1mcg/dL) and hypocortisolism (random cortisol 3mcg/dL). ACTH was not measured. Testosterone and gonadotropins were low. Upon later questioning, the Mae Sheikh-Ali, MD, Lina Aguirre, MD, Robert Wharen, MD, Leo Czervionke, MD, and Robert C. Smallridge, MD Objective: to demonstrate the advantage of using Dynamic MR Scan for detecting pituitary microadenoma. Case Presentation: A 55-year-old woman presented with irritability, fatigue, nervousness, tremulousness and palpitations.В Her mother had a history of hyperthyroidism.В On physical exam, her pulse = 60/min (on atenolol), and there was no proptosis or visual field defect.В She had a small, firm, diffuse goiter, mild tremor and brisk reflexes.В She had no symptoms or physical evidence of galactorrhea, acromegaly or Cushing’s syndrome.В Serum free T4 В = 3.0 ng/dL (normal < 2.8); free T3 = 558 pg/dL (< 420), and TSH = 1.7 mIU/L (increasing to 7 mIU/L after TRH). – 99 – ABSTRACTS – Pituitary Disorders Alpha-subunit = 1.3 ng/mL. Thyroid stimulating and binding inhibitory immunoglobulins were normal.В Thyroid ultrasound showed a goiter and pituitary MR showed sellar asymmetry but no discrete lesion. Discussion: The mild increase in alpha-subunit and sellar asymmetry suggested a pituitary tumor, but the family history of hyperthyroidism and TSH response to TRH suggested thyroid hormone resistance syndrome.В Conventional MR revealed enlargement of the pituitary gland on the left with deviation of pituitary stalk to the right of the midline.В A dynamic contrast enhanced MR scan of the pituitary revealed a discrete ovoid 6 mm in diameter relatively hypointense mass within the pituitary gland which became visible at 90 seconds post injection. An Octreoscan showed intense uptake in the pituitary region.В Transphenoidal surgery confirmed a TSH tumor (cells positive for TSH, alpha- subunit and rarely for GH and PRL). Three years latter, thyroid tests were normal while taking 25 mcg L- T4, and dynamic MR scan showed no tumor recurrence. Conclusion: This case illustrates the value of multimodality neuroimaging in detecting small pituitary tumors. – 100 – ABSTRACTS – Reproductive Endocrinology Conclusion: Idiopathic hypogonadotrophic hypogonadism is more common than hypergonadotrophic hypogonadism. Testosterone replacement offers men the opportunity to regain some of the vigor of their youth. Done while closely monitored, it is a relatively low-risk proposition that has many benefits, including boosting cognition, muscle mass, and bone density while decreasing abdominal fat. Restoration of a eugonadal state can restore well-being and in crease compliance with other aspects of health care. REPRODUCTIVE ENDOCRINOLOGY Abstract #900 MALE HYPOGONADISM IN TERTIARY CARE CLINIC Saeed Ahmed Mahar, MD, FCPS, Abdul Jabbar, and Najumul Islam Abstract #901 Introduction: Male hypogonadism is one of the most common endocrinologic syndromes. The diagnosis is based on clinical signs and symptoms plus laboratory confirmation via the measurement of low morning testosterone levels on two different occasions. Serum luteinizing (LH) hormone and follicle-stimulating hormone (FSH) levels distinguish between primary (hypergonadotropic) and secondary (hypogonadotropic) hypogonadism. Androgen replacement therapy in hypogonadal men has many potential benefits: improved sexual function, an enhanced sense of well-being, increased lean body mass, decreased body fat, and increased bone density. Objective: To study the presentation and type of hypogonadism. Methods: Medical records were reviewed of all the patients who attended the endocrine clinic at Aga Khan University Hospital Karachi, from January 2000 to December 2006 and were found to have low testosterone levels, were included in the study. The patients with diabetes mellitus were excluded from the study. Results: Sixty one (mean age 24 years) with Hypogonadotropic hypogonadism, and thirteen males (mean age 25 years) with Hypergonadotropic hypogonadism were enrolled in the study. In Hypogonadotropic hypogonadism, common presentations were lack of facial hairs (23%), decreased libido (21.3%), and small penis (19.7%). In Hypergonadotropic hypogonadism, most common presentations were small penis (30.8%), decreased Libido (23.1%), and infertility (23.1%). All patients with Hypogonadotropic hypogonadism had low pretreatment Testosterone levels as compared to Hypergonadotropic hypogonadism (46.13 В± 34.1 vs. 106.92 В± 76.6). Serum FSH and LH level were low in Hypogonadotropic hypogonadism patients. After treatment Axilary hair were increased in all groups of patients. Hypogonadotropic hypogonadism patients were more likely to be young (p=0.03), less likely to have over weight, more liely to have small penis size (p=0.05), sparse axillary hair (p=0.01), less pubic hair (p=0.02), low serum LH (p=0.002), and less likely to have Testosterone level (p=0.001). COMPLETE ANDROGEN INSENSITIVITY SYNDROME Sachin Kumar Jain, MBBS, MD, DM, FACE, Pramila Diwaker, and Ajay Ajamani Objective: To present a case of Complete Androgen Insensitivity Syndrome ( CAIS ). Case Presentation: 37 yr. old reared as a female, presented with primary amenorrhoea Patient had a normal female phenotype and had not ever pursued serious evaluation, was a known case of schizophrenia and was on treatment (Resperidone and Clonazepam) for last 13 yrs.В В There is history ofВ В some problem of sexual development in maternal grandmother’s sister, details of which are not available. Pt’s height-160.9 cms (mother’s ht150 cms, father’s ht-163 cms),which was close to target male height В / BMI-25.7 kg/m2 / female habitus / normal breast development / scanty axillary and pubic hairs В / illdefined swellings in both inguinal regions (gonads) / vaginal orifice admitted В only little finger / rest of the systemic examination was normal. Investigations revealed- normal hemogram and serum chemistry; testosterone 2.08 ng/ml (female<0.81); normal LH 7.55mIU /ml В & FSH 7.32mIU/ ml; serum Prolactin 51.9 ng/ml(up to 25 ng/mlВ increased levels? due to Antipsychotics use); Estradiol 37.4 pg/ml; Androstenedione 3.5 ng/ml(0.3-3.5); DHEAS 197 Вµg/dl (35-430);В TSH 4.37 ВµIU/ml; HCG stimulation test by 2000 IU of HCG intramuscularly for 3 days -S. Testesterone rose from 2.08 to 11.57 ng/ml; USG of abdomen -uterus, cervix, ovary not visualized, thin vaginal strip; MRI abdomen revealed – bilateral В undescended testes in inguinal region with left ependidymal cyst with thin strip of vaginal canal, however uterus, ovaries not visualized; В karyotype was В 46XY. Discussion: Patient had primary amenorrhoea with female phenotype, very few axillary & pubic hair, significant family history, height close to target male height, elevated basals Testosterone and marked rise in testosterone on HCG stimulation test and, bilateral В undescended testes, – 101 – ABSTRACTS – Reproductive Endocrinology no ovary, uterus and male genotype. Based on these, patient was diagnosed as having- Complete Androgen Insensitivity Syndrome. Patient underwent bilateral В gonad excision, which revealed testicular tissues on both specimen with atrophic seminiferous tubules, leydig cell hyperplasia, no spermatogenesis; left gonad revealed sertoli cell adenoma. Bilteral В inguinal hernia repair was done. Vaginal dilatation / reconstruction were not performed, as pt was not sexually active. Post-op testosterone wasВ 0.47 ng/ml with no rise in testosterone after HCG stimulation test; Estradiol 19.71 pg/ml; FSH 39.02 mIU/ml; LH(20.41 mIU/ml; Prolactin В 34.02 ng/ml. Patient В developed postmenopausal symptoms relieved after premarin 0.625mg/day. CAIS is an X-linked recessive disorder with prevalence between 1 in 20,000 to 1 in 60,000 male live births. 1-2% of phenotypic female with bilateral inguinal hernia have CAIS. It is the most common identifiable cause of male pseudohermaphroditism with karyotype XY and mutation in AR gene. At puberty, female habitus with primary amenorrhoea,scanty pubic & axillary hairs, height close to target male height, with testes usually undescended, vestigial mullerian structures; testicular histology reveals В there are sertoli cell only seminiferous tubules with sparse spermatogonia & absent spermatogenesis. Elevated LH, testosterone & estradiol with normal/mildly increased FSH seen upon hormonal evaluation along with positive HCG stimulation test. There is an increased risk of gonadal tumours in Defective Sexual Differentiation especially in presence of Y–chromosome. Conclusion: Our patient had CAIS with left sertoli cell adenoma. Unique feature being that patient presented at the age of 37 years with primary amenorrhoea. Abstract #902 GONADOTROPIN-INDEPENDENT PRECOCIOUS PUBERTY DUE TO TESTOTOXICOSIS and penile length was 8x3cm. Testes were prepubertal and measured 2 cm in greatest diameter. Laboratory studies showed suppressed LH at 0.3 IU/L and FSH at 0.5 IU/L with an elevated testosterone at 125 ng/dL. Thyroid function studies, 17-hydroxyprogesterone, androstenedione and DHEAS were normal. Testicular ultrasound was normal and bone survey was negative for bony dysplasia. His bone age was read between 9 and 10 years. Lupron stimulation showed no LH or FSH response. Genetic testing for familial-male limited precocious puberty (testotoxicosis) was positive.В He was started on anastrazole 1mg daily. At 4 months, bone age is unchanged, LH and FSH are suppressed, testosterone is 38 ng/dL and growth rate is 3.6 cm/year. Discussion: Testotoxicosis is a rare cause of GIPP. It is secondary to an activating mutation of the LH receptor. This is a sex-limited autosomal dominant disorder but sporadic cases can occur as may be the case in our patient. Other more common causes for GIPP such as congenital adrenal hyperplasia, McCune-Albright syndrome or malignancy were excluded in this patient. Our patient started with secondary sexual maturation at the age of 4 years and a very advanced bone age, as is the typical presentation for testotoxicosis. Treatments for this disorder are usually limited by poor final adult height and toxicity. Our patient was started on anastrozole, and bicalutamide may be added in the future depending on his response since this combination has been reported effective.В Genetic testing is important especially for counseling. Conclusion: Testotoxicosis should be considered after other more common causes of GIPP are ruled out. The rarity of this disorder limits the amount of patients enrolled in clinical trials to test different treatment options. So far aromatase inhibitors and anti-androgens seem to be efficacious in decreasing skeletal maturation and virilization. Long-term data on final adult height are lacking and ongoing trials will provide more information in the future. Naim Mitre Calderon, MD, Aida Lteif, MD Objective: To report a 5 year old boy with gonadotropin-independent precocious puberty (GIPP) secondary to testotoxicosis and to underline the importance of genetic testing. Case Presentation: A 5 year 9 month old boy presented with a history of increased penile and testicular size since the age of 4 years. He also had significant growth acceleration where his height increased from the 30th to greater than the 95th percentile. He developed pubic hair and was reported to be aggressive. There was no family history of early puberty. Physical exam showed a height z score of 2.2. There was one 0.5cm cafГ©-au lait spot on the anterior abdomen. Pubic hair was in Tanner stage II Abstract #903 SERTOLI-LEYDIG CELL TUMOR AS CAUSE OF SECONDARY AMENORRHEA Catalina I Poiana, MD, PhD, FACE, Mara Carsote, MD, Gabriel Banceanu MD, PhD, Maria Sajin, MD, PhD, Bogdan Stanescu, MD, PhD, and Mihail Coculescu, MD, PhD, FACE Objective: Sertoli-Leydig cell tumor is a type of sex cord stromal (SCS) tumor, often associated with androgens secretion, which sometimes can mimic menopause. – 102 – ABSTRACTS – Reproductive Endocrinology Case Presentation: We present the case of a 46 years old female, with secondary amenorrhea since age of 40. At that time, she was considered as premature menopause and no investigation was further performed. With time, hirsutism developed with marked frontal alopecia. On admission in our hospital, laboratory findings showed mild polyglobulia and a total cholesterol of 225 mg/dL. Testosterone values were 10 times above normal: 8.01 ng/ mL (range 0.14 to 0.76 ng/mL). The computed tomography scan revealed a tumor of 3.5 by 2.8 cm on the right ovary. Resection of the tumor was performed. There was no evidence of secondary dissemination. The pathology report revealed a Sertoli-Leydig cell tumor with intermediate grade of differentiation. The immunohistochemistry profile showed: inhibin and calretin highly positive, pancytokeratin intensely reactive, CD99 moderately positive, epithelial membrane antibody weakly reactive. Postsurgery, left leg thrombophlebitis complicated the evolution. The patient was well 3 months later, with decreasing levels of testosterone and slowly reducing hirsutism. However, the clinical exam showed a left thyroid nodule. The fine needle aspiration biopsy suggested a papillary carcinoma. Thyroidectomy with total neck lymphadenectomy was performed and the diagnosis of sclerosing type of papillary carcinoma (T2N0M0) was sustained. Discussion: The term of Sertoli-Leydig cell tumor usually refers to SCS tumors of testicular type and it is synonymous to arrhenoblastoma and androblastoma. They account for 3-10% of gonadal tumors. The main incidence is between 20 and 30 years, but it may occur at any age (from 2 to 80 years). Clinical manifestations do not correlate with the histological subtypes or clinical stage. In our case even if the cells from the tumor had intermediate grading, the clinical progression was slow. The most important immunohistochemical marker for the SCS tumors is inhibin, which is positive in almost 100% of cases. Calretin is considered as more sensitive, but less specific. In our case they were both intensely positive. Conclusions: Ovarian tumors are rare causes of amenorrhea and hirsutism. Nevertheless, they should be suspected if serum androgens are extremely high. We recommend increased awareness of endocrinologists to the possibility of misdiagnosis with premature menopause. The association with thyroid carcinoma is probable due to an epidemiological overlap, because papillary carcinoma is one of the most frequent forms of endocrine cancer. Abstract #904 COMPLETE ANDROGEN INSENSITIVITY CLINICAL PRESENTATION Pushpa A Viswanathan, MD, and Selma F Witchel Objective: To describe the variations in the clinical presentation of complete androgen insensitivity(CAIS). Case Presentation: A 17 1/2 year old female presented with primary amenorrhea. Following lack of withdrawal bleeding with medroxyprogesterone, additional evaluation included a karyotype, which showed 46XY, total testosterone 1161ng/dl and, free testosterone 129.2pg/ ml. A diagnosis of CAIS was made and patient referred for gonadectomy. Of significance was her past medical history. She had bilateral inguinal hernias at birth, which were repaired at birth and the “misplaced ovaries” were placed into the abdominal cavity. Family history was not available since the patient was adopted and androgen receptor (AR) mutation analysis not performed. This case illustrates the importance of careful evaluation of inguinal hernia and masses in infants and adults with female external genital development. A 4 day old baby girl was referred for evaluation of labial masses. Her genitalia were otherwise consistent with normal female external genital development. Testosterone level was 74.9ng/dl, FSH<0.3mIU/ml, LH<0.4mIU/ml, estradiol of 30pg/ml. Her repeat testosterone levels a week later was not high-40.3ng/dland remained low at 20.2ng/ dl. Karyotype was 46XY and absent uterus by ultrasound. Additional history revealed a maternal aunt diagnosed with CAIS at age 30 years. The aunt’s karyotype was 46XY. No mutations in her AR were identified by DNA sequence analysis, which included the promoter, coding exons, and all exon/intron boundaries. Patient underwent gonadectomy at the age of 6 months. Pathology revealed testicular tissue with sertoli cell predominant tubules. PLAP stain was negative indicating absence of neoplasia. Discussion: Androgen Insensitivity is a common cause of undermasculinization of a 46XY fetus.AR signaling is the key determinant of virilization of the male external genitalia. This is highlighted in the AIS, which presents with a wide ranging phenotype from normal female in CAIS to lesser degrees of genital ambiguity in PAIS. Here we describe two patients with CAIS who presented at different chronologic ages. Recently heterozygous mutations in genes other than in AR have been reported in PAIS, Coutant et al. JCEM 2007. Among a large cohort of patients with presumed AIS, AR mutations were not identified in 13 CAIS patients out of 57 patients; presentation was mainly with inguinal hernia. This raises the question of karyotyp- – 103 – ABSTRACTS – Reproductive Endocrinology ing in females with inguinal hernia, Ahmed et al, JCEM 2000.These two cases emphasize the index of suspicion needed for the accurate diagnosis of patients presenting with inguinal hernia. Although elevated testosterone levels are usually found in CAIS, absence in the newborn period does not exclude the diagnosis, Ahmed et al Arch Dis Child 1999. Conclusions: AR mutations can be identified in many patients with androgen insensitivity, but genetic abnormalities have not been identified in all. Testosterone levels may be within normal limits after birth in CAIS. All females with inguinal hernia especially with history of primary amenorrhea may benefit from karyotype analysis. Abstract #905 EFFECTS OF INTRATHECAL OPIOIDS ON THE HYPOTHALAMIC-PITUITARY- GONADAL AXIS IN A WOMAN WITH POLYCYSTIC OVARY SYNDROME sible advantage in efficacy of pain control compared to oral opioids. The effects of oral and intrathecal opioids on the hypothalamic-pituitary-gonadal axis have been described in the literature as adverse effects.В However, here we describe a case of a woman with polycystic ovary syndrome and chronic nonmalignant pain that required the intermittent intrathecal administration of opioids and demonstrate suppression of her hypothalamic-pituitarygonadal axis and improvement in her symptoms of hyperandrogenism during therapy that returned to baseline with discontinuation of therapy. Conclusion: This case illustrates the interesting effects of intrathecal opioids, but also may provide insight into the pathophysiology of polycystic ovary syndrome. В This raises intriguing questions about the role of the opioid system in polycystic ovary syndrome, and demonstrates changes in laboratory and clinical abnormalities with central disruption of the hypothalamic-pituitary-gonadal axis. Abstract #906 Marideli ColГіn Scanlan, MD, and Alan Burshell, MD Objective: Presentation of clinical and laboratory data that demonstrate the suppressive effects of intrathecal opioids on the hypothalamic-pituitary-gonadal axis in a woman with polycystic ovary syndrome. Case Presentation: A 35 year-old woman with a history of vitiligo, Hashimoto’s thyroiditis, Stiff-person syndrome, and polycystic ovary syndromeВ had a testosterone level of 100 ng/dL (treated with metformin) prior to requiring intrathecal opioids for her chronic pain.В In 2001, she began receiving intrathecal opioids, and her testosterone level, as well as her estradiol, LH, and FSH levels became undetectable (total testosterone <10 ng/dL, estradiol <10 pg/mL, LH <0.1mIU/mL, FSH <0.3 mIU/mL).В Over the next year, her levels became detectable, but remained low (total testosterone 21.4 ng/dL, estradiol 27 pg/mL, LH was not measured, FSH 1.4 mIU/mL).В Later, as the dosage of her intrathecal opioids decreased dramatically, the levels of testosterone, estradiol, LH, and FSH increased (total testosterone 49 ng/dL, estradiol 61 pg/mL, LH 12 mIU/mL, FSH 5.7 mIU/mL).В When she discontinued the intrathecal opioids, her levels returned to near baseline (testosterone 75 ng/dL, estradiol 86 pg/mL).В The patient experienced changes in her clinical symptoms of hyperandrogenism of hirsutism and acne that accompanied these biochemical changes. Discussion: Opioids have long been used to treat chronic nonmalignant pain, and the intrathecal route of administration is being used as an alternative more often due to the smaller dose needed, less expense, and a pos- GIGANTOMASTIA: BENIGN CONDITION IMPOSING RADICAL TREATMENT; CASE REPORT Simona Vasilica Fica, MD, PhD, Carmen Barbu, Madalina Constantin, Dana Terzea, and Ioan Lascar Objective: to report a case of gigantomastia, a rare benign disorder of the breast, marked by an extremely sudden and homogeneous increase of breast volume with the onset of puberty, leading to severe physical and psychological complications. Case Presentation: a 13-year-old premenarchal girl, with no previous medical history, was referred to our clinic in July 2007 for excessive breast enlargement up to 100 cm in thoracic circumference, developed in less than 5 months, associated with inflammatory and necrotic skin lesions. Juvenile bilateral gigantomastia was diagnosed after extensive endocrine, immune and imagistic studies, and treatment (progestin and non steroidal anti-inflammatory) was started. After 3 months of follow up with continuous enlargement of breasts and extension of epithelial necrosis with ulceration, the entire breast tissue was surgically removed; subcutaneous mastectomy was done considering the high rate of recurrence of gigantomastia reported after conservative surgery such as reduction mammaplasty. The histological pattern (extensive stromal fibrosis, ductal epithelium with moderate hyperplasia, and no acinus) is specific for gigantomastia and ruled out a malignant disorder. – 104 – ABSTRACTS – Reproductive Endocrinology Immunohistochemical study showed positive reaction for both estrogen and progesterone receptors in almost 90% of epithelial cells and the presence of nuclear proliferation factor Ki67 in both stromal and epithelial tissue. Discussion: There was no particular hormone overproduction in our case. However, taking into account the moment of the onset in our case, the role of the hormonal milieu as the promoting event remains highly probable, as well as the steroid receptor hypersensitivity suggested by the immunohistochemical investigation. There are some reported cases of inflammatory gigantomastia in a context of immune mediated diseases, outlining the relationship between the immunological factors and the hormonal factors. In our case there were no clinical signs of autoimmune disease or immune mediated condition, as well as no perilobular lymphocytic infiltrate. Conclusion: Although the pathogenesis of this condition is still unknown, our case highlights the steroid receptor hypersensitivity as an important mechanism in a particular paracrine regulation between stromal and epithelial breast tissue, both of them Ki67 positive. Moreover, in spite of the benign character of the disease, it needs radical surgical treatment due to rapid and severe complications and ineffectiveness of the antiestrogen therapy, as well as the frequent recurrence reported after a simple reduction mammaplasty. – 105 – ABSTRACTS – Thyroid Disease The observed decline in LDL-C induced by levothyroxine, although a modest 5.75%, is significant in terms of reduction for CAD (33). Furthermore, the increased levels of LDL-C in non-treated SCH patients were mild 3% but reached statistical significance. The Helsinki Heart Study has shown that only a 7% decrease in LDL-C levels is associated with a 15% reduction in the incidence of CAD(34). Physiological, TSH guided, levothyroxine treatment should be initiated in SCH as it may reduce morbidity and mortality in patients with this common syndrome. Conclusion: SCH has a negative impact on the lipoprotein profile in premenopausal women and may translate into a sizeable cardiovascular risk if untreated. THYROID DISEASE Abstract #1000 ATHEROGENIC LDL-C RISES IN UNTREATED SUBCLINICAL HYPOTHYROIDISM George Samir Mikhail, MBBCh, MSc, Sameer Alshammari, MD, FRCPC, Mohammed Alenezi, MD, FRCPC, Maged Mansour, MD, PhD, and Nesreen Khalil, MSc Objective: To evaluate the effects of physiological doses of Levothyroxine replacement on the lipoprotein profile in patients with SCH. Methods: We used a prospective double blind, placebo controlled study design. We enrolled one hundred and twenty patients with SCH mostly but not exclusively premenopausal women. Patients were randomly assigned to either a Levothyroxine treatment group (59 females and one male age rangedВ 15-53yrs) or a placebo group (59 females and one male age rangedВ 14-57). Total cholesterol (TC), low-density lipoprotein cholesterol (LDLC), high-density lipoprotein cholesterol (HDL-C) and triglycerides (TG) were measured before and 52 weeks after assignment to either group. Results: In the Levothyroxine treatment group, TC was 5.04В±0.98 mmol/L before and 4.74В±0.87 after treatment (P<0.0001), LDL-C was 3.30В±0.90 mmol/L before and 3.11В±0.77 after treatment (P<0.01), TG was 1.18В±0.71 mmol/L before and 0.95В±0.53 after treatment (P<0.002) and HDL-C was 1.20В±0.33 and 1.19В±0.32 (P=0.29) after treatment. In the placebo group, TC values before and after 52 weeks remained unchanged 4.99В±0.72, 5.04В±0.67 (P=0.16), HDL-C 1.15В±0.23, 1.10В±0.25 (P=0.88), TG 1.01В±0.66, 1.06В±0.59 (P=0.77) but LDL-C values rose from 2.79В±0.60 mmol/L to 2.89В±0.59 reaching statistical difference (P<0.016). After 52 weeks we compared the mean values of TC, LDL-C, HDL-C and TGВ in both groupsВ of patients those who received Thyroxine andВ of theВ control group. Total cholesterol showed a significant difference (p<0.029 at 95% C.I.) while LDL-C showed a high significant difference (p<0.0001 at 95% C.I.) in thyroxine receiving group to the control. The difference did not reach statistical significance in TG and HDL-C. Discussion: We used a prospective double-blind, placebo-controlled study design. Our patient selection was those with no prior known thyroid disease, previous surgery or radiation therapy of thyroid gland which indeed reflect the subset of patients that we address the question of whether to treat or not. Abstract #1001 IS THE SUGGESTED CHANGE OF THE UPPER LIMIT OF THE TSH REFERENCE RANGE FEASIBLE? Rashid O. Al Jawair, MD, Merill Edmonds, MD, FRCPC, FACP, Irene Hramiak, MD, FRCPC, and Sonya Tokmakejian, PhD, FCACB Objectives: It has been proposed to lower the upper limit of TSH from the conventional (presently 5.00 mIU/ L LHSC). We looked at the feasibility of the suggested change. Methods: We have looked at the distribution of TSH in 190 students tested under well defined conditions. Anti TPOAb were also measured when aliquots frozen at -800C were available. Results: There were 190 students age group 21-40 years old included in the study, 119 (62.6%) were males and 71 (37.4%) were females.В In individuals without a history of thyroid disease the median TSH was 2.40mIU/ L and the percentile distribution from 2.5%-97.5% is 0.4-6.87mIU/L. We have excluded three students with known thyroid disease in addition to two students who were diagnosed to have thyroid disease based on the laboratory finding. В Anti TPOAb was measured in 57(30%) students.В The anti TPOAb was positive (> 40U/ml) in three students, The first subject has been on Thyroxine supplement and the second unfortunately was measured four years later and there was no follow up. The result of the third subject was moderately increased which could have been explained by gross hemolysis. Conclusions: We concluded that changing TSH upper limit reference cutoff to 2.5 or 3.5mIU/L is not feasible since about 50% or about 28% respectively of TSH – 106 – ABSTRACTS – Thyroid Disease that a more aggressive approach to her management was required. A thyroidectomy was performed and radioiodine ablation therapy was given to ablate the peritoneal strumosis. Thyroid hormone suppressive therapy was also initiated. Conclusions: This is a report on a rare case of struma ovarii with peritoneal strumosis. Aggressive management with surgical excision of the lesions, radioiodine ablation therapy, and thyroid hormone suppression therapy was employed in spite of the benign pathology because of the risk of an unrecognized low-grade malignancy and the potential of malignant transformation. levels will be classified as above normal.В There is no evidence that starting these people on thyroid hormone will have any benefit. Abstract #1002 PERITONEAL STRUMOSIS: A CASE REPORT Judith M Castillo-Perez, MD, Francisco Correa, MD, Emmanuel Javier, MD Objective: To report a striking case of peritoneal strumosis. Case Presentation: A 37 year-old female presented with a two-month history of lower abdominal pain. MRI study showed a left adnexal mass measuring 4.8x5.1x3.0 cm and a 12x6x6 cm mass in the mid pelvis. The TSH was suppressed at 0.11uIU/mL with a normal free T4 of 1.33 ng/dl. She had no prior signs or symptoms of thyroid disease. On physical examination the thyroid was not enlarged, with no palpable nodules. The remainder of her examination was within normal limits. At age 28 y, she had a left ovarian cystectomy for a benign serous cystadenoma. At age 32 y, she had a right ovarian teratoma removed. A TAH-BSO was performed and several peritoneal implants were also excised. Pathology of the right ovary showed mature cystic teratoma composed exclusively of benign thyroid tissue consistent with struma ovarii. Peritoneal and recto-sigmoid implants were compatible with strumosis. The left ovary showed multiple cysts with no thyroid tissue present. Post-surgery, a wholebody iodine scan demonstrated focal areas of increased uptake in the abdomen and pelvis. An FDG-PET/CT performed showed non-FDG-avid, multiple abdominal subcutaneous and intraperitoneal nodules. Total thyroidectomy was done and pathology revealed focal chronic lymphocytic thyroiditis without evidence of malignancy. She later received 148 mCi of I131 to ablate the remaining strumosis. She is now on thyroid hormone suppressive therapy. Discussion: Struma ovarii occurs in about 2% of mature cystic teratomas. Peritoneal strumosis denotes presence of thyroid tissue in the peritoneal cavity, and is rare. Patients usually present with signs and symptoms related to a pelvic tumor and rarely present with hyperthyroidism. This patient has a benign struma ovarii with benign peritoneal strumosis. However, the presence of a well-differentiated follicular carcinoma with metastatic peritoneal lesions cannot be completely ruled out. The risk of malignant transformation of benign struma ovarii has also been reported. With this possibility, we decided Abstract #1003 MULTIDISCIPLINARY MANAGEMENT OF METASTATIC PAPILLARY THYROID CARCINOMA ARISING FROM MALIGNANT STRUMA OVARII Maeve Elizabeth Hutchinson, MBBCh, BAO, Ian D. Hay, MD, PhD, FACE, FACP, FRCP, Keith C. Bible, MD, PhD, Clive S Grant, MD, Geoffrey B Thompson, MD, and William F Young Jr, MD Objective: To describe 3 patients with malignant struma ovarii (MSO) managed via a multidisciplinary approach and followed for a combined period of 48 postoperative years. Case 1: A 46 year old woman in 1983 underwent ovarian resection for MSO. Five years later, diffuse lung metastases were noted and biopsy confirmed papillary thyroid cancer (PTC). Total thyroidectomy on her normal gland was performed, followed by radioactive iodine (RAI) treatment—cumulative I-131 dosage to date is 1200 mCi. The lungs remain the only metastatic site. Chest X-ray and serum thyroglobulin (Tg) levels are stable on levothyroxine (T4) treatment. Suppressed Tg in 1996 was 74.7ng/mL and 94ng/mL in 2007; TSH-stimulated Tg was 618ng/mL in 1996 and 549ng/mL in 2007. Despite persistent lung metastases at 24 postoperative years, she remains asymptomatic and desires no more RAI therapy. Case 2: A 28 year old woman in 1995 had, at salpingo-oophorectomy (SPO), a 13-cm ovarian mass; pathology showed PTC arising from MSO. In 2001 she developed abdominal fullness and a right ovarian tumor. Total abdominal hysterectomy, right SPO, appendectomy and omentectomy were performed, showing MSO with PTC involving all biopsied organs and 13 lymph nodes. Rapidly recurrent disease postoperatively prompted thyroidectomy. Post-thyroidectomy, TSH-stimulated Tg was 42,000ng/mL. She was treated with a cumulative dose of – 107 – ABSTRACTS – Thyroid Disease 950mCi I-131 and aggressive interposed abdominal debulking surgery. The patient is now 13 years postoperative, with negative whole body I-131 scintigraphy, FDG-PET and abdominal CT scans. Tg on a suppressive dose of T4 is 1.2ng/mL. Case 3: A 46 year old woman presented with thyrotoxicosis; I-131 uptake occurred in her goiter, mediastinum, and bilateral chest. CT suggested widespread metastases. Subsequent evaluation verified metastatic PTC originating in MSO with peritoneal carcinomatosis plus pleural space and mediastinal disease. Seven years before, she was treated for an ovarian tumor; re-evaluation of pathology revealed PTC in MSO. Thyroidectomy was performed—confirming Graves’ disease without intra-thyroidal PTC. Following surgical debulking of intra-abdominal and thoracic deposits her Tg was 249ng/ mL. Subsequently, she was treated with a total of 450mCi I-131 and T4 replacement. Eleven years following her first surgery there is no clinical evidence of PTC and her FDG-PET-CT scan is negative. Tg on a suppressive dose of T4 is 0.2ng/ml. Conclusion: MSO is both rare and challenging. Patients with MSO can receive sustained benefit from a considered and multidisciplinary approach. The coexistence of MSO and Graves’ disease is unique to our knowledge and further complicated the management. IU/L (30-235), TPO antibodies > 1000.0 IU/ml (0.0-3.9), Thyroid Stimulating Immunoglobulins (TSI) 54% (positive if >16%). Electrocardiogram showed atrial flutter with a rate of 117 beats/ minute. She was diagnosed with TPP based on her clinical presentation and laboratory findings of thyrotoxicosis. She was treated with intravenous potassium and intravenous then oral propranolol. Her symptoms improved within four hours and she was able to walk eight hours after admission. Thyroid uptake and scan showed a homogenously enlarged thyroid gland with elevated I123 uptake of 78.2% and 79.3 % at 5 and 24 hours respectively. She was then treated with 19.1 mCi of I-131 and was discharged on oral propranolol. On follow-up visit two weeks later, she had no further episodes of weakness. TSH was 0.02 uIU/ml (0.35-5.5), free T4 was 1.43ng/dl (0.58-1.64), serum potassium was normal at 4.1 mEq/ml and we continued her propranolol. Discussion: TPP is a well-known complication of thyrotoxicosis in Asian populations, predominantly affecting males. Only sporadic cases of TPP have been reported in other non-Asian populations, and it is rarely reported in Hispanic females. Paralysis is caused by severe hypokalemia that is a result of sudden intracellular shifting of potassium and is not due to potassium deficiency. Propranolol blocks the intracellular shifting of potassium and thus is important in treating and preventing the recurrence of TPP. However, treating the underlying cause for hyperthyroidism is the definitive treatment for TPP. Conclusion: TPP should be considered in the differential diagnosis of weakness in female and male patients of all races. Our case represents a rare occurrence of TPP diagnosed in a Hispanic female. Abstract #1004 THYROTOXIC PERIODIC PARALYSIS Hussam H. Alhawari, MD, Debra L. Simmons, MD, Fred H. Faas, MD, and Antoine Makdissi, MD Objective: To present a case of young Hispanic female who presented with generalized weakness and severe hypokalemia. She was later diagnosed with thyrotoxic periodic paralysis (TPP) in the setting of Graves’ disease. Case: A 21-year-old previously healthy Hispanic woman presented with a two-day history of recurrent transient episodes of generalized weakness lasting few hours. Her weakness was so profound such that she was unable to walk. The patient also complained of nausea, palpitations, and excessive sweating. On examination, she appeared anxious, had diffuse thyroid enlargement, tachycardia, motor strength of one out of five in both upper and lower extremities and absent deep tendon reflexes. Serum potassium was less than 1.0 mEq/ml, phosphorus 2.2mg/dl (2.5-4.5), magnesium 1.7mg/dl (1.8-2.9), TSH 0.01 uIU/ml (0.35-5.5), T4 total 18.3 mcg/dl (4.5-10.9), T3 total 3.4ng/ml (0.6-1.8), CK В 139 Abstract #1005 THYROGLOSSAL DUCT REMNANT: EXPERIENCES AT A TERTIARY CARE CENTRE Mohammed Ahmed, MD, FACP, FACE, Rafif Farhat, MD, Fatima Al-Zidjali, and Asma Tulbah, MD Objective: To define the clinical features, the natural history & the management of thyroglossal duct remnant (TGDR) during a 28-year period at a tertiary care center. Case presentation: 16 pts.were treated for TGDR between 1979 to 2006. Their case records, diagnostic procedures undertaken, the histopathological & followup (FU) data were reviewed. Results: There were 10 males & 6 females, aged 2-43 yrs (mean 12.2). All pts. – 108 – ABSTRACTS – Thyroid Disease presented with non-tender midline upper neck swelling, 5 had draining sinuses. All cases were diagnosed clinically; however, ultrasound was needed to confirm the diagnosis in 3 cases. I 123 thyroid scan was done in 7 pts. В MRI/CT were done in 3 pts. None of imaging procedures helped differentiate simple cysts versus those harboring malignancy. All pts. underwent Sistrunk procedure. TG sinuses were associated with recurrence in 3 pts. that required repeated excision.5 pts. (31%: 4 females/1 male, aged 830 years) had papillary thyroid carcinoma (PTC) of the TG duct that was diagnosed after Sistrunk surgery. Pts. were followed up to 10 years. TT (total thyroidectomy)/ bilateral neck dissection (BND) was done in 4 pts. followed by I 131 Rx for ablation of postop remnant. Three of these pts. are in remission, & the oldest pt. aged 30 years had recurrence requiring a 2nd surgery. The latter had 1.5 cm PTC in the cyst, had invasion of the neck muscles & the thyroid gland was free of cancer at the initial TT & BND. At re-exploration, lymph nodes were positive for carcinoma. Pt. received В I 131. At 20 months FU, she is in remission. Discussion: TGDRs manifesting as midline cystic neck swellings represent a developmental anomaly of thyroid. TGDR carcinoma is found in about 1% of the lesions. The Dx of carcinoma is seldom made preoperatively. The cysts are usually asymptomatic & the presentation of pts. with carcinoma is indistinguishable from the simple cyst. Sistrunk surgery is the treatment of choice. It consists of removal of the cyst, middle part of hyoid bone & the TG duct. Following appropriate Rx long term survival of pts. with TGDR carcinoma is excellent in majority cases. Conclusion: The possibility of TGD carcinoma should be entertained in pts. with TGDR Thyroid US, radioiodine scan, CT/MR imaging cannot reliably exclude the presence of carcinoma. PTC is the commonest malignancy in TGDR. The frequency ofВ PTC was very high (31%) in our series. An occasional pt. operated at a later age may have an aggressive course with recurrence. Excision of the cyst at an early age is therefore recommended to facilitate the Dx of underlying malignancy in the cyst, & also to prevent other complications such as infection, & sinus formation. Abstract #1006 RETROSPECTIVE STUDY OF RADIOACTIVE IODINE TREATMENT OF HYPERTHYROIDISM Jennifer Carter Wheaton, DO, Abid Yaqub, MD, Imran Choudhry, MD, and Bina Jain, MD Objective: To determine the incidence of hypothyroidism following radioactive iodine (RAI) treatment for hyperthyroidism and to study the relationship between pretreatment RAI uptake and treatment dose and the subsequent development of hypothyroidism. Methods: Retrospective chart review of patients treated with RAI for hyperthyroidism between 1995 and 2000. 180 charts were reviewed but 41 met the inclusion criteria. Data was collected regarding the cause of hyperthyroidism, initial RAI uptake, initial dose of RAI, number of RAI treatments, and post treatment thyroid status. Results: 70% of patients with Graves’ disease became hypothyroid after their first RAI treatment, 22% had recurrent or persistent hyperthyroidism, and 7% remained euthyroid. 45% of patients with toxic multinodular goiter developed hypothyroidism, 18% had recurrent or persistent hyperthyroidism, 27% remained euthyroid, and 9% had transient hypothyroidism. None of the patients with toxic adenoma became hypothyroid. There was no relationship between the dose of RAI or pretreatment RAI uptake and the likelihood of developing hypothyroidism. Discussion: A recognized consequence of RAI ablation is possible permanent hypothyroidism. Our study showed a relatively higher incidence of hypothyroidism following RAI treatment for hyperthyroidism as compared to previously published studies. However, consistent with other reported studies, we also found a relatively greater proportion of patients with Graves’ disease developing post-ablative hypothyroidism in comparison to those with toxic nodular goiters. Conclusion: Within this study, post-ablative hypothyroidismВ was more prevalent inВ Graves’ diseaseВ than in toxic nodular goiters.В Neither the magnitude of the administered dose nor the pretreatment RAI uptakeВ predicted the development of hypothyroidism. – 109 – ABSTRACTS – Thyroid Disease of age. Simultaneous occurrence of MTC and PTC in the same thyroid is rare. Somatic mutations in tumor suppressor genes and oncogenes were described in PTC, which include RET. The inherited RET mutation may predispose to other malignancies. Conclusion: Simultaneous occurrence of MTC and PTC is a rare phenomenon; only two cases have been reported in MEN 2A patients. However, MTC and microPTC association may be more frequent as originally thought. Abstract #1007 RECURRENT MEDULLARY AND SIMULTANEOUS MICRO-PAPILLARY THYROID CARCINOMA Suzette Adele Robinson, MBBS, Nandalal Bagchi, MD, PhD, and Abdul Abou-Samra, MD, PhD Objective: To report a MEN2A case of recurrent medullary thyroid carcinoma (MTC) and a simultaneous micro- papillary thyroid carcinoma (PTC). Case Presentation: This is a 47 y old African American female with elevated parathyroid hormone (PTH), a history of hemithyroidectomy for thyroid cancer at age 13 and left adrenalectomy at age 31 (details of surgeries unavailable). No family history for parathyroid, thyroid and adrenal diseases. Examination was significant for a 2cm left thyroid nodule. PTH was 109 pg/ml (7-53); Ca 11.7 mg/dl (8.2-10.6); Alb 3.5 g/dl (3.5-5.3); Mg 1.9 mg/dl (1.6-3.0); Phos 3.2 mg/dl (2.3-5.0); 25-OH vitamin D 7 ng/ml (20-47); Calcitonin 529 pg/ml (0.04.6);В Plasma free Metanephrine 1.65 and 2.73 nmol/L (0.0-0.49); Normetanephrine 4.22 and 4.66 nmol/L (< 0.90) and CEA 33.1 ng/ml (0.0-3.0). Ultrasound revealed a left thyroid lobe with two nodules; the largest was 2.5 x 1.8 cm with calcifications, hypo and hyperechogenecity. FNA cytology: single and cluster cells; most were plasmacytoid with granular cytoplasm, multinucleated with salt and pepper nuclear chromatin appearance, and reactive with calcitonin antiserum.В Abdominal MRI showed a right 3.8 x 2.4 cm adrenal mass consistent with a pheochromocytoma; no local or distant metastases. The patient was prepared with a and b blockers and had right adrenalectomy followed by thyroidectomy on the next day. Pathology confirmed the right pheochromocytoma and the medullary thyroid carcinoma. In addition, a 0.5 cm PTC, follicular variant was present in the thyroid specimen. Central node biopsy was significant for a 0.3 cm focus of medullary carcinoma seen within an involuted thymus tissue; it was not possible to distinguish extra thyroid extension from metastasis. Patient was discharged on prednisone, florinef and synthroid. RET proto- oncogene Cys634Arg mutation at exon 11 was identified. Discussion: MTC is rare accounting for 3-10% of thyroid cancer. Hereditary forms, such as MEN2A, accounts for only 15% of all MTC, occurs at younger age, and is caused by an activating mutation in the retinoblastoma proto-oncogene (RET). Somatic RET mutations are also found in 50% of sporadic MTC. MEN2A carriers usually develop bilateral MTC before 10 years Abstract #1008 SIGNIFICANCE OF CRP LEVEL RISE IN PATIENTS WITH SUB-ACUTE THYROIDITIS AND ITS ROLE IN PREDICTING THE NEED FOR GLUCOCORTICOID THERAPY Manash Pratim Baruah, MD, and Sonali Barman Bhuyan Objective: This study was aimed to find the significance of C-reactive protein (CRP) level rise in patients with sub-acute thyroiditis (SAT) and examine what level (of CRP) warrants the need for initiating Glucocorticoid therapy. Methods: CRP levels were measured in twenty-nine study subjects (12 Male, 17 Female, mean age 38.1 В± 8.6 year) with SAT and 19 patients with Graves’ disease (2 Male, 17 Female, mean age 36.8 В± 16.5 year) as controls at initial presentation. Erythrocyte sedimentation rate (ESR) was measured in all thirty patients with SAT by Westergren method. High resolution ultrasonography(HRUSG) was performed in 14 patients with SAT whereas thyroid scan was performed in 15 patients. Thyroid FNAC was performed in 11 patients. Sixteen patients with SAT received glucocorticoid therapy. Results: Elevated CRP level (cut off 5mg/dL) was seen in 18(62%) patients with SAT with a mean CRP level of 32.95 В± 4.17 mg/dL. However, all patients had normal CRP level in the control group with a mean CRP level of 4.09 В± 0.56 mg/dL. Median CRP level amongst the patients with SAT was 10.2 mg/dL. ESR was high amongst SAT patients (68.3 В± 4.11) mm after first hour (Westergren) and significantly correlated to that of CRP level (p<0.02). Glucocorticoid had to be initiated in 16(55%) patients of SAT, as they were showing no relief even after adequate usage of non-steroidal anti-inflammatory drugs (NSAID) at least for one week. Mean CRP levels amongst patients requiring glucocorticoid was 50.62 В± 4.82 mg/dL (median value 47.15 mg/dL) compared to 11.2 В± 1.54 mg/dL amongst those not requiring glucocor– 110 – ABSTRACTS – Thyroid Disease A women and this effect was manifested in the first 3 months after delivery. These data suggested that clinically significant numbers of women with HT have further exacerbation of their hypothyroidism after childbirth compared to nulliparous women. The mechanism of this decreased thyroid reserve requires further delineation but is likely to be similar to the enhanced thyroid cell apoptosis observed with transient post partum thyroiditis which in itself is a transient form of Hashimoto’s thyroiditis. However, in this category of patients the thyroid cell damage is usually permanent. ticoid (p<0.02) in patients with SAT. Discussion: CRP, which is a marker of inflammation, has not been widely studied in inflammatory thyroid disorders particularly in SAT. Glucocorticoid therapy is widely used to alleviate symptoms in patients with SAT. Our study is first of its kind comparing CRP levels in two major etiological groups of thyrotoxicosis. Moreover no previous study has prospectively tried to ascertain at what level of CRP steroid may be considered mandatory. Conclusion: The rise of CRP level in patients with SAT is statistically significant (p<0.02) compared to controls and correlates well with the rise in ESR. Moreover, it can guide in instituting glucocorticoid therapy who fails to respond after NSAID therapy. Abstract #1010 SKULL BASE METASTASIS: PRESENTING FEATURE OF DIFFERENTIATED THYROID CANCER Abstract #1009 PREGNANCY ACCELERATES THYROID FAILURE IN HASHIMOTO’S THYROIDITIS Mohammed Ahmed, MD, FACP, FACE, Ahmed Nazmi, MD, Mohammed Al-Harthy, MD, Imaduddin Kanaan, MD, and Hindi Al-Hindi, MD Terry F. Davies, MD, FRCP, FACE, Richard Haber, and Juan C. Galofre Objectives: To characterize salient features of skull base metastasis(SBM) from papillary thyroid cancer (PTC),outline the diagnostic strategies,& propose rational Rx guidelines. Case Presentation: A 47-yr man presented to Neurosurgical service with 5 mos. hx of headache, and diplopia due to 6th cranial nerve paralysis. CT Skull revealed a large expansile osteolytic lesion at rt. skull base that had eroded the central clivus, middle cranial fossa, rt. pertous apex, extended into the intracranial cavity centrally into the prepontine cistern & rt. cerebropontine angle. A dx of clival chordoma was made & pt. underwent transsphenoidal debulking; histopathological Dx: metastatic papillary thyroid carcinoma (PTC), immunostains were positive for thyroglobulin (TG), & thyroid transcription factor1.At our examination a lt. thyroid nodule was detected. FNA Dx: PTC. Seven yrs. ago pt. had undergone thyroid surgery at an outside hospital; no information could be tracked down. Neck/Chest CT:7mm hypodense lesion lt. thyroid lobe/multiple bilateral pulmonary nodules, right. mediastinal lesion, a 4x4x4.5 cm large right. posterior apical paravertebral pleural mass causing 3rd rib destruction & lytic lesions of the rt. 7th rib & T2 vertebra were detected. I123 whole body scan: intense uptake (15%) left thyroid bed, skull base, lungs, mediastinum multiple skeletal foci (right ribs, 4th lumbar vertebra, left. femur iliac bone), TG >5000 ug/l, TSH 4.8 mU/l, TG antibodies 64 u/ml.Pt. underwent completion thyroidectomty. Histopath: PTC lt. thyroid lobe, multiple soft tissue & lymph nodes deposits of PTC. Postop Objective: Clinical manifestations of autoimmune thyroid disease are common in the postpartum period and are considered secondary to the immune suppression which occurs in pregnancy. We hypothesized that patients with established Hashimoto’s thyroiditis (HT) should also experience an exacerbation in the post partum with further impairment of thyroid function. В Such clinical exacerbations would be revealed by a long term increase in the need for LT4 supplementation in the postpartum when compared with the pre-pregnancy dose. Methods: We performed a retrospective study review of 38 unselected pregnant В women with HT, aged 20-45 years. Of these women, 26 were euthyroid (TSH <4.5uU/ml) prior to pregnancy with a mean В± SD initial TSH of 2.1В±1.0 uU/ml (Group A). We also reviewed 32 age-matched non-pregnant women with HT as controls and a mean initial TSH of 1.8В±1.0 uU/ml (Group B). In Group A we measured the total LT4 supplementation (mg) taken during the 9 months before pregnancy (TS-1) and then the 9 months after pregnancy (TS-2). В Similarly, in Group B we measured the total LT4 supplementation (mg) consumed during two 9 month periods (TS-1 and TS-2) separated by an intermediate 9 months. The mean LT4 amounts (TS-1 and TS-2) were compared in the two groups using Student-t testing: Group A: TS-1: 23.5 В± 13.2; TS-2: 26.6 В±12.9 (p<0.01). Group B: TS-1: 25.2 В± 11.4; TS-2: 26.3 В±11.8 (p=ns). Results: Pregnancy induced a long-term 15% increase in LT4 requirements in the postpartum of Group – 111 – ABSTRACTS – Thyroid Disease pt. received I 131 x 2 using thyrogen (cumulative dose 510 mCi) under cover of steroids (because of intracranial mets.) for persistent uptake of I131 in skull base, bones & lungs. External beam radiation (XBR) to brain & mediastinum was given. Follow-up TG 889/TSH 119. Pt. is alive & fully functional at 15 months FU. Discussion: Skull base metastasis from differentiated thyroid cancer (DTC) is rare; only 20 cases are reported till 7/2007.В There is no clear consensus on management strategy for SBM from DTC. The reported overall survival ranged from < a yr. to > 10 yrs. from the detection of metastasis. Our case is unique because of extensive erosion of the skull base & the surrounding structures. It represented part of disseminated metastases involving lungs, mediastinum & skeletal system. Conclusions: Metastasis from DTC needs to be considered in the differential Dx of destructive skull base lesions. Histopatholigical confirmation is mandatory followed by debulking of skull base metastasis, total thyroidectomy, radioiodine, external beam radiation & longterm TSH suppression. Discussion: Painless thyroiditis is a self-limited disease typically associated with an abrupt onset of hyperthyroidism.В The thyrotoxicosis is usually mild and is due to inflammatory mediated damage of thyroid follicles with subsequent release of preformed thyroid hormone.В It is associated with low radioactive iodine uptake, and the diagnosis can be confirmed by biopsy revealing diffuse lymphocytic infiltration.В The ESR and WBC count are elevated in approximately half of affected patients.В The etiology is thought to involve an autoimmune process, but the precise mechanism remains unclear.В There is developing interest in the possibility that painless thyroiditis is mediated by cytokines released in response to infection or subclinical injury.В The temporal relation between symptom onset and immunization, coupled with the absence of antecedent infection leads us to believe that the influenza vaccine was the inciting factor in our patient’s thyroiditis.В There is a case report in Taiwan attributing subacute thyroiditis in a 25-year-old female to the influenza vaccine she received two days prior to symptom onset, but this is the first report in the United States postulating that the influenza vaccine appears to be responsible for a case of thyroiditis. Conclusion: We bring this case to the attention of medical practitioners because it is the first reported case in the U.S. speculating a link between the influenza vaccine and thyroiditis.В Certainly, even a strong temporal relationship does not equate to an absolute cause and effect, and more research is needed to elucidate the exact mechanism of painless thyroiditis. Abstract #1011 WORSE THAN THE FLU? THE INFLUENZA VACCINE AS A POSSIBLE CAUSE OF PAINLESS THYROIDITIS Rob Ennis, MD, and Hossein Gharib, MD, MACP, MACE Objective: To report a case of painless thyroiditis presumably caused by the influenza vaccine. Case Presentation: A previously healthy 51-yearold male presented to our institution with a 3 week history of fatigue, subjective fever, and sweats.В He dated the onset of symptoms to 1-2 days after receiving his first ever influenza vaccine. The initial evaluation suggested primary hyperthyroidism with suppressed TSH (0.01 mIU/L; normal 0.3- 5.0 mIU/L), elevated FT4 (3.3 ng/ dL; nl. 0.8-1.8 ng/dL) and T3 (228 ng/dL; nl. 80-190 ng/ dL).В The ESR was also elevated (60 mm/hr; normal 0-22 mm/hr).В He was subsequently referred to Endocrinology.В He denied upper respiratory symptoms and neck pain.В On exam, his thyroid was not tender or nodular but was slightly enlarged and diffusely firm.В A four hour RAIUВ scan revealed suppressed uptakeВ at 0.2%.В These findings were consistent with painless thyroiditis, and the temporal relation between symptom onset and vaccination strongly support the notion that the influenza vaccine was responsible for his thyroiditis. Abstract #1012 INTERFERON-ОІ INDUCED GRAVES’ DISEASE IN A PATIENT WITH MULTIPLE SCLEROSIS Harpreet Singh Bajaj, MD, and Robert Zimmerman, MD, FACE Objective: We report a case of a patient with Multiple Sclerosis (MS) who developed Graves’ disease after Interferon-ОІ (IFN-ОІ) treatment. This case supports the theory that IFN-ОІ can induce Thyroid Stimulating Immunoglobulins (TSIs) in high-risk patients and depicts a clear transformation of a normal Radioactive Iodine (RAI) study prior to therapy to one of classic Graves’ after initiation of IFN-ОІ treatment. Case presentation: An 18 year old female with relapsing-remitting MS was referred to Endocrinology clinic for evaluation of abnormal thyroid function tests (TFTs) and fatigue before initiation of IFN-ОІ therapy. She – 112 – ABSTRACTS – Thyroid Disease denied other hyperthyroid symptoms. Her TSH was low at 0.15 uU/mL (normal 0.4-5.5 uU/ml) with a normal free T4 and free T3 at 1.2 ng/dl (0.7-1.8 ng/dl) and 3.5 pg/ml (1.8-4.6 pg/ml) respectively. Her TSIs were just above normal at 158% (normal 70-150 %). A RAI study demonstrated normal, homogeneous 24-hour uptake of 18.4% (normal 5-25%) in her thyroid gland. She was cleared for IFN-ОІ treatment with close follow-up. Three weeks after the initiation of IFN-ОІ, the patient was still clinically and biochemically euthyroid. By three months of therapy, she had lost 7 pounds and was complaining of palpitations, sweating and dizziness. Her repeat TFTs were clearly in the thyrotoxic range (TSH 0.008, Free T4 3.1 and Free T3 15.1) and TSIs had increased significantly to 5156 %. A repeat RAI study demonstrated an increased, homogenous 24 hour uptake of 47.3%. Hence, a diagnosis of IFN-ОІ induced Graves’ disease was made and anti-thyroid treatment was started. Discussion: Thyroid dysfunction has been reported in about one-fourth of MS patients treated with IFN-ОІ, most often occurring within the first year of treatment. Hypothyroidism is the most common manifestation followed by IFN-ОІ induced thyroiditis. Graves’ is a rare cause of hyperthyroidism in this population and can be differentiated from thyroiditis by measuring TSIs or RAI uptake, as done in this case. Multiple studies substantiate the usefulness of baseline anti-thyroid antibody levels as the strongest predictive factor for future thyroid dysfunction development in IFN-ОІ treated patients. Conclusion: This case demonstrates the benefits of screening for anti-thyroid antibodies before initiation of IFN-ОІ therapy and of rigorous monitoring of high-risk patients during this treatment. With increasing usage of IFN-ОІ and other such biologic agents, there is a greater need for endocrinologists to be aware of hormonal complications associated with these medications and to understand the pathophysiology, investigation and treatment options for such complications. Case Presentation: This case presentation identifies a 62 year-old black female with a history of hypothyroidism who presented to an ophthalmologist with left unilateral proptosis.В Subsequent MRI demonstrated a 5x5 cm lesion in the left frontal lobe extending into the left orbit.В She was admitted for planned resection of suspected meningioma.В After mass resection via craniotomy, initial pathology was most consistent with metastatic disease, and a primary malignancy was sought.В Hypodensities of the thyroid gland were noted during CT scan, and subsequent thyroid ultrasound revealed a mass lesion in the left thyroid bed.В Final pathology of the intracranial lesion identified a well-differentiated follicular thyroid carcinoma.В This patient interestingly reported a left hemithyroidectomy twelve years prior secondary to a symptomatic goiter.В Pathology at that time was negative for malignancy.В Additionally, this patient had labwork that was consistent with primary hyperparathyroidism.В As there have been some reported cases of parathyroidhormone-secreting papillary thyroid cancers, tissue from the meatstatic lesion was stained for parathyroid hormone.В Stain for parathyroid hormone, however, was negative.В This patient had completion thyroidectomy with concominant parathyroidectomy, yielding appropriate resolution of hypercalcemia.В She is currently awaiting radioactive iodine ablative therapy. Discussion: Follicular thyroid carcinoma is the second most common type of thyroid cancer after papillary thyroid cancer. This well-differentiated tumor of the thyroid epithelium may represent up to thirteen percent of all thyroid cancers.В These typically present as nodules within the thyroid.В Metastatic disease at presentation uncommon, representing only seven percent of cases of follicular thyroid carcinoma.В The large retro-orbital mass seen in this case represented a solitary metastatic focus.В Such presentation is rare, though there have been a few reports of similar.В This particular cancer may spread through hematogenous dissemination and has a predilection for metastasis to bone and lung.В The skull is often among bony sites to which this disease can spread, and such appears to be the case with this patient. Conclusion: This presentation should serve as evidence to consider spread of malignancy such as follicular thyroid carcinoma in the differential diagnosis of a patient presenting with findings suggestive of retro-orbital mass effect. Abstract #1013 FOLLICULAR THYROID CARCINOMA PRESENTING AS UNILATERAL PROPTOSIS Ben Williamson Seale, MD, and William Nicholas, MD Objective: To demonstrate an atypical presentation of follicular thyroid carcinoma, such that this diagnosis may be considered in future patients with similar presentation. – 113 – ABSTRACTS – Thyroid Disease EUTHYROID GRAVE’S OPTHALMOPATHY: A CASE REPORT cedes the hyperthyroidism in 20 % of cases, patients with apparent euthyroid graves opthalmopathy should be followed over a period of time to detect hyperthyroidism at an early stage and to prevent complications. Anne Marie Van Hoven, MD, and Saima Khan, MD Abstract #1015 Abstract #1014 Objective: To discuss a case of Grave’s Ophthalmopathy in a euthyroid patient. Case Presentation: A 63 year old female with past medical history of hypertension presented with complaints of periorbital swelling and blurring of vision for 2weeks. It was associated with excessive tearing, redness and discomfort but no pain. It was not associated with double vision. On examination she had periorbital and conjunctival edema and injection, normal extra ocular movements, no nystagmus, no diplopia on extremes of gaze, no lid lag, stare or proptosis, normal fundi and thyroid examination. Labs showed normal kidney and liver function, TSH 0.812, free T4 0.9, total T4 5.8, total T3 113. TSI was checked and it was found to be positive. MRI head showed changes consistent with graves orbitopathy. Diagnosis of euthyroid graves orbitopathy was made and patient was started on steroids and significant improvement was seen within a month. At 6 months follow up, patient remained asymptomatic and thyroid functions remained normal. Discussion: Graves’s ophthalmopathy occurs in 25% - 50% of patients with Graves Hyperthyroidism. Euthyroid Graves ophthalmopathy is much less common, occurring in approximately 10% of patients with Graves ophthalmopathy (1).The initial activation of T cells in Graves’ ophthalmopathy is thought to be initiated by thyrotropin (TSH) receptor antigen. TSH receptor antibodies, and not just T cells, may play an important role in the eye disease by activating fibroblast and adipocyte TSH receptors. The volume of both the extra ocular muscles and retro orbital connective and adipose tissue is increased, due to inflammation and the accumulation of hydrophilic glycosaminoglycans. GAG secretion by fibroblasts is increased by activated T-cell cytokines. Risk factors for the development of Graves’ ophthalmopathy include genetics, female sex, smoking, and possibly radioiodine therapy. Ophthalmopathy appears before the onset of hyperthyroidism in approximately 20 percent of patients, concurrently in about 40 percent, in the six months after diagnosis in about 20 percent, and after treatment for Graves’ hyperthyroidism in the remainder (most commonly after radioiodine therapy). Conclusion: Grave’s Opthalmopathy may occur even in the absence of hyperthyroidism and therefore may be difficult to diagnose.В Since ophthalmopathy pre- RECURRENT SILENT THYROIDITIS Monica Agarwal, MD, Debra L. Simmons, MD, and Antonie Makdissi Objective: Recurrent silent thyroiditis is an unusual event in an uncommon disease. We present a rare case of silent thyroiditis with recurrence after 12 years. Case: 42 year-old Caucasian man presented in 1995 with fatigue and palpitations. He had a family history of hypothyroidism. The thyroid was not tender. TSH was 0.00 mIU/dL (0.4 – 6) with total T4 of 17.2 ug/dL (4.5 11.5). The 24-hour radioactive iodine uptake (RAIU) was 2%. He was diagnosed with silent thyroiditis. The RAIU three months later was 16%. Patient did not require thyroxine. In 2002, patient was admitted with atrial fibrillation. His TSH was 2.72 mIU/dL and total T4 was 10.7 ug/ dL. In 2007, he presented with fatigue. The thyroid was nonpalpable. TSH was 0.01 mIU/dL, total T4 17.6 ug/dL and thyroid peroxidase antibodies (TPO) were 103 IU/mL (0-60). The thyroid uptake and scan showed normal size thyroid with uptake of 1.7% (5-15%) at 24 hours. Thyroid ultrasound showed hypoechogenic thyroid gland. The 24 hour urine iodine was 227 ug/L (42-350) and whole body scan was negative for ectopic thyroid tissue. Two months later the patient became clinically hypothyroid. The TSH was 41 mIU/dL (0.4 -5.5). Hormone replacement was initiated, but tapered off by four months.В The TSH was 3.7 mIU/dL and 4.4mIU/dL at two and three months after discontinuation of synthroid. Discussion: Silent thyroiditis (or painless subacute lymphocytic) is one of the variants of painless thyroiditis. Others include Hashimoto’s (or chronic lymphocytic), drug-induced and postpartum thyroiditis. It is characterized by thyrotoxicosis associated with depressed values of the RAIU in the absence of excess body iodide stores. There is lack of a viral prodrome and tenderness in the thyroid bed. About 50% of patients have TPO antibodies. Following the thyrotoxic phase, there is a transient euthyroid phase then a hypothyroid phase before a long-term return to euthyroidism. Patients can be treated symptomatically with beta-blockers in the thyrotoxic phase. The literature discussing recurrence has been scarce and limited to case reports and series. To our knowledge, there have been only three cases where the recurrence has occurred – 114 – ABSTRACTS – Thyroid Disease over a span longer than 12 years. Repeated recurrences may need a more definitive treatment such as treatment with I131 or thyroidectomy. The constellation of clinical, biochemical and imaging data in our patient support at least two episodes of silent thyroiditis 12 years apart. Conclusion: Silent thyroiditis is normally a selflimited and nonrecurring disease. В This is a rare case of recurrent silent thyroiditis with at least two episodes 12 years apart. ter size and low iodine uptake. On the other hand, age, presence of multiple chronic diseases, polypharmacy, and poor medication compliance underscores the limitations encountered with surgery and long-term use of anti-thyroid medications. Theoretically, favorable results with 131I therapy could be expected, if thyroidal uptake of iodine is increased by a compound such as rh-TSH. Combined rh-TSH and radioiodine has been utilized for the management of euthyroid, multinodular goiter. To the best of our knowledge, this approach has not been tested for the treatment of toxic, multinodular goiter with low radioiodine uptake. Conclusion: The present case illustrates the beneficial effect of adjunct therapy with rh-TSH and radioactive iodine in decreasing the goiter size, and treatment of hyperthyroidism in elderly patients with toxic multinodular goiter and low iodine uptake. Close clinical monitoring of these patients is absolutely necessary, due to transient exacerbation of hyperthyroidism, and therefore potential risk of cardiovascular decompensation. Abstract #1016 ADJUNCT USE OF RECOMBINANT TSH (rh-TSH) WITH 131I IN THE TREATMENT OF TOXIC MULTINODULAR GOITER WITH LOW RADIOACTIVE IODINE UPTAKE Hema Padmanabhan, MBBS, MD, Rathnakara Sherigar, MD, and Ali Iranmanesh, MD Objective: To describe the effectiveness of adjunctive use of recombinant TSH (rh-TSH) with 131I radioiodine for treatment of toxic multinodular goiter with low iodine uptake in an elderly man Case presentation: A 94 year old male with toxic multinodular goiter and low radioactive iodine uptake, was treated with 15.4 mCu of 131I after thyroid gland was primed with rh-TSH. As a result, radioactive iodine uptake increased from a baseline of 2% (2 hr) and 6% (6 hr) to 14% (2 hr) on day 1, maximized at 61% (2 hr) and 79% (6 hr) on day 28, and returned to values of 3.6% (2 hr) and 3.9% (6 hr) by day 70. Concomitantly, serum FT4 concentration (normal range: 0.65-1.75 ng/ dL) increased from a pre-treatment of value of 2.11 to a maximum of 12 on day 3, with marked decrease to 4.9 on day 5 and a gradual decline to normal value of 1.67 by day 140. Circulating FT3 concentrations (normal: 2.34.5 pg/mL) followed a similar pattern at respective values of 4.9 and 10.5 for pre-treatment and day 5 post-treatment, but an earlier recovery to normality (4.5) by day 70. Pretreatment serum TSH concentration was less than 0.03 uIU/mL. The patient continued to be euthyroid without thyroid replacement at his last clinic visit (555 days post-treatment) with serum FT4, and TSH (normal: 0.483.94 uIU/mL) concentrations of 1 ng/dL and 1.9 uIU/mL, respectively. Recovery from hyperthyroidism was associated with a 71% reduction in the size of thyroid gland, as determined by ultrasound. Discussion: Management of toxic multinodular goiter in elderly could be challenging at times. Although preferred in most hyperthyroid states, treatment with 131I may not produce the best outcome due to the goi- Abstract #1017 FREE THYROXINE INDEX VERSUS FREE T4 IN THE ASSESSMENT OF THYROID FUNCTION Hema Padmanabhan, MBBS, MD, John Badlissi, MD, and Ali Iranmanesh, MD Objective: To compare free thyroxine index (FTI:В Total T4 x T3uptake/100)В and Free T4 in the evaluation of thyroid function. Methods: In this retrospective survey, the results of FT4 and concomitant FTI were reviewed in 417 subjects who had normal serum concentrations of TSH. Thyroid tests were performed in the Endocrine Laboratory as requested by primary care providers for various clinical indications. FT4, total T4, T3 uptake, and TSH were measured by chemiluminescent methodology, using 2 different fully automatic analysers, namely ACS-180 (Bayer Diagnostics Corp, MN), and Immulite 2000 (Siemens Diagnostics, CA). Free T4 was analyzed by analog method. Results: Of the 417 cases with normal TSH, FT4 was elevated in 26, while abnormally high FTI was observed in only one. В The results differed with the type of autoanalyser used. Of a total of 269 assays performed by Immulite 2000, FT4 was increased in 18 (specificity: 93%), as opposed to one subject with documented high FTI (specificity: 99.6%). On the other hand, specificity with ACS-180 was 95% (8 of 147) for FT4, and 100% for FTI (0 of 147). – 115 – ABSTRACTS – Thyroid Disease Discussion: The validity of FT4 results has been questioned in euthyroid patients with nonthyroidal illness, hereditary dysalbuminic hyperthyroxinemia, and the presence of thyroid antibodies. In healthy subjects, measurement of circulating free thyroxine (FT4) correlates well with thyroid status and with results obtained by equilibrium dialysis. Analog assays for FT4 produce inaccurate results because the T4 analog is sequestered by albumin. This is not overcome even by chemically blocking analogalbumin, because the chemically blocked FT4 assay appears to be “thyroxin-binding globulin” (TBG) dependent, producing inappropriately low FT4 results with low TBG concentrations and high values with high TBG. Equilibrium dialysis using chemical blockers, displace T4 analog from albumin, but in high concentrations, also displace it from TBG. Our data showed that FTI has a higher specificity than FT4. Of the 26 patients with high FT4, 12 were on drugs which are known to decrease the peripheral conversion of T4 to T3. Conclusion: FT4 by analog methods has a higher false-positive rate compared to FTI. This is possibly due to the prevalence of non thyroidal illnesses and use of drugs( such as beta-blockers, amiodarone and corticosteroids), which are known to decrease peripheral conversion of T4 to T3, at the expense of increased circulating concentrations of reverse T3 and FT4. We, therefore, conclude that FTI is a more specific test for evaluating thyroid functions. dL (0.7-1.7), free T3 - 6.9 pg/mL (2.3-4.2), thyrotropinbinding inhibiting immunoglobulin (TBII) showed 30 % inhibition (<16), glucose was 492 mg/dL and hemoglobin A1c was 15%. Anti thyroid peroxidase antibodies (TPO) was less than 10 IU/mL (<34.9) and thyroid stimulating immunoglobulins (TSI) was less than 75% (<125). Thyroid ultrasound showed multiple hypoechoic nodules; the largest was 1.2 cm in the left mid to lower lobe with prominent vascularity. The 123I thyroid scan showed heterogeneous 55% uptake (normal 10-30%), with an area of increased uptake in the left lobe. The patient was treated with 10.9 mCi of 131I.В Two weeks later a post-treatment thyroid scan with oblique views confirmed Graves’ disease with a superimposed hot nodule in the left mid to lower pole corresponding to the largest nodule seen on ultrasound. Discussion: The clinical and biochemical presentation of hyperthyroidism in this patient (exophthalmos; smooth, bilaterally enlarged thyroid gland; elevated uptake; diffuse enhancement on scan; and elevated TBII) is consistent with Graves’ disease. In addition, the nuclear scan showed a “hot” nodule in the precise location of the dominant nodule on thyroid ultrasound. Marine and Lenhart described “cold” and “cool” adenomatous nodules in Graves’ disease.В Although other authors have used the term Marine-Lenhart syndrome to describe AFTN in euthyroid Graves’, there are only a few documented cases such as ours, with confirmed “hot” nodules in the presence of thyrotoxic Graves’ disease. Conclusion: The co-existence of Graves’ disease and autonomously functioning nodules is rare. Although overwhelmingly adenomas, carcinoma has been reported in this setting. Re-evaluation of the nodule, including consideration of biopsy, should occur following initial therapy. Abstract #1018 HYPERTHYROID GRAVES’ DISEASE AND A SIMULTANEOUS HOT NODULE Marina Strizhevsky, DO, Yun Feng, Katherine Groh, and Adrienne M. Fleckman, AACE Abstract #1019 PAPILLARY THYROID MICROCARCINOMA PRESENTING AS SOLITARY LATERAL CYSTIC NECK MASS: A RARE PHENOMENON Objective: To report and review the literature on the coexistence of Graves’ disease and autonomously functioning thyroid nodules (AFTN). Case Presentation: A 43-year-old deaf Hispanic woman with a history of diabetes mellitus and hyperthyroidism was admitted for uncontrolled diabetes. The patient was diagnosed with hyperthyroidism one year ago but did not follow up. Her only complaint referable to the thyroid was increasing fatigue for several months. Physical exam was remarkable for left-sided exophthalmos and stare, without lid lag. The thyroid was enlarged (50-60g), smooth and firm, without bruit or distinct nodules. TSH was <0.03 mU/L (0.38-5.5), free T4 - 2.8 ng/ Maria Paulina Santos Parong, MD, Jennifer Wheaton, DO, Abid Yaqub, MD, Thomas Dougherty, MD, and Paul Durst, MD Objective: To describe an unusual presentation of Papillary Thyroid Microcarcinoma and subsequently reaffirm the need for careful and meticulous diagnosticВ evaluation ofВ such cases. Case Presentation: A 32 year old male patient presented with a 6 year history of solitary, cystic, nontender, – 116 – ABSTRACTS – Thyroid Disease Case Presentation: A 47-year-old woman presented with anterior neck discomfort and a palpable thyroid mass. Thyroid ultrasound revealed a 1.2 x 0.8 x 1 cm heterogeneously hypoechoic right thyroid nodule. TSH was normal at 0.639 mIU/l. FNA biopsy showed scant cellularity. A hemorrhage into the thyroid was suspected. At follow-up in four weeks the patient complained of rightsided neck pain. The thyroid gland was tender. Ultrasound demonstrated an enlarging hypoechoic area in the right thyroid lobe.В Neck CT was negative for abscess, ESR was elevated at 56 mm/hr, TSH was mildly suppressed at 0.18 mIU/L. Diagnosis of subacute thyroiditis was made. Subsequently the patient developed left-sided neck pain and an extension of the hypoechoic areas into the left lobe.В Two weeks of prednisone resulted in marked symptomatic improvement, and a decrease in hypoechoic areas. After discontinuation of prednisone the symptoms recurred but the patient refused a repeat course of steroids. Discussion: Diagnosis of subacute thyroiditis is usually based on the presence of typical findings of neck pain, diffuse tender goiter, elevated ESR, characteristic phases of thyroid function change from hyperthyroidism to hypothyroidism with subsequent normalization, low radioactive iodine uptake on scintigraphy. Diagnosis is more difficult in atypical cases with absence of significant pain or tenderness or only with focal thyroid gland involvement. FNA biopsy can help to rule out a neoplasm. Thyroid ultrasound can be very useful in differentiating subacute thyroiditis from other disorders. It typically shows heterogeneously hypoechoic areas with ill-defined borders and no flow on color Doppler. The ultrasound picture is not pathognomonic of subacute thyroiditis, but the changing findings on ultrasonography with a decrease in hypoechoic areas after administration of steroids and eventual complete disappearance of lesions help to confirm the diagnosis. Conclusion: Subacute thyroiditis should be considered in the differential diagnosis of a thyroid nodule. The typical features of subacute thyroiditis such as neck pain, elevated ESR, suppressed TSH, hypoechoic areas on ultrasound, response to steroids and a clinical course help to establish the diagnosis. Serial ultrasound can be very useful in diagnosis and monitoring of disease progression, especially in atypical cases. 4 x 5 cm left sided neck mass.В CT of the neck showed a large cystic structure in the lateral neck suspicious for cystic hygroma versus branchial cleft cyst.В The mass was excised and the final pathologic report revealed a focus of papillary thyroid carcinoma arising in the wall of a branchial cyst.В Repeat review of the same pathology specimen and use of special stains revealed lymph nodal architecture consistent with cystic degeneration of a metastatic lymph node thus proving a metastatic spread from an undetected primary thyroid lesion.В The patient underwent total thyroidectomy with left modified radical neck dissection and was found to have a 4mm papillary thyroid carcinoma in the left lobe of the thyroid. Discussion: Papillary Thyroid Microcarcinoma (PTMC), defined as being less than 10mm in size, is generally considered to be slow growing with relatively good prognosis.В Some reports however indicate that with delay of diagnosis, there maybe increased risk of recurrence andВ mortality.В Mazzaferri and Jhiang in their analysis of 1355 patients with thyroid cancer reported that mortality rate was increased 2-3 fold with a year delay in diagnosis.В Although PTMC could be associated with cervical lymphadenopathy, the affected nodes are usually solid and multiple.В A presentation of PTMC with a solitary cystic lateral neck mass isВ uncommon.В В About 35 cases have been reported in literatureВ so far.В When PTMC presents this way,В it is often challenging to differentiate between the occurence of malignant degeneration of an aberrant lateral thyroid tissue versus a metastatic lesion from an undetected primary thyroid cancer. Conclusion: Our case report describes an uncommon presentation of PTMC.В It is important for physicians to be aware that PTMC can also present initially as a solitary cystic neck massВ as appropriate and timely diagnosis would clearly affect further management and care of such patients. Abstract #1020 SERIAL ULTRASONOGRAPHY IN THE DIAGNOSIS OF SUBACUTE THYROIDITIS PRESENTING AS A THYROID NODULE Anna Leonidovna Marina, MD, and Jann M. Johnston, MD, FACE Objective: We report an unusual case of subacute thyroiditis presenting as a thyroid nodule in a patient followed by serial ultrasonography to demonstrate the role of serial ultrasound in the diagnosis of this disorder. – 117 – ABSTRACTS – Thyroid Disease progression from symptomatic hyperthyroidism to overt hypothyroidism in just six weeks. Conclusion: This is the first described case of a patient with serologic autoimmunity,В abnormal thyroid function, andВ lymphocytic infiltration in the thyroid elements of a large cystic teratoma. Patients with ovarian tumors or other foci of ectopic thyroid tissue should be monitored closely for the development of thyroid dysfunction. Abstract #1021 BENIGN CYSTIC TERATOMA CONTAINING THYROID TISSUE WITH LYMPHOCYTIC THYROIDITIS IN A PATIENT WITH THYROTOXICOSIS PROGRESSING TO HYPOTHYROIDISM Susan Jane Adamcik, MD, Manfred Blum, MD, and Priya Kundra, MD Abstract #1022 Objective: To present a case of a woman with thyrotoxicosis preceding removal of a benign cystic teratoma containing thyroid tissue with lymphocytic thyroiditis. Case Presentation: A 55 year old Russian woman presented on May 30, 2007 for evaluation of a pelvic mass. She described multiple courses of iodine treatment in Russia for unknown reason, the last one year previously. There was no family history of thyroid disease.В She lived thirty miles from Chernobyl in 1986. She denied recent viral illness or neck trauma.В Examination was notable for an irregular tachycardia at 130, a non-tender thyroid, and a palpable abdominal mass. Laboratory evaluation revealed a TSH of 0.009uIU, Ft4 of 8.92, TPO Ab>1000, TG Ab of 370 with nonelevated ESR and TSI.В Abdominal ultrasound revealed an 11x9x10cm mass in the pelvic midline. В I131 whole body scan on July 5, 2007 revealed <1% uptake in the neck and an area of uptake posterior to the bladder within the region of the pelvic mass.В Repeat Ft4 level was 1.01 and 24hr urinary iodine was 170u/L.В On July 17, 2007, TSH was 48.17, Ft4 was 0.57 and the patient started levothyroxine.В Thyroid ultrasound revealed a heterogeneous thyroid without focal nodule.В She underwent bilateral salpino-oophorectomy on August 8, 2007 with removal of a benign 14.5x8x8cm cystic teratoma of the left ovary containing 1cm2 of thyroid tissue with lymphocytic infiltration.В Three months later, the patient still requires levothyroxine. Discussion: Mature cystic teratomas account for 10-20% of all ovarian neoplasms and contain components of all three germ layers, including thyroid tissue.В They have been associated with certain autoimmune diseases including autoimmune hemolytic anemia and rare encephalitides via production of antibodies against teratoma neoplastic cells.В Thyroid hyperfunction with thyroid autoantibodies and lymphocytic thyroiditis has been described in patients with struma ovarii, but there are only five reported cases of histologic thyroiditis within a benign cystic ovarian teratoma. В Antithyroid antibodies were detected in two cases and none demonstrated abnormalities in thyroid function.В Our patient not only had high titers of anti-thyroid antibodies, but a dramatic METASTATIC PAPILLARY THYROID CANCER PRESENTING AS A PARASELLAR MASS Adalberto D. Gonzalez-Pantaleon, MD, Elias Siraj, MD, FACE, and Colleen Veloski, MD Objective: To report a case of papillary thyroid carcinoma presenting with brain metastasis. Case Presentation: A 55-year-old male presented with headaches and diplopia of 6 months duration. Brain MRI revealed a 4.5 x 2.7 cm parasellar mass extending into the sphenoid, cavernous sinus, and prepontine cistern. Further evaluation revealed a thyroid mass, which on fine needle aspiration was indeterminate. Since the location of the mass was atypical for pituitary adenoma, a transphenoidal biopsy was performed. Initial pathology was suggestive of pituitary adenoma. Subsequent immunostainings were positive for thyroglobulin and TTF-1, strongly suggesting a metastatic thyroid carcinoma. Serum thyroglobulin (TG) level was >3000 ng/dL. There was no evidence of significant hypopituitarism. Total thyroidectomy was performed and final pathology showed follicular variant of papillary thyroid carcinoma (PTC) with vascular invasion. Transphenoidal debulking was performed but was limited by significant intraoperative bleeding. Whole brain radiation therapy (WBRT) was administered due to worsening of cranial nerves palsies. Radioactive iodine (RAI) therapy (200 mCi I 131) was given and post treatment scan showed foci of iodine avid metastases in the cranial vault, thyroid bed, chest, and abdomen. After initial improvement of neurological deficits, the patient is now showing evidence of progression, and the TG level remained high despite suppressive levothyroxine therapy. He is being evaluated for possible repeat RAI therapy, WBRT and/or chemotherapy as part of a study protocol. Discussion: PTC is the most common thyroid malignancy, and is usually discovered as a thyroid nodule. The incidence of distant metastatic disease at presentation is rare. Brain metastases occur in 1% of all cases and are – 118 – ABSTRACTS – Thyroid Disease necessaries to evaluate the impact of different treatments kinds over cardiovascular system in patients with GD. associated with poor prognosis. There is no consensus regarding the management of PTC metastatic to the brain. Surgical resection of metastatic lesions has been shown in some studies to increase survival. The role of postoperative adjuvant WBRT is not clearly defined, but may be effective in reducing recurrence. If the metastases are iodine avid, RAI therapy may improve prognosis, but can cause rare side effects such as acute cerebral edema. Conclusions: PTC presenting with brain metastasis is rare but is associated with poor prognosis. Although no guidelines are available, surgical resection seems to be the best therapeutic option to improve outcomes. Postoperative WBRT and RAI therapy are reasonable additional treatment options. Abstract #1024 COCAINE USE AS A PRECIPITATING FACTOR FOR THYROTOXIC PERIODIC PARALYSIS Angel Rodolfo Alejandro, MD, and Anup Sabharwal, MD Objective: To report a case of Thyrotoxic Periodic Paralysis (TPP) in a 37 year old woman precipitated by cocaine use on two isolated occasions. Case Presentation: A 37 year-old African American woman presented with bilateral lower extremity paralysis and upper extremity weakness. She had required hospitalization one month prior for a similar episode. At that time, she was found to have a serum potassium of 1.6 mmol/l, and her muscle weakness resolved following potassium replacement. She was discharged home with only potassium supplementation. After discharge, labs revealed a TSH of <0.004 ВµIU/ml, a free T-4 of 3.50 ng/ dl (normal 0.93-1.70 ng/dl), and a urine screen was positive for cocaine. On the recent hospitalization, she complained of palpitations and heat intolerance, and admitted to cocaine use the night before. Positive physical findings included tachycardia, absent deep tendon reflexes, and decreased motor strength in all extremities. EKG revealed prominent U-waves and a prolonged QT interval. Serum potassium was found to be 1.8 mmol/l. Her muscle weakness resolved following potassium replacement. She was discharged home with methimazole 10mg daily. In follow up, she is both clinically and biochemically euthyroid and has had no further episodes of paralysis reported. Discussion: TPP is a reversible electrolyte and motor disorder which is characterized by hypokalemia and acute muscle weakness in the setting of hyperthyroidism. This patients experience leads us to believe that cocaine use may have precipitated the attacks of TPP. В The pathophysiology of TPP involves over activation of the Na+-K+ATPase pump with resultant hypokalemia and paralysis. Hyperthyroidism results in a hyperandrenergic state with Гџ-adrenergic stimulation directly activating the Na+-K+ATPase pump. Excess thyroid hormone increases the sensitivity of the Гџ-adrenergic receptors, further increasing the catecholamine induced activation of the Na+-K+ATPase pump. Additively, cocaine use also induces an adrenergic surge which may have further precipitated this patient’s TPP by over activation of the Na+-K+ATPase pump. Abstract #1023 CARDIAC EFFECTS OF SUBCLINICAL HYPERTHYROIDISM (SH) IN PATIENTS WITH GRAVE’S DISEASE Hernando Vargas Uricoechea, MD Objective: To evaluate some cardiac effects of SH in patients with GD. Methods: 40 women with SH (main group) due to GD, demonstrated by TSH levels <0,4 mUI/ml and normal levels of FT3 and FT4, with radiologic criterias established by thyroid ultrasonography and nuclear imaging with radioiodine uptake (131I), were matched with 40 healthy women (adjusted by age) who had normal levels of thyroid hormone; all they for make cardiac tests (doppler echocardiography, 24-h holter ECG and 24-h ambulatory blood pressure monitoring). Patients with active treatment for GD and patients intaking drugs that injure the cardiac rhythm/function were precluded. Results: The diurnal Systolic Blood Pressure (SBP) average was 140 mmHg in main group, and 128 mmHg in control group (P=0.03). The nocturnal SBP average in main group was 144 mmHg, and 127 mmHg in control group (P=0.04). Differences in Diastolic Blood pressure levels, were not found. The heart rate average in main group was 90 bpm and 73 bpm in control group (P=0.02). В Echocardiography showed diastolic dysfunction, defined like reduction in E/A in main group, compared with control group: 0.91 [0.85;0.96] vs. 1.24 [1.18;1.3] (P=0.03). 8 women in main group (20%) revealed criterias for ventricular hypertrophy; nobody revealed these criterias in control group (P=0,002). Conclusion: SH in patients with GD is related with relevants and importants cardiac effects. Clinical trials are – 119 – ABSTRACTS – Thyroid Disease levels < 1 ng/ml; no visible uptake in the thyroid bed was observed in 20/21 patients (95.2%) from Group A and 17/19 patients (89.5%) from Group B. No statistical differences between the two groups were observed for both ablation criteria (Fisher exact test). Discussion and Conclusion: The use of rhTSH for preparation of low risk DTC patients to ablation therapy with low doses of 131I (50 mCi) is safe and effective, exposes the patients to lower radiation doses and avoids the discomfort due to hypothyroidism. It might be the optimal ablation procedure in this group of patients. Conclusions: Cocaine’s catecholamine effect on the Na+-K+ATPase pump may be a precipitating factor of TPP in this patient. It is important to recognize that treatment of hyperthyroidism remains the primary goal in the management of TPP. This is illustrated by the fact that despite continued cocaine abuse, this patient, who remains euthyroid on anti-thyroid medication, has not had any further episodes of paralysis. Abstract #1025 LOW DOSE RADIOIODINE POSTSURGICAL REMNANT ABLATION IN THYROID CANCER: COMPARISON BETWEEN HORMONE WITHDRAWAL AND USE OF rhTSH IN PATIENTS AT LOW RISK Abstract #1026 IVIG THERAPY IN THE TREATMENT OF GUILLAIN-BARRE SYNDROME, RESULTING IN IMPROVEMENT OF COEXISTING GRAVES’ DISEASE Enrico Papini, MD, FACE, Chianelli M., MD, Papini Laura Todino V., MD, Graziano F., MD, Guglielmi R., MD, and Signore A., MD Javeria Ahmed, MBBS, and Thomas Hughes, MD Objective: To present a case of Guillain-Barre syndrome (GBS) with concomitant Graves’ disease. Therapy with intravenous immunoglobulin (IVIG) resulted in decline of thyroid stimulating immunoglobulin (TSI) and resolution of the hyperthyroid state. Case Presentation: A 46 yo white female was admitted with a one week history of progressive numbness, tingling and weakness of her bilateral lower extremities (BLE), which was rapidly progressive. She denied any other focal weakness (diplopia, dysarthria, dysphagia). The only recent infection was a left otitis media about 2 months prior. Exam was significant for a palpable thyroid gland with fullness at the isthmus, sinus tachycardia, resting tremor, and 4/5 BLE strength, absent deep tendon reflexes and distal BLE hypoesthesia. Work up for secondary causes of neuropathy was negative. TSH was reported to be 0.02 mIU/mL, FT4 2.5 ng/dL (0.581.64) and TT3 245 ng/dL (87-178). TSI was elevated at 246%. В She was started on a beta-blocker with return to normal sinus rhythm. Plasmapheresis was initiated for treatment of GBS, but was changed to IVIG after lack of improvement in neurological symptoms. RAIU & scan was consistent with Graves’ disease, and showed a 24 hour uptake of 75%. RAI ablation was planned, but this was delayed due to the extended hospital course to treat GBS. Repeat TFTs subsequent to IVIG therapy showed resolution of her hyperthyroid state, with TSH 0.11 mIU/ L, FT4 0.8 ng/dL. TSI decreased to within normal range (97%). Discussion: Guillain-Barre syndrome and Graves’ disease both have underlying autoimmune etiologies. Objective: To compare the efficacy of low dose (50 mCi) 131I ablation in low risk patients with differentiated thyroid cancer (TNM stage pT1-T2, pN0, M0) randomized to using L-T4 withdrawal vs rhTSH stimulation. Methods: All patients, on the day of treatment, underwent 131I neck scintigraphy and radioiodine uptake; post-therapy whole body scan (WBS) was also acquired 4-6 days after the therapeutic dose of 131I. Neck ultrasound examination (US) was performed at time of treatment to assess the completeness of thyroidectomy. Efficacy of ablation therapy was assessed after 6-12 months by WBS, Tg and TgAb measurement following L-T4 withdrawal. Patients positive to Tg autoantibodies were excluded from the study. Patients were raned in two groups: Group A, preparation with L-T4 withdrawal; 24 patients received 131 I (54.6+/-5.9 mCi) after 37 days of L-T4 withdrawal and 20 days of T3 replacement. On the day of treatment TSH, Tg, TgAb were measured; Group B, stimulation by rhTSH; 21 patients received 131I (53.2+/-4.9 mCi) 24 hours after the 2nd injection of rhTSH (0.9 mg). TSH, Tg and TgAb were measured on the day of treatment and after two days. Result: All patients showed visible uptake in the thyroid bed at the post-therapy WBS. In Group B, however, six patients did not show any visible uptake in the thyroid bed at the pre-therapy scan and, on average, lower neck uptake was observed (4.7+/-4.5% vs 1.4+/-1.41%, Group A vs Group B, p=0.004). High ablation rates have been observed in both groups of patients. At follow up, after L-T4 withdrawal, 18/20 patients (90.0%) from Group A and 14/18 patients (77.7%) from Group B had serum Tg – 120 – ABSTRACTS – Thyroid Disease Although GBS may be associated with other endocrinopathies, the coexistence with Graves’ disease has only rarely been reported. IVIG is now the standard of care in the treatment of GBS. There are reports of IVIG use in severe cases of Graves’ associated ophthalmopathy. Our patient represents a rare instance of resolution of hyperthyroid symptoms and reduction of TSI as a result of IVIG therapy for her GBS. Conclusion: In selected and rare cases, IVIG may be considered as an alternative therapeutic option in the management of severe hyperthyroid patients. and 16 of the RET proto-oncogene.В However, tumor cells were not tested for RET proto-oncogene rearrangements or mutations. Work up for hyperparathyroidism and pheochromocytoma was negative. Discussion: Simultaneous occurrence of papillary and medullary carcinoma as two distinct tumors is very rare. While some case reports argue against any embryological or genetic association between these tumors, others suggest a common origin. Obtaining serum calcitonin levels prior to surgery would have been a useful approach.В Levels >100 pg/ml would strongly suggest presence of medullary thyroid carcinoma.In addition, recent evidenceВ indicates that measurement of calcitonin in FNA biopsy specimens maybe helpful in diagnosing MTC. Conclusion: It is likely that two carcinomas in our case do not share common genetic or embryological background. Increased vigilance for medullary thyroid carcinoma is needed in a person with thyroid nodules and elevated levels of carcinoembryonic antigen. Abstract #1027 SIMULTANEOUS OCCURENCE OF PAPILLARY AND MEDULLARY THYROID CARCINOMA Yuriy Gurevich, DO, and Alina Gouller, MD Objective: To describe a case of simultaneous occurrence of papillary and medullary thyroid carcinoma and review pertinent literature. Case Report: A 54-year-old woman presented for evaluation of multinodular goiter incidentally discovered on whole body PET scan, which revealed two hypermetabolic foci in the thyroid gland.В PET scan was performed for assessment of elevated carcinoembryonic antigen.В The patient was asymptomatic.В There was no history of radiation exposure or family history of thyroid cancer. She was clinically and biochemically euthyroid.В Ultrasound examination of the thyroid revealed a 16 x 12 x 7 mm hypoechoic nodule with punctuate calcifications at the junction of the isthmus and left lobe.В There were two hypoechoic nodules measuring 24 x 19 x 21 mm and 18 x 16 x 18 mm in the superior and inferior poles of the left thyroid lobe, respectively. Fine needle aspiration of the nodule in the left superior pole was interpreted as epithelial neoplasia with Hurthle cell changes and atypical features.В The isthmus nodule biopsy results were consistent with papillary thyroid carcinoma. Patient underwent total thyroidectomy.В Surgical pathology of the nodule in the superior pole of the left lobe was consistent with medullary thyroid carcinoma with focal capsular invasion.В Diagnosis was confirmed by immunoreactivity to chromogranin, cacitonin, CEA, synaptophysin and lack of reactivity to thyroglobulin. Pathology of the second nodule revealed papillary thyroid carcinoma with extrathyroidal invasion. This tumor was immunoreactive to thyroglobulin only. DNA analysis of the peripheral leukocytes indicated that there were no mutations in exons 10, 11, 13, 14, 15, Abstract #1028 A CASE OF PROPYLTHIOURACIL INDUCED HEPATIC FAILURE Alvin Ng, MBBS, and Kwang-Wei Tham. MB, BCh Objective: To report a case of propythiouracil induced hepatic failure. We highlight the pitfalls of diagnosis and discuss the non-thionamide strategies for controlling thyrotoxicosis. Case Presentation: A 38 year old female with Graves’ disease presented with progressive painless jaundice over a few days. She had developed pruritus after taking carbimazole and was switched to propylthiouracil 6 weeks ago. Clinically, she was mildly thyrotoxic with a Burch and Wartofsky score of 20. Investigations showed hyperbilirubinemia, elevated alkaline phosphatase and transaminases and coagulopathy. Her Thyroid Stimulating Hormone (TSH) was <0.006 mU/L and free Thyroxine (fT4) was 26.6 pmol/L. Liver biopsy showed submassive necrosis of hepatocytes. Her thyrotoxicosis was controlled with propranolol 20 mg qid, lithium carbonate 250 mg bid, cholestyramine 4mg tid, IV hydrocortisone 100 mg 6 hourly and IV sodium iodide 1g over 24 hours. On the 7th day of admission she received a living donor graft from her husband in a 12 hour surgery uneventfully. On the 23rd day after the last iodide dose, 30 mCi of radioiodine was given to render her hypothyroid. – 121 – ABSTRACTS – Thyroid Disease after delivery she developed symptoms of thyrotoxicosis.В At this time TSH was <0.01 and free T4 was 10.44.В RAI uptake and scan revealed a homogenous 24-hour uptake of 73%.В Levothyroxine was discontinued and the patient was started on methimazole.В When symptoms persisted, the patient sought treatment at our hospital.В Upon admission, TSH was <0.01, free T4 was 2.02, and TSI was 357%. Methimazole was discontinued due to marked transaminase elevation and the patient received 10mCi of I-131 for definitive treatment. Discussion: Hyperthyroidism is known to occur early in the course of Hashimoto’s thyroiditis and is commonly termed “Hashitoxicosis.” Following this phase, during which the inflamed thyroid leaks preformed hormone, the injured gland loses synthetic ability and hypothyroidism ensues.В Patients who have already entered the hypothyroid phase of Hashimoto’s thyroiditis are not expected to subsequently develop thyrotoxicosis.В A handful of case reports in the literature, however, describe patients that have transitioned from one form of autoimmune thyroid disease to another.В These studies show that the same patient may express one or more of the different TSH receptor antibodies in addition to anti-TPO or antithyroglobulin antibodies.В We suggest that our patient’s relatively low level of anti-TPO antibodies was insufficient to completely destroy her thyroid.В During the postpartum period, her immune state likely altered such that TSI became the predominant antibody in circulation.В В This allowed her clinical expression of disease to shift toward thyrotoxicosis. Conclusion: Transformation of Hashimoto’s hypothyroidism to Grave’s hyperthyroidism is extremely rare but can occur.В When hypothyroid patients have unexpected symptoms or changes in thyroid function tests, especially during pregnancy or the postpartum state, this unlikely diagnosis should be entertained and treated accordingly. Discussion: It is crucial to recognize that liver dysfunction may be a consequence of thyrotoxicosis. Cardiac failure with hepatic congestion can cause hyperbilirubinemia while autoimmune hepatitis and hemolytic anemia have been associated with Graves’ disease. Up to 60% of hyperthyroid patients have at least one abnormal liver biochemistry. However, it was unlikely that an uncontrolled state of thyrotoxicosis was the cause in this case as the history and temporal sequence strongly favoured PTU induced hepatic injury. Beta–blocker can ameliorate the adrenergic effects and block conversion of T4 to T3 while high dose corticosteroids inhibit hormone secretion and also block conversion of T4 to T3. Its immunosuppressive effects may be beneficial considering the purported mechanism of immune-mediated damage by PTU. Iodide acutely inhibits organic binding but this is transient. Its main action is to inhibit hormone release. Lithium also inhibits hormone secretion but unlike iodide, it enhances the retention of RAI in the gland and increases its efficacy. In thyrotoxicosis, there is increased entero-hepatic circulation of thyroid hormones and cholestyramine sequesters these hormones in the gut. Conclusion: PTU induced hepatic injury must be distinguished from hepatocellular dysfunction resulting from thyrotoxicosis itself as the management in both situations are very different. When thionamide is contraindicated, there are other medical modalities which can be used in a synergistic manner to control thyrotoxicosis with success. Abstract #1029 DEVELOPMENT OF GRAVE’S HYPERTHYROIDISM IN A WOMAN WITH HASHIMOTO’S HYPOTHYROIDISM Diane E. Fresca, MD, and Xiangbing Wang, MD, PhD Objective: To report a case of Grave’s hyperthyroidism in a postpartum woman previously treated with thyroid hormone replacement for Hashimoto’s hypothyroidism. Case Presentation: A 32-year-old female was diagnosed with Hashimoto’s thyroiditis three months after a miscarriage.В At the time of diagnosis TSH was 32, free T4 was 0.8, anti-TPO antibodies were 67.7, and 24-hour RAI uptake was 13%.В Four months after initiation of treatment with levothyroxine the patient became euthyroid and remained stable until becoming pregnant in August 2006.В During her first trimester, TSH rose to 98 and her levothyroxine dose was increased.В В Thyroid function tests normalized and the patient remained euthyroid through her uncomplicated delivery.В Six months Abstract #1030 IODINE DEFICIENY IN CENTRAL NEW JERSEY: A CASE REPORT Alexander Kulczycki, MD, and Xiangbing Wang, MD, PhD Objective: To recognize iodine deficiency (ID) as a reemerging cause of goiter in central New Jersey (CNJ). Case presentation: A 29 year-old Hispanic female living in CNJ presented to Endocrinology clinic for evaluation of possible hyperthyroidism. She complained of weight gain, dysphagia, hand tremors, polydipsia, breast – 122 – ABSTRACTS – Thyroid Disease tenderness, hot flushes, and amenorrhea with inducible menses. On physical exam a diffusely enlarged thyroid gland and galactorrhea were noted. All other examinations were all within normal limits (WNL). CBC, metabolic panel, prolactin, FSH, LH, testosterone, insulin levels were WNL. Thyroid chemistries were WNL: TSH 2.05miU/L, free T4 1.2ng/dL, total T3 158ng/dL. The TPO antibody level was elevated at 213.3iU/mL. Pituitary MRI demonstrated no micro- or macroadenomas or any other intracranial pathology. An iodine-123 uptake and scan demonstrated a 24-hour uptake of 72% (hyperthyroid range) and a diffusely enlarged gland with no focal nodules. A 24-hour collected urinary iodide level showed no detectable urinary iodide. Further discussion with the patient revealed that she actively avoided consumption of iodized salt and seafood. Based on these findings, the patient was diagnosed with ID. Discussion: In the early 1900s ID was identified as the leading cause of widespread endemic goiter in the United States. Since the introduction of iodine supplementation of salt and other foods (bread, meat, milk, etc) starting in the 1920s, though, ID has been virtually unheard of in this country. ID can still be observed in remote developing nations and some developed nations like Denmark that only initiated iodine replacement programs within the past ten years. Among certain ethnic subgroups, where there is over-dependence on foods high in groitrogens (cassava/yucca, millet, sweet potatoes, cabbage) ID can also be observed. Consequently, the mechanism of ID in this case included 1) avoidance of iodized salt and seafood and 2) consumption of goitrogenic foods which might inhibit iodine absorption. Further investigation, such as screening the patient’s family members for ID, remains to be done. Conclusion: We report a case of goiter caused by ID in CNJ. Given that iodine levels in processed foods have been decreased in recent years and the use of goitrogenic foods in certain increasingly prevalent ethnic subgroups, iodine deficiency should again be included in the differential diagnosis of goiter in the United States. A full diet history and 24-hour iodine level are necessary to confirm the diagnosis. Fortunately, the treatment is as simple as adding iodized salt to the diet. Abstract #1031 PREDICTIVE VALUE AND DISCRIMINANT CALCULATION IN DIAGNOSE THYROTOXICOSIS IN HYDATIDIFORM MOLE PATIENTS Nanny Natalia Mulyani Soetedjo, MD, Sri Hartini, and K.S. Kariadi Objective: Tyrotoxicosis in hydatidiform mole patients is not uncommon and may create a severe problem. It was progress rapidly but silently and may emerge suddenly as an alarming situation. There are no specific thyroxic signs and symptoms which lead to prompt recognition and treatment. Thus to able to establish the diagnosis of thyrotoxicosis the determination of high fT4, fT3 and TSH <0,1 mIU/ml is crucial but it requires some time to get the results. Methods: The inability to get the result in time will cause the diagnosis is established too late and makes the critical condition unavoidable especially after the mole evacuated. A study with the purpose to create a simple procedure to enable the clinicians to diagnose thyrotoxicosis more instantly concluded that prediction. Factors were pulse rate > 100/mt or uterine size is > 20 weeks, and discriminant calculation, with high accuracy. To reevaluate the accuracy of the predictive factors and the discriminant calculation, we analyzed hydatidiform mole patients from January 2002 until December 2005. Result: There were 105 patients, aged range between 16-50 years old. Thyrotoxicosis was found in 76 (72,4%) patients. Using predictive factors criteria, 36 patients who had pulse rate Ві 100/mt, 32 (88,9%) of them had thyrotoxicosis and among 55 patients who had uterine size > 20 week, 40 (72,7%) patients was found thyrotoxicosis. Discussion: In patients who had combination of В predictor factors, calculation with Discriminant formula there was no thyrotoxicosis. Among 69 patients who had pulse rate < 100/mt, 44 (63,8%) patients had thyrotoxicosis (p=0,006), with discriminant calculation there was 32 (46,4%) patients D<0 (p=0,724). Among 50 patients who had uterine size < 20 weeks, 36 (72%) patients had thyrotoxicosis (P=0,934), whom with discriminant calculation was found 47 (94%) patients D<0 (<0,001). Among 11 patients who had pulse rate < 100/mt and had uterine size < 20 week, with discriminant calculation there was found all patients D<0 (p<0,001). – 123 – ABSTRACTS – Thyroid Disease Conclusion: Predictive values seem capable to diagnose thyrotoxicosis. If there was no predictive values, discriminant calculation could be used to diagnose thyrotoxicosis in hydatidiform mole. goiter in the absence of clinical symptoms, as seen in our case, is distinctly unusual. Conclusion: Primary thyroid lymphoma, though rare, should be considered in all patients with Hashimoto’s thyroiditis who present with unusually large goiters or acute onset of rapid enlargement of thyroid gland. Abstract #1032 AN UNUSUAL PRESENTATION OF THYROID LYMPHOMA Abstract #1033 AUTO-INFARCTION OF A HURTHLE CELL NODULE AFTER FNA Anjali Bhagra, MBBS, and Vahab Fatourechi, MD Objective: To discuss an unusual presentation of primary thyroid lymphoma. Case presentation: A 51 year old man presented with an asymptomatic neck mass that had gradually increased in size over 5 years. Clinical examination revealed an asymmetrically enlarged, non-tender thyroid gland, with the right lobe measuring 9 cm. Symptoms of thyroid dysfunction or mechanical compression were absent. Fine-needle aspiration demonstrated extensive lymphocytic infiltration and cytologic features consistent with Hashimoto’s thyroiditis. Computed tomography (CT) of the neck showed massively enlarged right thyroid lobe (9 cm) causing marked tracheal deviation to the left. Thyroid function tests were within normal range. Given the significant cosmetic disfigurement related to the thyroid mass, the patient elected to proceed with surgical excision. Right lobectomy and isthmectomy were performed by standard cervical exploration. Pathology confirmed severe Hashimoto’s thyroiditis with atypical lymphoid follicles, suspicious for thyroid lymphoma. The lymphoid follicles stained positive for CD20, CD10 and bcl-6 and showed kappa light chain restriction, confirming a diagnosis of follicular lymphoma (Grade IIIA). Discussion: Primary thyroid lymphoma should be considered in the differential diagnosis of patients with thyroid nodules, because the prognosis and treatment differ from other diagnostic entities. Thyroid lymphoma is rare, with an estimated annual incidence of 2 per million and a 4:1 female predominance. Autoimmune thyroiditis confers a relative risk of 67. Half of all cases of thyroid lymphoma arise in the background of autoimmune thyroiditis. Thyroid lymphoma usually presents acutely as a rapidly enlarging goiter, often larger than 5 cm with substernal extension and mechanical compressive symptoms. “B symptoms” (fever, night sweats, weight loss) may be rarely present. When lymphoma is suspected, immunohistochemical staining / flow cytometry of thyroid core biopsy are necessary for diagnosis. The diagnosis of primary thyroid lymphoma in the setting of a long standing Deepa Sundararajan, MD, Maneet Kaur Narula, MD, and Harmeet Singh Narula, MD, FACE Case Presentation: A 44 year oldВ woman was seen in Endocrine clinic for an incidentally discovered thyroid nodule found on routine physical exam. A 3 cm nodule was easily palpable in Left mid-thyroid. On sonogram the nodule was solid & another nonpalpable 1.5 cm solid nodule was seen in Rt mid-thyroid. FNA of the dominantВ Left thyroid nodule was performed in the office and was consistent with a Hurthle cell lesion. One week after the FNA, the patient complained of pain and increasing swelling in the nodule; examination in the office confirmed a mild increase in the nodule which was tender; thyroid sonogram confirmed the nodule to have increased in size from 3.2x2.4 cm to 3.4x3.2 cm, solid with cystic areas. Her discomfort improved significantlyВ with Ibuprofen; Thyroid function studies, ESR and White countВ remained normal, ruling out infection & subacute thyroiditis. On repeat examination 1 month later, the dominant Lt Thyroid nodule was much smaller, 1cm on palpation.В On repeat thyroid sonogram, the nodule was 1.9x1.2cm, cystic. Three months later, the nodule was nonpalpable and measured 1.3cm on sonogram, again cystic.В It measured 9mm on sonogram 6 months later. The right sided nodule was benign onВ FNA and remained stable at 1.5 cm (solid) duringВ follow-up. The sudden enlargement of the nodule after the FNA and its subsequent dramatic decrease in its size and change in characteristics from solid to cystic all point to the auto-infarction in the Hurthle cell nodule post FNA Discussion & Conclusion: Thyroid nodules may occasionally infarct post FNA.В Hurthle cell nodules may have an increased predilection for auto-infarction post FNA as the nodule may outgrow its blood supply. Endocrinologists need to be aware of this presentation, as patients may present with acute pain & enlargement of the nodule post FNA, raising concern for bleeding or infection of the nodule. – 124 – ABSTRACTS – Thyroid Disease thyroidism also improved off of antithyroid medication, suggesting that treating celiac disease might also help thyroid abnormalities. Conclusion: Routine screening for celiac disease should be highly considered for patients with both hyperthyroidism and iron-deficiency anemia. Treating celiac disease may reduce morbidity and improve quality of life in patients with hyperthyroidism and celiac disease. Abstract #1034 HYPERTHYROIDISM, IRON-DEFICIENCY ANEMIA AND CELIAC DISEASE. Cindy Huang, MD, Amy Toscano-Zokor, DO, and Xiangbing Wang, MD, PhD Objective: To report a case of Graves’ hyperthyroidism associated with iron-deficiency anemia and celiac disease. Case Presentation: A 37 year old woman with no significant past medical history presented to Endocrinology clinic with one year history of palpitations, tachycardia, anxiety, diarrhea and weight loss. Clinical and biochemical findings were consistent with overt hyperthyroidism. TSH 0.02 mIU/L (0.4-5.5), free T4 2.9 ng/dL (0.8-1.8), T3 388 ng/dL (60-181), and thyroid uptake showed increased 24 hour uptake at 65%. Thyroid ultrasound showed diffusely enlarged thyroid with no focal lesion. Patient was started on Methimazole 10mg bid and Propranolol 40mg bid for symptom control. She developed facial rash after starting Methimazole, so it was discontinued. Blood tests showed H/H 10.9/33.3%, and iron studies revealed iron-deficiency anemia. Patient was referred to Gastroenterology for workup of anemia and chronic diarrhea. She was found to have positive antigliadin antibody and positive tissue transglutaminase IgG antibody consistent with celiac disease. Endoscopic small bowel biopsies were suggestive of celiac disease. Patient was then placed on gluten-free diet, with gradual improvement of diarrhea and anemia. Two months after gluten-free diet, patient was no longer anemic with H/H 14.4/41.4%, and her symptoms improved. She remained clinically euthyroid, and blood test showed TSH 0.04 mIU/L, free T4 1.1 ng/dL, T3 115 ng/dL. Discussion: The prevalence of celiac disease in patients with Graves’ hyperthyroidism was 4.5% as compared with 0.9% in age and sex matched healthy controls, and previous studies recommended routine screening for celiac disease in patients with Graves’ hyperthyroidism. A substantial number of patients with iron deficiency anemia were found, on small bowel biopsy, to have mucosal abnormalities compatible with the diagnosis of celiac disease. The association of hyperthyroidism, celiac disease and iron deficiency anemia is clinically important because early treatment of celiac disease may prevent or reverse extraintestinal manifestations, including osteoporosis, anemia, fatigue, and may reverse some thyroid abnormalities. In this case, patient’s anemia significantly improved on gluten-free diet. Her symptoms of hyper- Abstract #1035 THYROTOXIC PERIODIC PARALYSIS IN A PATIENT OF RECURRENT HYPERTHYROIDISM 50 YEARS AFTER RADIOIODINE THERAPY Sheng-Fong Kuo, MD, and Jen-Der Lin, MD Objective: Thyrotoxic periodic paralysis (TPP) is uncommon associated disorder of hyperthyroidism characterized by muscle paralysis and hypokalemia due to a massive intracellular shift of potassium. This condition mainly affects Asian young adult male of 20 to 40 years old. Case presentation: This study reports a TPP case occurring 50 years after radioiodine therapy for hyperthyroidism. The 82-year-old male patient presented to our emergency department with slurred speech and muscle weakness (especially bilateral lower limbs) in August, 2006. His potassium level was 1.56 meq/L (Normal: 3.04.8), then. Serum creatine phosphokinase level was 243 U/L (Normal: 15-130) and serum phosphate level was 2.0 mg/dL (Normal: 2.4-4.7). The serum cortisol level was normal and arterial blood gas revealed mild metabolic alkalosis combined with mild respiratory alkalosis. After potassium chloride infusion totally about 200 meq in two days, the serum potassium returned to normal and he regained his muscle power. The serum free T4 level was 1.99 ng/dL (Normal: 0.89-1.76), TSH was 0.043 uIU/mL (Normal: 0.35 - 5.50) and thyroid auto-antibody (TBII) was positive. The patient had diabetes and was treated with oral anti-diabetes agents and insulin. He had hyperthyroidism 50 years ago and was treated with radioiodine therapy. He was well thereafter without symptoms and sign of hyperthyroidism. However, prior to this acute paralysis, he had suffered from insomnia, anxiety, and weight loss for half a year, and he visited Psychiatry clinic and take medications for treatment. Finally, he was treated with methimazole for hyperthyroidism and had no more TPP attack since then. Discussion: Recurrent hyperthyroidism in an elderly patient long time after radioiodine therapy with the initial presentation of TPP is rare. Although TPP usually affects – 125 – ABSTRACTS – Thyroid Disease middle-aged male patients, it can affect elderly patients as well. The symptoms and sign of hyperthyroidism are usually not apparent in elderly patients as the present case. Effective control of hyperthyroidism is indicated to prevent the recurrence of paralysis. Conclusion: TPP is a curable disorder that resolves when a euthyroid status is achieved, and it can affect elderly patient as well as young adult. Prompt diagnosis and immediate treatment is important for such a patient. Conclusions: PPT appears to be rare among Nigerian women. The cause of this apparent rarity could not be due to the study design. It is recommended that a longer вЂ�span’ of follow up in the post partum period and studies in other centres using a larger sample size should be undertaken so as to determine the prevalence rates in other parts of the country. Abstract #1036 REVERSAL OF MENSTRUAL ABNORMALITIES BY TREATING SUBCLINICAL HYPOTHYROIDISM Abstract #1037 PREVALENCE OF POSTPARTUM THYROIDITIS AMONG NIGERIAN WOMEN Lee Pletts Goscin, MD, PhD Bilkisu Mohammed Mubi, MBBS, and Prof Augustine E. Ohwovoriole Objective: To report objective improvements including reversal of menstrual abnormalities and infertility by treating subclinical hypothyroidism. Case Presentation: The NHANES III and Colorado Health Studies showed normal TSH for women is 0.5 to 2.5.В In our clinical practice 40 women and 3 men with TSH from 3.0 to 7.5 and symptoms of hypothyroidism were treated with appropriate doses of Levothyroxine.В The Levothyroxine was adjusted on a case by case basis to decrease the symptoms.В Four women with Amenorrhea and Oligomenorrhea returned to normal menstrual cycles.В One man with NIDDM showed a marked improvement in Erectile Dysfunction (ED).В Another young 47-year-old married man was able to restore his marital relationship and start on a second job.В The third man had increased energy and improved cholesterol. Discussion: After the NHANES III and Colorado Health Studies suggested a smaller normal range for TSH in white women, patients with typical hypothyroid symptoms had both TSH and free T4 measured. В Of 46 women who were identified over three years 44 chose to take Synthroid.В The difference between these 44 women and previous studies that showed no improvement on Levothyroxine is that each woman was titrated to her optimal dose for her. Conclusion: This study shows that significant morbidity from premature menopause, increased cholesterol, decreased ability to function at work, obesity and marital relationships can be improved by treating subclinical hypothyroidism. Objective: Post partum thyroiditis (PPT) is an autoimmune disorder that presents in women with transient thyroid dysfunction, elevated thyroid peroxidase antibodies (TPOab) and thyroid ultrasound abnormalities during the first year after parturition. Several epidemiological studies from different parts of the world have reported a prevalence of PPT ranging from 1.1 to 16.7%. However, the prevalence of PPT among Nigerian women has not been reported. This study set to determine the prevalence of PPT among post partum women in Northern Nigeria. Methods: This was a cross sectional case control study in which 85 women who were six weeks to nine months post partum and an equal number of age matched controls were studied for PPT. Relevant medical history and physical examination for thyroid dysfunction were carried out in the two groups of women. Blood samples for serum assays of total T3 (TT3), total T4 (TT4) and TSH and TPOab were taken and analysed using ELISA method. Data were analysed using the statistical software SPSS. Results: PPT was found in only one case, presenting with thyrotoxicosis and high titres of TPOab (1.2 %). All the control subjects had normal thyroid function test. The Mean В±SD of serum TT3, TT4 and TSH in the study and control subjects were similar and comparable, 1.33 В±0.37 and 1.07В В±0.36 ng/ml; 102.13В±11.29 and 93.33В В±19.34 nmol/l; and 1.77В В±1.08 and 1.57В В±1.08 mIU/L, p> 0.05 respectively. High titres of TPOab was found in 1 (1.2%) of study subjects and 3 (3.5%) of control subjects, p > 0.05. – 126 – ABSTRACTS – Thyroid Disease oil), nitric oxide (Mona Vie and nitroglycerin), and carbonic anhydrase inhibition (acetazolamide) all similarly stimulate cerebral perfusion. Conclusion: Hyperthyroidism causes a pseudoAlzheimer’s pattern of abnormal cerebral metabolism which resolves with either natural or pharmacologic cerebral perfusion stimulants, independent of their mechanism of action. Abstract #1038 MILD HYPERTHYROIDISM CAUSES A PSEUDO-ALZHEIMER’S PATTERN OF CEREBRAL METABOLISM WHICH IS REVERSIBLE WITH CEREBRAL PERFUSION STIMULANTS Harold Thomas Pretorius, MD, PhD, and Nichole Richards Abstract #1039 Objective: Compare cerebral metabolism in hyperthyroidism and Alzheimer’s disease. Methods: Brain SPECT used 12 to 25 mCi Tc-99mHMPAO intravenous (IV) in a dark, quiet room.В Basal perfusion served as aВ marker of metabolism.В Cortical metabolic and perfusion indices (CMi and CPi) compared patients before and 1 hr after Mona Vie (acai fruit juice) or known cerebral perfusion stimulants:В 500 mg acetazolamide IV or 0.6 mg nitroglycerin sl in 15 min or 10 g fish oil (Lovaza) oral in 3 hrs.В Normal CMi (61+-10)% and CPi (65+-9)% were fromВ 20 patients withВ minor complaints and low likelihood of disease. Results: Decreased memory was noted in 3 hyperthyroid patients,В 1 with toxic nodular goiter andВ 2 with Graves’ disease,В without evidence of coexisting Hashimoto’s thyroiditis, who hadВ borderline lowВ CMi (50+-5)% but significant regional parieto-occipital and mesial temporal defects, defined by regional CMi (40+8)%,В calculated as the product of regional activity and the ratio of active global (in a 60% isocontour) to regional cortical areas, divided by total cerebral activity (in a 30% isocontour).В В TheВ similar Alzheimer’s pattern inВ 2 cases was more pronounced, withВ much lowerВ CMi and regional CMi of (30+-10)%.В In early Alzheimer’s andВ in hyperthyroidism the regional perfusion defects resolved with Mona Vie or any of the other perfusion stimulants, resulting in normal CPi (58+-5)%.В There was no consistent effect on patient symptoms within several months of therapy with Lovaza; however, symptoms tended to remit after successful therapy of hyperthyroidism. Discussion: Multiple reports from the prospective Rotterdam study show a > 300% increased incidence of Alzheimer’s disease in hyperthyroidism, the mechanism of which is unknown, but from the results here likely involves specific cerebral metabolism defects.В Epidemiological studies suggest lower rates of Alzheimer’s disease with increased fish consumption, although more recent reports question if the beneficial effects of natural fish may be compromised by increasing levels of neurotoxic pollutants, such as mercury.В It is intriguing that multiple mechanisms, including dependence on prostaglandins (fish ASSOCIATION OF SINGLE NUCLEOTIDE A/G POLYMORPHISM IN CYTOTOXIC T- LYMPHOCYTE ANTIGEN 4 (CTLA 4) GENE (49 EXON 1) IN PATIENTS WITH AUTOIMMUNE THYROID DISEASE Rakesh Kumar Sahay, MBBS, P.L. Rekha, PhD, M. Ishaq, PhD, P. Srinivas Rao, MD, and G.C. Reddy, MD, DM Objective: To investigate for a possible allelic association of the single nucleotide polymorphism (CTLA4A/ G) in exon 1 of the cytotoxic T lymphocyte antigen-4 (CTLA4) gene with autoimmune thyroiditis. Back ground: CTLA-4 is a co stimulatory molecule expressed on activated T (TH) cells, and functions as a negative regulator of T cell activation. We investigated the distribution of the CTLA4 exon 1 polymorphic types (49 A/G at codon 17) in Graves’ disease and Hashimotos thyroiditis. This dimorphism results in an amino acid exchange (Thr/Ala) in the leader peptide of the expressed protein and reduces the inhibitory function of CTLA4 and contributes to the pathogenesis of auto immune diseases. Method: A total of 383 subjects comprising of 128 patients with hypothyroidism, 60 with hyperthyroidism, 150 age and sex matched healthy controls and 45 first degree relatives participated in the present study. Genotyping was done by PCR using a set of sequence specific primers (PCR-SSP) Results: Table 1 depicts the distribution of CTLA 4 genotypes among the patients and the controls. Analysis of the results indicated highest risk associated with GG genotypes in patient groups when compared to the control population (П‡2 17.341, Pc 0.000. Odd’s Ratio 3.923 with 95% CI 2.057-7.472). Frequency of genotype GG was observed to be higher in both the groups of patients (Hashimoto’s thyroditisВ as well as GD) compared to other genotypes. However Chi square analysis indicated that the risk associated with GG genotype is higher towards developing Grave’s disease (П‡2 24.508, Pc 0.000. Odd’s – 127 – ABSTRACTS – Thyroid Disease Ratio 6.551 with 95% CI 3.057-14.027) when compared to Hashimotos (П‡2 8.561, Pc 0.003. Odd’s Ratio 2.951 with 95% CI 1.469-5. 919). Further, the results were analysed to study if there exists a negative correlation between any of the genotypes and thyroid dysfunctions. For this, statistical analyses were done for genotypes AA and AG against other genotypes in patients in general as well as hypothyroid cases and hyperthyroid cases separately. Analysis of the results indicated a negative correlation between genotype AA among patients in general (П‡2 12.725, Pc 0.000. Odd’s Ratio 0.287 with 95% CI 0.147-0.565).The association was analysed to be stronger in patients with GD (П‡2 17.12, Pc 0.000. Odd’s Ratio 0.179 with 95% CI 0.08-0.4) compared to those with Hashimotos (П‡2 6.15, Pc 0.013. Odd’s Ratio 0.376 with 95% CI 0.82-0.779). When analysis was done for genotype AG, a strong negative association was observed with patients in general (П‡2 6.09, Pc 0.014, Odd’s Ratio 0.544 with 95% CI 0.0.342-0.864,) as well as with Grave’s Disease (П‡2 5.906, Pc 0.015. Odd’s Ratio 0.397 with 95% CI 0.196-0.802,) compared to the control population. Such an association was not statistically significant in patients with hypothyroidism. Further, the distribution of CTLA 4 genotypes among the patients’ group were compared with that among the unaffected first degree relatives of patients with Hashimotos and Grave’s Disease (Table 1). In both the groups of FDRs frequency of susceptible genotype GG was observed to be nil. Statistical analysis revealed a significant difference in the distribution of GG genotype in patients with Hashimotos thyrodidits (П‡2 5.311, Pc0.021, Odd’s Ratio Inf.) as well as Grave’s disease (П‡2 8.97, Pc0.003, Odd’s Ratio Inf.) compared to the respective FDRs control group. Conclusion: Genotype as well as allele frequency studies indicate polymorphism at position 49 of CTLA4 gene as a candidate locus involved in the predisposition of thyroid dysfunctions. Though reports are available on this line from various other populations, to our knowledge reports from Indian series of patients are lacking. Case presentation: An elderly female patient with advanced metastatic follicular thyroid cancer received Thyrogen (Genzyme Corp) to stimulate RAI uptake using the compassionate use protocol. Within 24 hours, the patient developed respiratory failure requiring intubation and ICU admission. To our knowledge, this is the first report of Thyrogen-associated respiratory failure in follicular thyroid cancer. The patient had longstanding multinodular goiter, which enlarged despite suppressive levothyroxine therapy. FNA results were suggestive of a follicular carcinoma. The patient had subtotal thyroidectomy and postoperative RAI ablation with 75 mCi. Pathology revealed low-grade follicular carcinoma with vascular capsular invasion. Whole body scan showed uptake only in the neck.В Over the next few years, she had debulking surgeries for local recurrences with spread into the mediastinum and surrounding the internal jugular vein. Despite this, she again developed a new mass in the thyroid bed and had pulmonary metastates. Whole body I 131 scan and a PET scan were negative. Two years later, she had additional local recurrence with tracheal compression and left vocal cord paralysis; she refused further surgery. When Thyrogen became available, palliative use (two consecutive doses of Thyrogen, followed by RAI administration) was planned. The patient received the first dose of 0.9 mg Thyrogen IM and 24 hours later, she experienced severe shortness of breath and required endotracheal intubation. CT scan showed a bulky neck mass encasing the trachea, and pulmonary metastases. CXR had a nonspecific pulmonary edema pattern.В After negative evaluation for other causes of respiratory failure, she received 120 mg Solumedrol IV and was successfully extubated two days later. She lived for a year after the hospitalization. Discussion: Respiratory failure associated with Thyrogen administration has been reported in metastatic papillary cancers and in large goiter. Possible mechanisms are low-grade inflammation and oxidative stress linked to TSH increase. Alternative treatment options in this case include: pretreatment with glucocorticoids and the use of lower doses of Thyrogen to stimulate RAI uptake. Clinicians should be aware of respiratory failure as a potentially life threatening complication of Thyrogen use in patients with large thyroid tumors, including follicular cancers. Abstract #1040 THYROGEN-ASSOCIATED RESPIRATORY FAILURE Catalina Norman, MD, Anna C. Freitag, MD, and Nancy J. Rennert Objective: To report a case of Thyrogen-associated respiratory failure in advanced follicular thyroid cancer and to review the mechanisms and treatment of this potentially life threatening complication. – 128 – ABSTRACTS – Index Adrenal Disorders Author AlAssad, Hani AlAssad, Hani AlbarrГЎn, Alfredo Reza Alsoutary, Khalil M Alsoutary, Khalil M Amin, Alpesh AГ±el, Marguerite ГЃngeles, Arturo Armas, Laura A. G. AvendaГ±o, Edgar AvendaГ±o, Edgar Bhatt, Surya Prakash Bravo, Emmanuel Brietzke, Stephen Bulchandani, Deepti Cardenas, Elva Clemente, Javier Dale, Thompson H. Diab, Dima L. Doshi, Krupa Drake III, Almond Dube, Simmi Dubey, T. N. Espinet, Rafael Farrokhi, Farnoosh Gajula, Sonia Gardner, David Gardner, Michael Gomez-Perez, Francisco GГіmez-PГ©rez, Francisco J. Green, Kim Guifarro, Maria Alejandra Ramos Hamrahian, Amir H. Hanna-Moussa, Abdullah Harindhanavudhi, Tasma Harper, Rene J. Harrell, Michael Ilahi, Marium Isales, Carlos Karounos, Dennis – 129 – Abstract No Page 102 103 108 102 103 105 115 108 120 108 122 121 101 110 105 122 111 121 101 101 118 107 107 116 111 109 112 112 122 108 114 108 101 110 115 119 117 120 119 114 2 2 5 2 2 4 9 5 12 5 13 13 1 7 4 13 7 13 1 1 11 5 5 10 7 6 8 8 13 5 9 5 1 7 9 11 10 12 11 9 ABSTRACTS – Index Adrenal Disorders (Cont.) Author Kelly, Rebecca Khan, Asma Sohail Khan, Khurshid Khan, Uzma Khaya, Saba Kurukulasuriya, Lilamani Romayne G. Llerena, Luis A. Longo, Santo Lugar, Richard May, John Meyer, Claudine G. Mezitis, Spyros Mihailescu, Dan Nachnani, Jagdish S. Nanda, Sudip Odeke, Sylvester Pamula, John Panunti, Brandy Pretorius, Harold Thomas Ramos, Ma Alejandra Reyes, Edgardo Reynolds, L. R. Richards, Nichole Rios, Juan Manuel Rivera, Luis Raul Ruiz Rull, Juan Rull, Juan Shad, Fariha Sharma, V. K. Sulaimani, Riad Sulaimani, Riyadh Tanawuttiwat, Tanyanan Taneja, Deepa Tannock, Lisa Valentin, Esperanza ValentГn, Esperanza VanHoven, Anne Marie Vedula, Ramya Smita Velasco, German – 130 – Abstract No Page 112 113 110 113 104 109 111 121 112 105 118 100 115 105 121 118 121 104 117 122 108 114 117 108 116 122 108 111 107 102 103 115 114 114 122 108 106 106 100 8 8 7 8 3 6 7 13 8 4 11 1 9 4 13 11 13 3 10 13 5 9 10 5 10 13 5 7 5 2 2 9 9 9 13 5 4 4 1 ABSTRACTS – Index Adrenal Disorders (Continued) Author Weinberg, Andrew Yasmeen, Tahira Zalzaleh, Ghassan Diabetes Mellitus Author Abbassy, Aly Abdel Latif Aboderin, A. O. Adamu, Abdullah Ndaman Adeyemi-Doro, Adekunle Adeyemi-Doro, Adekunle Adhiarta, I. G. N. Aguilar-Salinas, Carlos Aguirre, Lina Ahmad, Imteyaz Akinlade, Akinyele Taofiq Alejandro, Rodolfo Alejandro, Rodolfo Alejandro, Rodolfo Aljohani, Naji Jameel Anumah, Felicia Ohunene Arbab, Tarig Sayed Mustafa Arbab, Tarig Sayed Mustafa Attallah, Hamdee Baddor, Nahed Baidal, David A. Baidal, David A. Baidal, David A. Bakari, Adamu Girei Bakari, Adamu Girei Bakhru, Nitasha Bamiro, S. B. Bamiro, S. B. Bansal, Alka Bays, Harold Beel, Ruth Behnke, Andrew John Behnke, Andrew John Bello-Sani, Fatima – 131 – Abstract No Page 100 115 115 1 9 9 Abstract No Page 206 211 205 254 253 247 213 255 215 232 225 231 227 218 203 256 207 221 206 227 231 225 200 219 216 253 254 212 230 245 245 246 203 18 20 17 45 45 41 21 46 22 32 28 32 29 24 16 46 18 26 18 29 32 28 15 24 23 45 45 21 31 40 40 41 16 ABSTRACTS – Index Diabetes Mellitus (Cont.) Author Benzon, Melissa Bernetti, Karina Bulchandani, Deepti Burke, Brian Bushati, Besa Button, Eric Ceriello, Antonio Chaudhary, Umair Javaid Cheang, Mary Chertow, Bruce Chinenye, Sunday Coker, Adekemi Olabisi Cuevas-Ramos, Daniel Cure, Pablo Cure, Pablo Curry, Andrea Daru, Patrick Drake III, A. J. Eaton, Crystal Emanuele, Mary Ann Emanuele, Nicholas Faradji, Raquel N. Faradji, Raquel N. Faradji, Raquel NoemГ Farrokhi, Farnoosh Fasanmade, Olufemi Adetola Fasanmade, Olufemi Adetola Fasanmade, Olufemi Adetola Fonseca, Vivian Andrew Foster, Scott Fox, Kathleen M. Froud, Tatiana Froud, Tatiana Froud, Tatiana Gavin III, James R. Ghetany, Mohamed Kamal Goldberg, Ronal Goldfine, Allison B. Gomez-Perez, Francisco – 132 – Abstract No Page 245 231 240 239 244 226 226 220 218 233 234 204 213 227 231 227 235 228 240 224 224 225 231 227 214 254 204 253 222 226 223 231 227 225 223 206 237 222 213 40 32 37 37 40 29 29 25 24 33 34 17 21 29 32 29 35 30 37 27 27 28 32 29 22 45 17 45 26 29 27 32 29 28 27 18 36 26 21 ABSTRACTS – Index Diabetes Mellitus (Cont.) Author Gorn, Lisa Goscin, Lee Pletts Grandy, Susan Gress, Todd W. Guevara, Ximena Guevara, Ximena Guevara, Ximena Hamburg, Mitchell Hasan, Mumtaz Hasan, Mumtaz Hasan, Mumtaz Herrada, Eva Hudson, Sandra G. Ikem, Innocent Ikem, Innocent Ikem, Rosemary Temidayo Ikem, Rosemary Temidayo Ikem, Rosemary Temidayo Imran, Syed Ali Imran, Syed Ali Imran, Syed Ali Inankur, Aysha Emily Ishibashi, Hirotaka Ismail-Beigi, Faramarz Iwuala, Sandra Iwuala, Sandra Jamil, Muhammad Shahid Jamil, Muhammad Shahid Jawa, Ali Asghar Jawa, Ali Asghar Jawa, Ali Asghar Jawa, Ghazanfar Jawa, Ghazanfar Jing, Ming Johnston, Jann Jones, Michael Jones, Michael R. Karches, Kelli Keaveny, Andrew – 133 – Abstract No Page 225 249 223 233 242 241 243 240 220 236 215 231 251 210 209 211 209 210 220 236 215 239 226 229 253 254 220 215 236 220 215 236 220 229 244 230 222 216 255 28 42 27 33 38 38 39 37 25 35 22 32 43 20 19 20 19 20 25 35 22 37 29 30 45 45 25 22 35 25 22 35 25 30 40 31 26 23 46 ABSTRACTS – Index Diabetes Mellitus (Cont.) Author Khan, Alina Khan, Zaffer Yab Khoo, Teck-Kim Kolawole, Babatope Kummer, Mark A. Kupin, Warren Leitao, Cristiane Bauermann Leitao, Cristiane Bauermann Lenz, Oliver Lohano, Suresh Lohano, Vasdev Lopez, Norma Lubitz, Sara Elisabeth Ludwig, Sora Martin, Kimberly Mathur, Sandeep Kumar McBride, Nancy McCallum, James McCallum, James Mcgarvey, Megan Elizabeth McNeil, Rebecca McQuillen, Kelly Meek, Shon Messinger, Shari Messinger, Shari Messinger, Shari Mineo, Davide Mineo, Davide Mokshagundam, Sri Prakash L. Monroy, Kathy Monroy, Kathy Morris, Margaret Murray, Robert Nabhan, Fadi Adel Nachnani, Jagdish S. Naidu, M.U.R. Narasimhan, Kanakasabai Newton, Christopher Alan Odetoyinbo, Babatunde – 134 – Abstract No Page 237 212 202 211 251 231 227 231 231 217 217 224 248 218 229 212 214 216 238 238 255 218 255 227 231 225 231 227 217 227 225 218 218 224 240 250 208 228 211 36 21 16 20 43 32 29 32 32 23 23 27 42 24 30 21 22 23 36 36 46 24 46 29 32 28 32 29 23 29 28 24 24 27 37 43 19 30 20 ABSTRACTS – Index Diabetes Mellitus (Cont.) Author Ogbera, Anthonia Okeoghene Ogbera, Anthonia Okeoghene Ogbera, Anthonia Okeoghene Ogbera, Anthonia Okeoghene Ogbera, Anthonia Okeoghene Ohwovoriole, Efedaye Ola, Bola Ola, Bola Olaogun, Matthew Onyemelukwe, Geoffrey C. Onyemelukwe, Geoffrey C. Paturi, Bhanu Teja Pileggi, Antonello Pileggi, Antonello Pinto, Miguel E. Pinto, Miguel E. Pinto, Miguel E. Probst-Riordan, Julie Puepet, Fabian Rahman, Ibrahim Abdel Rao, P.V. Rasool, Tahir Rasool, Tahir Reddem, Sreekanth Reddy Reiher, Alexandra Rempel, Brenda Ricordi, Camillo Ricordi, Camillo Ricordi, Camillo Rizvi, Ali Rodbard, Helena Wachslicht Rull-Rodrigo, Juan Saenz, Aleida Sakal, Saad Santhanam, Prasanna Selvaggi, Gennaro Selvaggi, Gennaro Shah, Vipul Sheikh-Ali, Mae – 135 – Abstract No Page 254 253 234 232 201 204 210 209 209 200 219 250 231 227 243 242 241 248 235 206 250 236 215 250 224 218 227 225 231 208 223 213 227 252 233 231 227 244 255 45 45 34 32 15 17 20 19 19 15 24 43 32 29 39 38 38 42 35 18 43 35 22 43 27 24 29 28 32 19 27 21 29 44 33 32 29 40 46 ABSTRACTS – Index Diabetes Mellitus (Cont.) Author Shen, Garry Shokry, Hazem Sincaroe, James Smith, Steven Soetedjo, Nanny Natalia Mulyani Soghikian, Maida Sonny, Chinenye Tanenberg, Robert Jay Tarigan, Helen C. Tharavanij, Thipaporn Tharavanij, Thipaporn Truitt, Kenneth Truitt, Kenneth E. Uchenna, Doris Ukoli, Christiana Uloko, Andrew Enemako Unachukwu, Chioma Usharani, P. Valdes, Paloma Almeda Varon, Juan Carlos Villena, Jaime E. Villena, Jaime E. Villena, Jaime E. Watwe, Veena Wittlin, Steven Yamanouchi, Toshikazu Yashmaina, Sridhar Zafar, Muhammad Abu Zafar, Muhammad Abu Zaheer, Jawad Zaheer, Jawad Zaheer, Jawad Hypoglycemia Author Agarwal, Monica Agosto, Agosto Ahmad, Khraisat Alejandro, Rodolfo – 136 – Abstract No Page 218 206 224 202 247 238 201 228 247 227 231 230 222 234 235 235 234 250 213 237 243 241 242 221 226 226 250 215 236 215 220 236 24 18 27 16 41 36 15 30 41 29 32 31 26 34 35 35 34 43 21 36 39 38 38 26 29 29 43 22 35 22 25 35 Abstract No Page 301 306 300 303 48 51 48 49 ABSTRACTS – Index Hypoglycemia (Cont.) Author Aljaghbeer, Eshraq Nazir Allende, Myriam Almeda-ValdГ©s, Paloma Almeda-ValdГ©s, Paloma Baidal, David A. Bernetti, Karina Cruz, Sidney Cuevas-Ramos, Daniel Cuevas-Ramos, Daniel Cure, Pablo Elbein, Steven Faradji, Raquel N. Froud, Tatiana Gabriel, Barnard San GГіmez-PГ©rez, Francisco J. GГіmez-PГ©rez, Francisco J. Harindhanavudhi, Tasma Kowalczyk, Joseph Leitao, Cristiane Bauermann Mateo, Jose Garcia Mihailescu, Dan Mineo, Davide Pileggi, Antonello Rabell, Vilma Ramirez, Margarita Ricordi, Camillo Rull, Juan Rull, Juan Saenz, Aleida Santiago, Monica Singh, Sant P. Tanawuttiwat, Tanyanan Tharavanij, Thipaporn Thomas, Tarita Uribe-Uribe, Norma Uribe-Uribe, Norma Ventura-Gallegos, Jose Luis Yasmeen, Tahira Zarate-Diaz, Xeily – 137 – Abstract No Page 300 306 305 302 303 303 300 302 305 303 301 303 303 304 302 305 304 304 303 306 304 303 303 306 306 303 305 302 303 306 300 304 303 304 305 302 302 304 305 48 51 50 49 49 49 48 49 50 49 48 49 49 50 49 50 50 50 49 51 50 49 49 51 51 49 50 49 49 51 48 50 49 50 50 49 49 50 50 ABSTRACTS – Index Hypoglycemia (Cont.) Author Zarate-Diaz, Xeily Zentella-Dehesa, Alejandro Lipid Disorders Author Attallah, Hamdee Baker, Mary Bakry, Elsayed Bhatt, Surya Prakash Crisostomo, Analyn Eledrisi, Mohsen Handa, Rohini Haq, Seema Joosub, Omran Nanda, Sudip Saghier, Sadaf Scofield, Hal Sultan, Mohammed Zambare, Suchitra V. Metabolic Bone Disease Author Adachi, Jonathan D. Agarwal, Niti Ajamani, Ajay Bodenner, Donald Boonen, Steven Borretta, Giorgio Brown, J. Castro-Magana, Mariano Cesario, Flora Clarke, Bart L. Dedrick, Rebecca Delmas, P. D. Dube, Simmi Dubey, T. N. Fatourechi, Vahab Flores, Mauricio Ernesto GarcГa, Franklin – 138 – Abstract No Page 302 302 49 49 Abstract No Page 400 402 401 403 401 401 403 402 401 403 402 402 401 400 52 53 52 53 52 52 53 53 52 53 53 53 52 52 Abstract No Page 517 502 502 505 518 519 511 516 519 515 504 511 510 510 522 516 501 64 56 56 57 64 65 61 63 65 63 57 61 60 60 66 63 55 ABSTRACTS – Index Metabolic Bone Disease (Cont.) Author Gianotti, Laura Grant, Kenneth Grauer, Andreas Grauer, Andreas Grauer, Andreas Greenspan, Susan L. Hughes, Thomas A. Jain, Sachin Kumar Jasson, Lavi Karmegan, Satish Kline, G. LaCroix, Andrea Laura, Monsalve Levin, Robert Lindsay, Robert Lindsay, Robert Magro, Giampaolo Manandhi, Aswatharayan Mazhari, Alaleh McClung, Michael R. Mendoza, Ana Miller, Paul D. Moraghan, Thomas Morales, Pedro E. Moses, Arnold M. Moses, Arnold M. Movva, Arun Kumar Mukherjee, Akta Patel Nabhan, Fadi Adel Paulo, Jr, Remberto Cuenca Placzkowski, Kimberly Ann Rao, Ambika Ratti, Jyothi Redman, Carolyn Rieke, Suzanne Roux, Christian Roux, Christian Rubin, Daniel Saag, Kenneth – 139 – Abstract No Page 519 520 518 517 513 504 506 502 501 520 511 504 501 509 517 504 519 520 512 518 523 518 521 501 503 514 503 500 512 508 515 520 520 505 500 517 513 509 504 65 65 64 64 62 57 58 56 55 65 61 57 55 59 64 57 65 65 61 64 67 64 66 55 56 62 56 55 61 59 63 65 65 57 55 64 62 59 57 ABSTRACTS – Index Metabolic Bone Disease (Cont.) Author Sabharwal, Anup Sarabu, Brijmohan Schiefer, Amanda Reagan Sharma, V. K. Silverman, Stuart Singh, Harinder Siris, Ethel Subbarayan, Sreevidya Kannoorpatti Tassone, Francesco Tebben, Peter J. Torres, Mira S. Venkatesh, Swamy Watts, Nelson B. Watts, Nelson B. Watts, Nelson B. Watts, Nelson B. Yeh, James Young, Lisa Young, Lisa Zaidi, Syeda Sadia Zhou, Xiaojie Zhou, Xiaojie Zhou, Xiaojie Obesity Author Chaudhary, Umair Javaid Hasan, Mumtaz Imran, Syed Ali Jamil, Muhammad Shahid Jawa, Ali Asghar Jawa, Ghazanfar Ali Zaheer, Jawad Other Author Abrams, Cynthia Abu-Lebdeh, Haitham S. Ahmed, Mohammed Al-Harthi, Saud – 140 – Abstract No Page 524 514 522 510 504 520 504 521 519 508 523 520 513 517 504 511 516 507 524 506 517 518 513 67 62 66 60 57 65 57 66 65 59 67 65 62 64 57 61 63 58 67 58 64 64 62 Abstract No Page 600 600 600 600 600 600 600 69 69 69 69 69 69 69 Abstract No Page 707 704 702 702 73 72 71 71 ABSTRACTS – Index Other (Cont.) Author Allende, Myriam Anumah, Felicia Ohunene Apovian, Caroline M. Asnani, Sunil Bejnariu, Cristina Iuliana Bhatt, Bankim Bin-Abbas, Bassam Black, Dennis Bone, Henry Boonen, Steve Chow, John T. Colle, Ann Di Luozzo, Gabriele Eriksen, Erik Fink Fomin, Svetlana Foote, Robert L. Gambhir, Kanwal Giannini, S. Jacob, Jubbin Jagan Jacob, Jubbin Jagan Kazlauskaite, Rasa Khaodhiar, Lalita Komarovskiy, Kateryna Lewi, Jack E. Lipede, Adefunke Omosefe Lippuner, K. Lowery, Supna Bhagat Martinez, Meliza Mason, Elizabeth Mechanick, Jeffrey I. Mesenbrink, Peter Miller, Paul D. Miller, Ralph Nunlee-Bland, Gail O’Brian, John Odonkor, Wolali Ogbera, Anthonia Osorio, Jorge Ivan Martinez Pathak, Ram D. – 141 – Abstract No Page 720 710 703 700 719 716 702 711 711 711 704 718 705 711 700 704 707 711 709 708 714 703 706 717 701 711 718 720 718 705 711 711 713 707 718 707 701 717 712 81 75 71 70 80 79 71 76 76 76 72 80 72 76 70 72 73 76 74 74 77 71 73 79 70 76 80 81 80 72 76 76 77 73 80 73 70 79 76 ABSTRACTS – Index Other (Cont.) Author Pathak, Sumedha Ram Rabell, Vilma Raikhelkar, Jayashree Ramirez, Margarita Reynolds, L. R. Richardson, Donald Sakal, Saad Scurlock, Corey Sellmeyer, Deborah Semega-Janneh, Mariama Shukla, Pratik R. Signalov, Mikhail Singh, Madhurita Singh, Navjot Singh, Navjot Skag, Arne Suciu, Pavel Taneja, Deepa Tannock, Lisa Usdan, Lisa S. Vahedi, Marjan Velinova, Silvia Via, Michael Wermers, Robert A. Williams, James T. Win, Hla Winer, Nathaniel Pituitary Disorders Author Abelev, Zinoviy Adeyemi-Doro, Adekunle Adeyemi-Doro, Adekunle Aguirre, Lina Ahmed, Mohammed Ahmed, Mohammed Ahmed, Mohammed Akhter, Natasha Al-Ahmed, Saleh – 142 – Abstract No Page 712 720 705 720 713 718 721 705 711 707 716 716 708 709 708 711 719 713 713 703 707 714 705 704 707 715 706 76 81 72 81 77 80 82 72 76 73 79 79 74 74 74 76 80 77 77 71 73 77 72 72 73 78 73 Abstract No Page 816 824 804 829 818 811 826 823 826 92 97 85 99 93 89 98 96 98 ABSTRACTS – Index Pituitary Disorders (Cont.) Author Al-Dabagh, Hiba Al-Harathi, Mohammed Al-Harthi, Saud Al-Hindi, Hindi Al-Jaghbeer, Eshraq Al-Lawati, Zahraa Al-Sheef, Mohammed Alfonso, Bianca Allende, Myriam Atkinson, John Attri, Navneet Augustine, Jaimie M. AvendaГ±o, Edgar Bakkari, Shakir Beniwal, Poonam Blumenthal, Stanley Buciuc, Razvan F. Bushnik, Tamara Butler, Paula Carpenter, Robert J. Clyde, Patrick W. Czervionke, Leo Dababo, M. Dankert-Hsu, Nicole M. Dodis, Regina Duggal, Jasleen Kaur Dulipsingh, Latha Ekpebegh, Chuks Eray, Esin Erickson, Dana Faiman, Charles Falls, William L. Fasanmade, Olufemi Fasanmade, Olufemi Fleckman, Adrienne M. Glusman, Joan Group, The Pasireotide Acromegaly Study Hamrahian, Amir H. Harindhanavudhi, Tasma – 143 – Abstract No Page 819 811 818 811 801 820 826 816 827 805 801 809 817 811 801 823 812 820 801 800 802 829 818 800 828 801 822 824 821 805 821 800 804 824 816 808 808 821 823 93 89 93 89 83 94 98 92 98 85 83 88 92 89 83 96 89 94 83 83 84 99 93 83 99 83 95 97 95 85 95 83 85 97 92 87 87 95 96 ABSTRACTS – Index Pituitary Disorders (Cont.) Author Iwuala, Sandra Omozehio Joshi, Prajesh Kanaan, Imaduddin Kanaan, Imaduddin Kanaan, Imaduddin Kantorovich, Vitaly Kassim, Thaslim Ahamed Katznelson, Laurence Khalfin, Alla Khan, Uzma Koch, Christian A. Kunecka, Paulina LaRochelle, Jeffery S. Lewi, Henry L. Lindsay, Robert M. Lorenz, Robert R. Lteif, Aida Ludlam, William Henry Lugaro-Gomez, Ana Mallhi, Kanwal Mann, Klaus Marlar, Victor Richard Marwan, Shaheen Mayberg, Marc R. Mogul, Harriette Nader, Nicole Stephanie Narula, Harmeet Singh Narula, Harmeet Singh Narula, Maneet Kaur Narula, Maneet Kaur Nazmi, Ahmed Nicholas, William C. Nimmo, Teresa Allison Nunlee-Bland, Gail Odeniyi, Ifedayo Adeola Odeniyi, Ifedayo Adeola Odonkor, Wolali Ohwovoriole, Augustin Patterson, Marc – 144 – Abstract No Page 804 816 818 826 811 803 802 820 807 814 812 828 800 820 813 821 810 809 827 801 808 812 818 809 807 810 815 825 815 825 818 812 803 819 804 824 819 824 810 85 92 93 98 89 84 84 94 86 91 89 99 83 94 90 95 88 88 98 83 87 89 93 88 86 88 91 97 91 97 93 89 84 93 85 97 93 97 88 ABSTRACTS – Index Pituitary Disorders (Cont.) Author PГ©rez, Francisco J. GГіmez Petersenn, Stephan Rabel, Vilma Ramirez, Margarita Ramirez, Jr., Sofronio Cruz Ramos, Ma. Alejandra Reddy, Ashwini Rennert, Nancy J. Roberts, Brian Rull, Juan Sabir, Anas Sathananthan, Airani Scheithauer, Bernd Seale, Benjamin W. Semega-Janneh, Mariama Shakir, K.M. Mohamed Shakir, K.M. Mohamed Sheikh-Ali, Mae Singh, Sarabjeet Siraj, Elias Smallridge, Robert C. Smith, Earl Soler, Simonette Spain, David A. Srinivasan, Lakshmi Steinberg, Gary Stringer, Jonathan Strizhevsky, Marina Sundararajan, Deepa Sundararajan, Deepa Tanawuttiwat, Tanyanan Tchong, Leo Unger, Nicole Valentin, Esperanza Valenzuela, Evana Veloski, Colleen Vouyiouklis, Mary Warner, Christopher J. Weil, Robert J. – 145 – Abstract No Page 817 808 827 827 822 817 814 828 820 817 804 805 805 812 819 802 800 829 801 806 829 801 822 820 820 820 803 816 825 815 823 806 808 817 828 806 813 800 821 92 87 98 98 95 92 91 99 94 92 85 85 85 89 93 84 83 99 83 86 99 83 95 94 94 94 84 92 97 91 96 86 87 92 99 86 90 83 95 ABSTRACTS – Index Pituitary Disorders (Cont.) Author Wharen, Robert Yudt, William M. Zerikly, Rahfa Kurdi Reproductive Endocrinology Author Ajamani, Ajay Banceanu, Gabriel Barbu, Carmen Burshell, Alan Calderon, Naim Mitre Carsote, Mara Coculescu, Mihail Constantin, Madalina Diwaker, Pramila Fica, Simona Vasilica Islam, Najumul Jabbar, Abdul Jain, Sachin Kumar Lascar, Ioan Lteif, Aida Mahar, Saeed Ahmed Poiana, Catalina I. Sajin, Maria Scanlan, Marideli ColГіn Stanescu, Bogdan Terzea, Dana Viswanathan, Pushpa A. Witchel, Selma F. Thyroid Disease Author Abou-Samra, Abdul Adamcik, Susan Jane Agarwal, Monica Ahmed, Javeria Ahmed, Mohammed Ahmed, Mohammed Al Jawair, Rashid O. – 146 – Abstract No Page 829 802 821 99 84 95 Abstract No Page 901 903 906 905 902 903 903 906 901 906 900 900 901 906 902 900 903 903 905 903 906 904 904 101 102 104 104 102 102 102 104 101 104 101 101 101 104 102 101 102 102 104 102 104 103 103 Abstract No Page 1007 1021 1015 1026 1010 1005 1001 110 118 114 120 111 108 106 ABSTRACTS – Index Thyroid Disease (Cont.) Author Al-Harthy, Mohammed Al-hindi, Hindi Al-Zidjali, Fatima Alejandro, Angel Rodolfo Alenezi, Mohammed Alhawari, Hussam H. Alshammari, Sameer Badlissi, John Bagchi, Nandalal Bajaj, Harpreet Singh Baruah, Manash Pratim Bhagra, Anjali Bhuyan, Sonali Barman Bible, Keith C. Blumenthal, Manfred Castillo-Perez, Judith M. Chianelli, M. Choudhry, Imran Correa, Francisco Davies, Terry F. Dougherty, Thomas Durst, Paul Edmonds, Merill Ennis, Rob Faas, Fred H. Farhat, Rafif Fatourechi, Vahab Feng, Yun Fleckman, Adrienne M. Freitag, Anna C. Fresca, Diane E. Galofre, Juan C. Gharib, Hossein Gonzalez-Pantaleon, Adalberto D. Goscin, Lee Pletts Gouller, Alina Grant, Clive S. Graziano, F. Groh, Katherine – 147 – Abstract No Page 1010 1010 1005 1024 1000 1004 1000 1017 1007 1012 1008 1032 1008 1003 1021 1002 1025 1006 1002 1009 1019 1019 1001 1011 1004 1005 1032 1018 1018 1040 1029 1009 1011 1022 1037 1027 1003 1025 1018 111 111 108 119 106 108 106 115 110 112 110 124 110 107 118 107 120 109 107 111 116 116 106 112 108 108 124 116 116 128 122 111 112 118 126 121 107 120 116 ABSTRACTS – Index Thyroid Disease (Cont.) Author Guglielmi, R. Gurevich, Yuriy Haber, Richard Hartini, Sri Hay, Ian D. Hramiak, Irene Huang, Cindy Hughes, Thomas Hutchinson, Maeve Elizabeth Iranmanesh, Ali Iranmanesh, Ali Ishaq, M. Jain, Bina Javier, Emmanuel Johnston, Jann M. Kanaan, Imaduddin Kariadi, K. S. Khalil, Nesreen Khan, Saima Kulczycki, Alexander Kundra, Priya Kuo, Sheng-Fong Lin, Jen-Der Makdissi, Antoine Makdissi, Antonie Mansour, Maged Marina, Anna Leonidovna Mikhail, George Samir Mubi, Bilkisu Mohammed Narula, Maneet Kaur Narula, Harmeet Singh Nazmi, Ahmed Ng, Alvin Nicholas, William Norman, Catalina Ohwovoriole, Augustine E. Padmanabhan, Hema Padmanabhan, Hema Papini, Laura Todino V. – 148 – Abstract No Page 1025 1027 1009 1031 1003 1001 1034 1026 1003 1016 1017 1039 1006 1002 1020 1010 1031 1000 1014 1030 1021 1035 1035 1004 1015 1000 1020 1000 1036 1033 1033 1010 1028 1013 1040 1036 1016 1017 1025 120 121 111 123 107 106 125 120 107 115 115 127 109 107 117 111 123 106 114 122 118 125 125 108 114 106 117 106 126 124 124 111 121 113 128 126 115 115 120 ABSTRACTS – Index Thyroid Disease (Cont.) Author Papini, Enrico Parong, Maria Paulina Santos Pretorius, Harold Thomas Rao, P. Srinivas Reddy, G. C. Rekha, P. L. Rennert, Nancy J. Richards, Nichole Robinson, Suzette Adele Sabharwal, Anup Sahay, Rakesh Kumar Seale, Ben Williamson Sherigar, Rathnakara Signore, A. Simmons, Debra L. Simmons, Debra L. Siraj, Elias Soetedjo, Nanny Natalia Mulyani Strizhevsky, Marina Sundararajan, Deepa Tham, Kwang-Wei Thompson, Geoffrey B. Tokmakejian, Sonya Toscano-Zokor, Amy Tulbah, Asma Uricoechea, Hernando Vargas Van Hoven, Anne Marie Veloski, Colleen Wang, Xiangbing Wang, Xiangbing Wang, Xiangbing Wheaton, Jennifer Wheaton, Jennifer Carter Yaqub, Abid Yaqub, Abid Young, Jr, William F. Zimmerman, Robert – 149 – Abstract No Page 1025 1019 1038 1039 1039 1039 1040 1038 1007 1024 1039 1013 1016 1025 1004 1015 1022 1031 1018 1033 1028 1003 1001 1034 1005 1023 1014 1022 1029 1030 1034 1019 1006 1006 1019 1003 1012 120 116 127 127 127 127 128 127 110 119 127 113 115 120 108 114 118 123 116 124 121 107 106 125 108 119 114 118 122 122 125 116 109 109 116 107 112
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