Basic Laboratory Tests
Basic Blood Chemistry Tests
Test
Alternative
Names
Units
Usual
Normal Range
Examples of conditions in
which abnormal values
occur
Albumin, serum
Albumin
g/dL
3.8-5.2 g/dL
Bilirubin, Total
Bili. Total
mg/dL
0.2-1.5 mg/dL
Blood Urea Nitrogen
Creatinine, serum
Lactate Dehydrogenase
BUN
Creatinine
LDH (LD)
mg/dL
mg/dL
U/L
9-25 mg/dL
0.7-1.5 mg/dL
50-150 U/L
Protein, Total
Aspartate Aminotransferase
Tot Protein
AST (SGOT)
g/dL
U/L
6.1-8.2 g/dL
0-33 U/L
Alanine Aminotransferase
ALT (SGPT)
U/L
0-45 U/L
Alkaline Phosphatase
Alk. Phos.
U/L
30-125 U/L
Gammaglutamyl
Transpeptidase
GGT (GGTP)
U/L
0-65 U/L
Globulin
Globulin
g/dL
2.1-3.9 g/dL
Glucose
Glucose
mg/dL
60-109 mg/dL
Fructosamine
Hemoglobin A1c
Fructosamine
HbA1c,
Glycosylated
Hemoglobin
(GHb)
Cholesterol
mg/dL
%
1.2-2.0 mg/dL
3.0-6.0%
Low levels may occur with
malnutrition, liver disease,
malabsorption, kidney
disease. Elevated levels are
uncommon but may be seen
in dehydration.
Liver dysfunction, biliary tract
disease/obstruction, Gilbert’s
syndrome (isolated),
hemolysis (isolated)
Kidney (renal) disease
Kidney (renal) disease
Tumors, hemolysis,
liver, heart, lung and
kidney diseases
See Albumin and Globulin
Viral hepatitis, fatty liver,
alcohol abuse, cirrhosis,
muscle injury, drug reactions,
macroenzyme (isolated)
Viral hepatitis, fatty liver,
alcohol abuse, cirrhosis,
drug reactions
Biliary tract disease,
gallstones, tumors, drug
reactions, bone
disease/injury, pregnancy,
growing children/adolescents
Biliary tract disease,
alcohol abuse, fatty liver,
drug reactions
Elevated levels can occur
with infections, inflammation,
autoimmune diseases and
various cancers. Low levels
can occur with liver disease,
inherited abnormalities in
globulin production, and in
kidney disease.
Diabetes mellitus,
hypoglycemia
Diabetes mellitus
Diabetes mellitus
mg/dL
140-199 mg/dL
Familial hyperlipidemia,
Total Cholesterol
HDL Cholesterol
LDL Cholesterol
Total Cholesterol/HDL
Cholesterol ratio
LDL Cholesterol/HDL
Cholesterol ratio (LDLHDL
ratio)
Triglycerides
Uric Acid
Triglycerides
UA
mg/dL
mg/dL
0-15 mg/dL
2-7 mg/dL
Prostate specific antigen
PSA
nanograms per
milliliter (ng/mL)
0-4 ng/mL
Carbohydrate deficient
transferrin
Hemoglobin associated
acetaldehyde
NTproBNP
CDT
%
0-2.5%
HAA
micromoles per
liter (ìmol/L)
picograms per
milliliter (pg/mL)
<10.5 ìmol/L
mg/L
Low risk <1,2 mg/L
Mod risk 1-2-1.9
mg/L
High risk >2 mg/L
Coronary disease, vascular
disease
HIV infection
HIV infection
Hepatitis B infection
Previous Hepatitis B infection,
Hepatitis B vaccination
Current or previous Hepatitis
B infection
Current Hepatitis B infection
Hepatitis C infection
C-reactive protein
HDL
LDL
Chol/HD
L ratio
LDL/HD
L ratio
Pro-Brain
naturetic
peptide, N
terminal
fragment
CRP
mg/dL
mg/dL
No units
35-80 mg/dL
0-129 mg/dL
<5.0
No units
0.9-5.3
<125 pg/mL
HIV antibody, serum
HIV antibody, urine
Hepatitis B surface antigen
Hepatitis B surface antibody
HBsAg
HBsAb
Non-reactive
Non-reactive
Non-reactive
Non-reactive
Hepatitis B core antibody
HBcAg
Non-reactive
Hepatitis B “e” antigen
Hepatitis C antibody
HBeAg
HCVAb
Non-reactive
Non-reactive
hypothyroidism, liver disease,
kidney disease, diabetes,
medications, obesity, cigarette
smoking, alcohol consumption
Gout, renal failure, malignancy
Prostate cancer,
benign prostate
hypertrophy, prostatitis
Excessive alcohol
consumption, liver disease,
inherited conditions and in
normal individuals
Various types of heart disease
Blood Chemistry Tests
Indicators of Carbohydrate Metabolism: Glucose, Glycosylated Hemoglobin (Hemoglobin A1c) and Fructosamine
Glucose measurements are made to determine if there is a disorder of carbohydrate metabolism. Such disorders include
diabetes mellitus and various forms of hypoglycemia. Diabetes usually results in elevated glucose levels while disorders
associated with hypoglycemia may result in low glucose levels. However, normal glucose values do not exclude the
possibility that abnormal carbohydrate metabolism may exist. Glucose level rise after meals and fall with fasting so it is
important to note when the blood samples were obtained in relation to the last meal. The degree of blood glucose
elevation may be an indicator of the severity of diabetes or of how well the diabetes is being controlled. But since
glucose levels often vary considerably throughout the day, fructosamine or glycosylated hemoglobin levels may give a
better indication of longer-term diabetes control. Improper preparation or delays in analyzing blood samples can result in
erroneously low glucose values, a condition termed glycolysis. Glycolysis not only may result in erroneously low glucose
values but may also cause laboratory measurements of creatinine to be erroneously high.
Glycosylated hemoglobin (Hemoglobin A1c).
Hemoglobin is the oxygen carrying protein within red blood cells. When hemoglobin comes into prolonged contact with
glucose, some glucose may become chemically attached to the hemoglobin molecule resulting in what has become
known as glycosylated hemoglobin (GHb) or hemoglobin A1c (HbA1c). Glycosylated hemoglobin levels rise and fall in
direct proportion to blood glucose levels. Glycosylated hemoglobin levels reflect average blood glucose levels over the life
span of the red blood cell, about 120 days. Therefore glycosylated hemoglobin concentrations are more useful indicators
of long-term diabetes control than are individual blood glucose measurements. The American Diabetes Association
recommends that a glycosylated hemoglobin values be kept at 7% or less.
Fructosamine
Similar to the way glycosylated hemoglobin is formed, blood glucose may become chemically attached to the protein,
albumin, to form fructosamine. As with glycosylated hemoglobin, fructosamine levels rise and fall in direct proportion to
blood glucose levels. But because the life-spam of the albumin molecule is shorter than that of the hemoglobin molecule,
fructosamine levels reflect average blood glucose concentrations over a shorter period of time, usually thought to be the
preceding 3 to 6 weeks.
Indicators of Lipid Metabolism: Total Cholesterol, HDL Cholesterol, LDL Cholesterol, TC/HDL ratio
Cholesterol, Total Cholesterol
Cholesterol is a lipid (fat) that is an essential component of cell membranes and is required for the synthesis of
various hormones. Cholesterol is both absorbed from food and synthesized by the liver. Excess amounts of
cholesterol may be deposited in arteries resulting in atherosclerosis and predisposing to the risk of heart attack and
stroke. Cholesterol circulates in the body bound to various forms of protein. The size and composition of these “lipoprotein” particles determine their potential for causing atherosclerosis.
HDL Cholesterol, LDL Cholesterol, Cholesterol/HDL Ratio
The forms of cholesterol commonly measured at the time of insurance underwriting include total cholesterol, high density
lipoprotein cholesterol (HDL cholesterol or “HDL”) and low density lipoprotein cholesterol (LDL cholesterol or “LDL”). LDL
particles transport cholesterol to the tissues and result in the deposition of cholesterol in arterial walls resulting in
atherosclerosis. HDL particles transport cholesterol back to the liver for further metabolism and thereby reduce the risk of
atherosclerosis. The total cholesterol/HDL cholesterol ratio (TC/HDL) has been shown to be an important predictor of the
risk of atherosclerosis, with lower cholesterol/HDL ratios being associated with less risk. Conversely, elevated LDL levels
and lower HDL/LDL ratios are associated with an increased risk of atherosclerosis. In some studies, low total cholesterol
levels and total cholesterol levels that are falling without treatment have also been associated with increased mortality
risk, primarily cancers and other non-cardiovascular diseases.
Total cholesterol, HDL and LDL concentrations vary from day-to-day by up to 13% in a given individual. Ideally, lipid
measurements should be made after a 12-hour fast since HDL levels may decrease slightly after meals. However,
eating has little effect on total cholesterol levels.
Lipid
Normal/Optimum/Desirable
Borderline
Increased Risk
Total Cholesterol
<200 mg/dL
200-239 mg/dL
>240 mg/dL
HDL Cholesterol
>60 mg/dL
40-59 mg/dL
< 40 mg/dL
LDL Cholesterol
<100 mg/dL
100-159 mg/dL
>160 mg/dL
Total Cholesterol/HDL ratio
<3.5
Triglycerides
<150 mg/dL
>5
150-199 mg/dL
> 200 mg/dL
Modified from Hunninghake DB, Pasternak RC, Smith SC, et al: Third Report of the Expert Panel on Detection, Evaluation and
Treatment of the High Blood Cholesterol in Adults (Adult Treatment Panel III) Circulation 2004; 110: 227-239
Triglycerides
Triglycerides are a major transportation and storage form for lipids. Triglycerides are produced in the intestine after meals
and by the liver. Elevated triglyceride concentrations are risk factors for coronary disease and may be a marker for insulin
resistance and pre-diabetes. Triglyceride concentrations above 1,000 mg/dL may cause acute pancreatitis. Triglyceride
levels can be markedly elevated after meals. Therefore triglycerides should be measured after a minimum of a 9 hour fast.
Indicators of Kidney (Renal) Function: Glomerular Filtration Rate (GRF), Creatinine, and BUN (Blood Urea
Nitrogen)
The kidneys’ main functions are to regulate salt and water balance in the body and to filter waste products from protein
metabolism.
Blood entering the kidneys travel through a myriad of branching arteries until reaching structures called glomeruli that
consist of portions of capillaries twisted into what resemble microscopic tufts, each about the size of a pin head. Each
kidney contains about 1 million glomeruli. The walls of the glomerular capillaries are very thin and contain pores allowing
the fluid portion of the blood to be filtered into collecting tubules which drain into a series of progressively larger tubules,
eventually emptying into the ureters and ultimately the bladder. The tubules secrete and reabsorb salts, water and other
chemicals to produce urine.
Creatinine
A common measure of kidney function is the Glomerular Filtration Rate (GFR), defined as volume of blood filtered by all
the glomeruli each minute. Unfortunately, GFR cannot be measured directly. So instead, estimates of GFR (eGFR) are
made using calculations based on the volume of blood that is completely filtered (cleared) of a given substance each
minute. The most common substance used for this calculation is blood creatinine, a normal product of muscle
metabolism.
Since blood creatinine is filtered by the glomeruli, deterioration in GFR will result in elevated creatinine levels. But blood
creatinine levels are also affected by the amount of muscle mass present and the dietary consumption of meat and protein
supplements which are also metabolized into creatinine. Since muscle mass is usually greater in men than women and
usually decreases in both sexes with age, blood creatinine concentrations must be interpreted in light of age, gender and
build. Finally, the most commonly used analytical method to measure blood creatinine (Jaffe reaction or alkaline picrate
method) may be affected by the presence of several factors. Glucose, protein, urea, ascorbic acid (vitamin C) and
glycolysis (metabolism of glucose in poorly prepared blood samples) may result in falsely increased creatinine
concentrations as determined by the Jaffe reaction.
Estimated GFR (eGFR)
Because blood creatinine concentrations may be affected by factors other than GFR, various mathematical equations have
been devised to estimated GFR (eGFR) from blood creatinine concentrations after adjusting for many of these other
factors. Most equations adjust for age, sex and race. Some adjust for build and other factors. Although some equations
perform better than others, all are imperfect. The most commonly used equations are those developed by Levey and used
in the Modification of Diet in Renal Disease (MDRD) study and those developed by Rule at the Mayo Clinic. The National
Kidney Foundation has defined 5 stages of chronic kidney disease based on GFR estimated from the MDRD equation.
National Kidney Foundation Stages of Chronic Kidney Disease
2
Stage
Description
eGFR (ml/min/1.73 m )
Recommended Actions
—
At increased risk
≥60 (with chronic kidney
disease risk factors)
Screening; chronic kidney disease risk reduction
1
Kidney damage with normal
or increased GFR
≥90
Diagnosis and treatment; treatment of comorbid conditions;
slowing progression; cardiovascular disease risk reduction
2
Kidney damage with mild
decreased GFR
60–89
Estimating progression
3
Moderately decreased GFR
30–59
Evaluating and treating complications
4
Severely decreased GFR
15–29
Preparation for dialysis or kidney transplantation
2
Stage
Description
eGFR (ml/min/1.73 m )
Recommended Actions
5
Kidney failure
<15 or dialysis
Kidney transplantation or dialysis (if uremia present)
Modified from National Kidney Foundation: K/DOQI clinical practice guidelines on hypertension and antihypertensive agents in chronic
kidney disease. Am J Kidney Dis 43(5 Suppl 1):S1–290, 2004.
BUN
Protein metabolism produces ammonia, a toxic substance that is further metabolized by the liver into urea. Urea is
removed from the blood by the kidneys. The laboratory blood test for urea is termed “Blood Urea Nitrogen” or BUN.
BUN concentrations rise with reductions in GFR. BUN can also rise with dehydration and upper gastrointestinal
bleeding. BUN levels may be reduced in liver disease and by malnutrition.
Liver Function Tests: ALT, AST, Alkaline phosphatase, GGT, Total Bilirubin
Five laboratory assays are commonly called liver function tests (LFTs), although these tests are neither specific to the
liver nor true measures of liver function. In most cases, elevated LFTs indicate possible liver cell injury (ALT and AST) or
interruption of bile flow or cholestasis (ALP, GGT). Only bilirubin, a metabolic breakdown product hemoglobin, is a direct
measure of liver function.
Alanine Aminotransferase (ALT or SGPT) and Aspartate Aminotransferase (AST or SGOT)
Alanine aminotransferase (ALT) and aspartate aminotransferase (AST) are both found within liver cells. When liver cells
die or are damaged, these enzymes are released into the circulation where they can be measured, allowing them to be
considered markers for liver injury. Despite their similarities, they differ somewhat in their specificity for the liver disease.
ALT is found in other tissues, including the kidney, lung, pancreas, red blood cells and skeletal muscle. However, its
concentration is by far highest in the liver and ALT is therefore considered relatively specific for liver disease.
AST is also found in many tissues, including the heart, brain, skeletal muscle and kidney. It is more evenly
distributed than ALT, so its elevation is considered less specific for liver cell injury. It may also occasionally be occur
as a larger-thannormal molecule called a macro-enzyme. If this macro-enzyme is present, erroneously high AST
levels (sometimes increased many fold) may be reported using conventional assays.
There may be substantial overlap between the diseased and non-diseased state when ALT and AST values are
mildly elevated. Thus, mild elevations may not necessarily indicate significant disease. However, as ALT and
AST levels rise, the likelihood of significant liver dysfunction increases.
Alkaline Phosphatase (Alk. Phos. or ALP)
Alkaline phosphatase (Alk. Phos.) is found in a number of tissues. Eighty percent of Alk. Phos. comes from the
liver or bone; most of the rest comes from the intestine.
Levels may be elevated in normal women during pregnancy due to the Alk. Phos. production by the placenta and
in children and adolescents due to Alk. Phos. production by bone growth. Individuals with blood groups B and O
have increased intestinal Alk. Phos. levels after fatty meals. Alk. Phos. values normally increase between the
ages of 40 and 65, especially in women. In addition, some medications may interfere with Alk. Phos. assays.
In the liver, Alk. Phos. is produced by bile duct cells. Obstruction of bile ducts leads to increased Alk. Phos. synthesis.
Such obstruction may by caused by hepatitis, drug reactions, gallstones, tumors, scarring (cirrhosis), or other diseases.
Gamma-glutamyltransferase (GGT)
Gamma-glutamyltransferase (GGT) is the most sensitive marker for biliary tract disease but its specificity is low due to
two factors. First, it is found in many tissues including the heart, brain, pancreas, kidney, spleen and seminal vesicles.
Second, its production can be increased or induced by substances such as alcohol, barbiturates and phenytoin (Dilantin).
Elevated levels due to increased production do not indicate cell damage. In addition, GGT levels increase with age, body
mass index (BMI) and male sex. This poor specificity limits GGT’s usefulness in diagnosing liver disease. Its principal role
in clinical practice is determining whether elevated alkaline phosphatase levels are likely due to liver or biliary tract
disorders. If both alkaline phosphatase and GGT levels are elevated, a liver or biliary cause of the alkaline phosphatase
elevation is likely; if the GGT level is normal other possible causes for the alkaline phosphatase elevation are more likely.
An isolated GGT elevation has not been found to be a good predictor of significant underlying liver disease.
Bilirubin
Bilirubin is produced when hemoglobin is metabolized. In its native form, bilirubin is insoluble in water. In the liver,
glucuronic acid molecules are attached (conjugated) to bilirubin to make it water soluble. Conjugated bilirubin is then
excreted in the bile. Conjugated bilirubin levels in the serum do not increase until the liver loses half of its functional
capacity. However, most mild elevations of total bilirubin in asymptomatic individuals are due to increased levels of
unconjugated bilirubin. Insurance laboratories commonly test only for total bilirubin levels and unless specifically asked to
do so, do not report results for conjugated and unconjugated bilirubin levels.
The most common cause of elevated unconjugated bilirubin levels in asymptomatic individuals is Gilbert’s syndrome, an
inherited defect in the enzyme that conjugates bilirubin. Gilberts syndrome is not associated with any significantly
increased mortality risk. Other causes of elevated unconjugated bilirubin levels include hemolysis, abnormalities in red
blood cell production, and severe liver disease.
Elevations in conjugated bilirubin may be caused by liver disease, bile duct obstruction, medications and some inherited
disorders.
Proteins: Total Protein, Albumin, Globulin, Albumin to Globulin ratio
Although many cells in the body produce proteins that circulate in the blood, the vast majority of proteins are produced by
the liver. All proteins are made from building blocks called amino acids. Proteins are the basic components of cells, body
tissues, enzymes, hormones, antibodies, and clotting factors. The two major classes of circulating proteins are albumin
and globulins. Normally, the concentration of albumin is twice that of globulins, i.e. the normal albumin/globulin ratio is 2:1.
Low albumin/globulin ratios may be due to low albumin levels or increased globulin levels. Therefore the total protein
concentration, albumin concentration and the total globulin concentration must all be considered as well as the ratio of
albumin to globulin.
Albumin
Albumin is the major protein in the blood, comprising about 60% of total blood protein. Albumin is synthesized by the liver
and serves three main functions: 1) It is the main contributor to osmotic pressure, the chemical property of solutions that
determines the movement of fluid across membranes and maintains fluid balance in blood and tissues. Low albumin
levels can result in the leakage of fluid out of blood vessels, producing tissue swelling (edema). 2) Albumin is a major
transport protein for many hormones, drugs and other molecules 3) Albumin, because it is a large molecule, 584 amino
acids long, serves as a cache for amino acids which can be reused to make other proteins. For that reason, albumin is
one of the first proteins to be catabolized (broken down) when malnutrition occurs. Low blood albumin levels may also
result from protein malabsorption or impaired synthesis due to liver disease or increased losses of albumin through the
kidneys or intestines. Studies have shown that albumin levels of 3.8 mg/dL or less are associated with an increased
mortality risk in the elderly. Elevated albumin levels are uncommon but are occasionally seen with dehydration.
Globulins
Globulins are the second major class of circulating proteins besides albumin. There are many types of globulins including
antibodies, enzymes, and transport proteins. Globulins can be separated by a chemical procedure called electrophoresis.
When electrophoresis is performed on blood that is devoid of clotting proteins (serum) it is called “serum protein
electrophoresis” (SPEP). SPEP separates serum proteins into an albumin fraction and a globulin fraction which, in turn, is
further separated into five globulin subgroups termed alpha1, alpha2, beta, delta and gamma. The gamma fraction consists
of antibodies, also called immunoglobulins. Antibodies bind to various components of parasites, bacteria and viruses to
help fight infections. They can also bind to proteins and other substances, sometimes resulting in inflammation and what
has been called “autoimmune disease.” Elevated globulin levels can occur with infections, inflammation, autoimmune
diseases, multiple myeloma, leukemia, lymphoma and cancers. Low globulin levels can occur with liver disease, inherited
abnormalities in globulin production including hyogammaglobulinemia and other immunodeficiencies, and in nephrosis (a
type of kidney disease in which protein is lost in the urine).
Tumor markers: Prostate Specific Antigen, Lactate Dehydrogenase (LDH)
Prostate specific antigen (PSA)
Prostate specific antigen (PSA) is a protein that is produced by prostate tissue. Prostate cancer tissue produces more PSA
than normal prostate tissue and PSA testing is done to detect prostate cancer, hopefully at an early stage when a cure is
possible. However, besides prostate cancer, elevated PSA levels can also result from an enlarged prostate gland (benign
prostatic hypertrophy or BPH), prostate inflammation or infection (prostatitis), and prostate trauma as might occur from a
digital prostate examination or from a biopsy. Although higher levels of PSA usually are more suggestive of cancer, the
values reached with some benign conditions, particularly prostatitis, can be quite high. The major difficulty in the
interpretation of PSA values, especially when PSA elevations are modest, is the great overlap between benign disease
(primarily BPH) and prostate cancer. Several factors are often considered to help make this distinction including whether
PSA values are increasing or decreasing, the rate of increase in PSA elevations, and estimates of the size of the prostate
gland and whether the level of PSA seems appropriate for the gland size. In many cases, a prostate biopsy in necessary to
determine whether prostate cancer is the cause of PSA elevations. However, a normal prostate biopsy does not necessarily
rule out prostate cancer. A prostate biopsy commonly done by inserting needles into the prostate gland may miss the area
where a cancer is located, especially if the biopsy is not done under ultrasound guidance or involves only a small number or
samples. Repeated biopsies over a period of time may even be necessary to diagnosis prostate cancer.
Lactate dehydrogenase (LDH)
Lactate dehydrogenase (LDH) is an enzyme that is found in virtually all tissues including red blood cells, liver, heart, lung,
kidney and muscle. In general, necrosis or destruction of tissue will lead to an increase in LDH levels. Five different forms
(isoenzymes) of LDH have been identified. The concentration of each isoenzyme varies depending on the organ. Thus,
the pattern of isoenzyme elevation may indicate the tissue of origin. Examples of clinical conditions associated with LDH
elevations include myocardial infarction, hepatitis and muscle injury. Probably the most common cause for increased LDH
levels on insurance testing is hemolysis due to red blood cell destruction during collection, transportation or storage of the
blood sample. Despite its non-specific nature, an important use of LDH is the evaluation of malignancies. Isolated,
unexplained elevations of LDH to more than 2 to 3 times normal are suspicious for a possible malignancy. In general, the
degree of LDH elevation is related to the volume of tumor present. Higher LDH levels in patients with cancer are generally
associated with a greater tumor burden and poorer prognosis. Any increase in LDH levels above baseline values in an
individual with a known or treated malignancy is highly suspicious for recurrent disease.
Uric Acid
Uric acid is produced by the liver as a byproduct of the metabolism of purines, compounds that are found in meat and
meat products. Elevated uric acid levels (hyperuricemia) may be due to increased dietary consumption of foods rich in
purines or decreased excretion of uric acid in the urine. Other conditions can also cause hyperuricemia, including various
malignancies, hemolytic anemia, psoriasis, renal failure, endocrine disorders, excessive alcohol consumption and some
medications. Elevated uric acid levels may result in gout or uric acid kidney stones. There is also evidence that
hyperuricemia increases the risk of coronary artery disease.
Alcohol markers: Carbohydrate Deficient Transferrin (CDT) and Hemoglobin Associated Acetaldehyde (HHA)
Carbohydrate deficient transferrin (CDT)
Transferrin is a protein that transports iron. Eight different types of transferrins exist. The type of transferrin depends upon
the number of carbohydrate chains that are attached to the parent transferrin molecule. In normal serum, most transferrin
has four carbohydrate chains, but some normal circulating transferrin molecules have two or three chains and others have
five or more chains. In alcoholics, there is an increase in the amount transferrin having zero to three chains. These are
called carbohydrate deficient transferrin (CDT) forms. An increase in the amount of CDT has been proposed as a test for
chronic excessive alcohol consumption and a number of studies have suggested that CDT can help distinguish alcoholics
consuming large amounts of alcohol from light social drinkers and abstainers.
HAA (hemoglobin associated acetaldehyde)
Alcohol is metabolized in the liver to acetaldehyde and blood acetaldehyde levels rise following alcohol ingestion.
Acetaldehyde is able to chemically bind to various tissue proteins, including hemoglobin. The presence of hemoglobin
associated acetaldehyde, or HAA, in the blood has been used as an indicator of chronic excessive alcohol consumption.
However it is still not entirely certain what amount and duration of alcohol consumption is necessary to cause elevated
HAA levels in the serum. Other factors that either increase the amount of blood acetaldehyde or decrease the metabolism
of acetaldehyde may also cause elevated HAA levels.
Markers of Infection: Human Immunodeficiency virus (HIV), Hepatitis B virus (HBV), and Hepatitis C virus (HCV)
serology
Human Immunodeficiency Virus Antibody Testing (HIV antibody)
Infections with the Human Immunodeficiency Virus (HIV) cause the Acquired Immunodeficiency Syndrome (AIDS) in
which there is a progressive loss of cells crucial for normal functioning of the immune system. This results in increased
susceptibility to multiple other viral, bacterial and protozoan infections and the occurrence of a variety of tumors. Although
many medications have been developed to treat HIV infections, HIV infections remain incurable and result in premature
death. Two types of HIV viruses have been identified. Most infections are caused by the type 1 virus (HIV-1). A small
number are caused by the type 2 virus (HIV-2).
Three to six weeks after infection with HIV-1 or HIV-2, antibodies directed against various components of the virus
particles are produced in sufficient amounts to be detectable. Sometimes it can take up to 6 months for antibody tests to
become positive, however. These antibodies can be detected in whole blood, dried blood spots, urine and oral fluid
(saliva).
The most common test for HIV antibodies is an enzyme-linked immunosorbent assay (ELISA). Although the false
positive results for ELISA HIV testing are uncommon, positive ELISA tests must be confirm ed by another testing
method, usually a Western Blot test, before being reported. However Western Blot tests can be inconclusive for the
presence of HIV infection and there are several conditions that can produce false positive Western blot tests results. In
situations where Western Blot tests are indeterminate or when a false positive Western Blot test is suspected, the
presence of HIV infection is usually confirmed with a polymerase chain reaction (PCR) test that detects the actual
genetic material (RNA) of the virus.
Hepatitis B Testing
The hepatitis B virus consists of an internal core consisting of protein, enzymes and genetic material surrounded by an
outer protein coat. The various tests for hepatitis B refer to various components of the virus particle including:
Hepatitis B surface antigen (HBsAg) testing detects material from the outer protein coat. The surface antigen becomes
detectable approximately 4 weeks after an individual is infected with the virus. The presence of the antigen indicates an
active infection with hepatitis B. The surface antigen disappears with resolution of the infection. Prolonged detection of the
surface antigen beyond six months after acute infection indicates a chronic carrier state which may or may be associated
with elevated liver function tests.
Hepatitis B surface antibody (anti-HBs, HBs antibody or HBsAb) testing detects antibodies to the outer protein coat of
the virus. The surface antibody usually becomes detectable several weeks after the disappearance of the surface antigen.
Its presence generally indicates resolution of the infection and development of lifelong immunity. The surface antibody
may eventually become undetectable in some individuals with a remote, resolved hepatitis B infection. Individuals who are
vaccinated against hepatitis B, and who have an adequate immune response to the vaccine, will also develop a
detectable surface antibody test.
The presence of Hepatitis B core antibody (anti-HBc, HBc antibody or HBcAb) indicates the development of an antibody
to the inner core protein of the virus. It usually becomes detectable shortly before elevation of the liver tests and near the
time of onset of clinical illness. There are two forms of the core antibody, IgM and IgG. The IgM type indicates an acute
infection. This form gradually disappears and is replaced by the IgG variety, usually by about 6 months after an acute
infection. The IgG core antibody is an indicator of a prior infection and remains present for life. In individuals with a remote
infection who have lost the surface antibody, the core antibody may be the only indicator of previous disease. Those
persons who are vaccinated for hepatitis B are not exposed to the core proteins and do not develop the core antibody.
Thus, the presence of an isolated hepatitis B surface antibody indicates vaccination as opposed to a prior infection.
Hepatitis “e” antigen (HBeAg) is a remnant resulting from the production of new viral particles. During an acute infection it
appears later than the surface antigen and its presence is an indicator of active viral production. It is an important marker
of active disease and a highly infectious state. HBeAg is an indicator of increased mortality and morbidity risk. Conversely,
the absence or disappearance of HBeAg is a good prognostic sign.
Hepatitis C Antibody Testing
Hepatitis C antibody (anti-HCV, HCV antibody, or HCVab) develops in response to infection with the hepatitis C virus. The
antibody usually takes 4-10 weeks to appear after exposure but may take up to 3 to 6 months to develop. Unlike some
other types of antibodies, the hepatitis C antibody does not eliminate the virus. Since 75-85% of individuals with hepatitis
C develop persistent disease, the presence of the antibody is usually an indicator of chronic infection. However, a minority
of individuals may clear the virus from their system without treatment. In resolved infections, the levels may gradually
diminish over time and disappear after many years. In addition, some individuals may have a false positive screening test
for Hepatitis C. Additional specialized testing may be necessary to differentiate those persons with a positive hepatitis C
antibody test who are actively infected from those who have a false positive test or those who have cleared the virus and
are no longer infected.
Other markers of heart and vascular diseases: hs-CRP and NTproBNP
hsCRP
C-reactive protein (CRP) is a protein produced by the liver in response to a variety of inflammatory conditions. Tests for
CRP have traditionally been used to assess disease activity in a variety of inflammatory conditions such as infections,
rheumatoid arthritis and appendicitis. There is also some evidence to suggest that CRP may play a part in causing
atherosclerosis. More recently the test for CRP has been modified to detect smaller CRP elevations previously considered
to be within the normal range. This modified test is known as highly sensitive C-reactive protein (hs-CRP) test. Some
studies have shown that low levels of inflammation, detectable by hsCRP elevations, are associated with increased death
rates in individuals with and without a prior diagnosis of coronary artery disease. For this reason hsCRP is sometimes
used to assess the risk of coronary artery disease.
NTproBNP
B-type natriuretic peptide (BNP) is a protein that is released by the heart muscle in response to pressure overload or
cardiac muscle stretching. BNP stimulates the kidneys to eliminate salt and water and causes blood vessels to dilate and
blood pressure to fall. BNP is formed in the heart muscle cells as part of a larger protein called proBNP. ProBNP is then
cleaved into two parts: an inactive fragment called NTproBNP and the active form, BNP. Both BNP and NTproBNP are
useful laboratory tests to screen for a variety of heart problems including congestive heart failure, coronary artery disease,
left ventricular hypertrophy, valvular heart disease, and pulmonary hypertension. Because NTproBNP is more stable in
blood specimens than BNP, NTproBNP is preferred for insurance laboratory testing. BNP and NTproBNP levels are
higher in women than men and increase with age and in kidney disease. Studies have shown an increased risk mortality
risk in individuals having elevated BNP or NTproBNP levels.