Jpn. J. Infect. Dis., 64, 367-372, 2011
Original Article
Usefulness of Tumor Marker CA-125 Serum Levels for the Follow-Up of
Therapeutic Responses in Tuberculosis Patients with and without Serositis
Wei-Chang Huang1, Chih-Wei Tseng2, Kai-Ming Chang1,3,
Jeng-Yuan Hsu1, Jiann-Hwa Chen4, and Gwan-Han Shen1,4,5*
1Division
of Chest Medicine, Department of Internal Medicine,
Taichung Veterans General Hospital, Taichung;
2Division of Gastroenterology, Department of Medicine,
Buddhist Dalin Tzu Chi General Hospital, Chia-Yi;
3Department of Life Sciences and 4Institute of Molecular Biology,
National Chung Hsing University, Taichung; and
5Department of Respiratory Therapy, China Medical University, Taichung, Taiwan, ROC
(Received January 19, 2011. Accepted June 14, 2011)
SUMMARY: The aim of this study was to determine the usefulness of cancer antigen 125 (CA-125) serum levels in patients with tuberculosis (TB) with and without tuberculous serositis. A total of 64 TB
patients with a mean age of 58.17 ± 19.05 years were enrolled in this observational case series study. All
patients underwent blood sampling for the measurement of CA-125 serum levels before treatment. If
the CA-125 serum levels were found to be elevated, the patients underwent blood sampling in the initial
treatment phase, continuation treatment phase, and every 6 months thereafter for 2 years. The treatment outcomes of the pulmonary TB group were evaluated using chest radiography and sputum examinations, and those of the tuberculous serositis group were evaluated on the basis of the amounts of fluid
determined by ultrasound. All patients in the tuberculous serositis group and 45z of the patients in the
pulmonary TB group had elevated CA-125 serum levels before treatment. The pretreatment mean
CA-125 serum level was significantly higher in the tuberculous serositis group than in the pulmonary TB
group. CA-125 serum levels decreased along with improvement in anti-TB treatment outcomes in both
the groups. In conclusion, the CA-125 serum levels in combination with clinical responses, chest
radiography, and sputum examinations, can offer better monitoring of therapeutic responses in anti-TB
treatment.
cells of the fallopian tube, endometrium, and mesothelial cells lining the pleura, pericardium, and peritoneum
(2). Elevation in CA-125 serum levels occur in a number
of diverse cancerous and non-cancerous conditions,
particularly those with serosal involvement (3–6).
Therefore, CA-125 cannot be considered a useful diagnostic tool, but it can be helpful in the therapeutic follow-up of tuberculous serositis patients with serosal involvement.
The aim of this study was to determine the usefulness
of measuring the CA-125 serum levels for monitoring
the therapeutic responses of TB patients with and
without tuberculous serositis.
INTRODUCTION
Tuberculosis (TB) is one of the leading causes of mortality worldwide and has become a global public health
emergency. Early diagnosis and treatment are the most
important strategies to control TB. In addition, early
detection of treatment failure is very important because
of increasing incidences of multidrug-resistant tuberculosis (MDR-TB) (1). Although novel diagnostic tools for
serologic tests, including QuantiFERON-TB Gold InTube and T-spot.TB, have been developed for rapid and
accurate diagnosis of TB, the results of these tests have
not been correlated with disease activity or therapeutic
responses. Standard methods such as chest radiography,
sputum acid-fast staining, and mycobacterial cultures
used for evaluating therapeutic responses of pulmonary
TB patients are not effective for the evaluation of extrapulmonary TB and tuberculous serositis, including
pleurisy, pericarditis, and peritonitis.
Cancer antigen 125 (CA-125) is a high molecular
weight glycoprotein that is expressed on the epithelial
MATERIALS AND METHODS
Patients: We conducted an observational case series
study involving 70 patients diagnosed with TB between
January 2000 and January 2007 at the Taichung Veterans General Hospital. Female patients with cancerous
and non-cancerous gynecologic conditions, such as
ovarian cancer, endometriosis, and pregnancy were excluded by medical chart review. Among the diagnosed
patients, 3 were with active pulmonary TB combined
with lung diseases (2 with bronchiectasis and 1 with interstitial lung disease) and 3 with active pulmonary TB
combined with tuberculous pleurisy were excluded.
Thus, we enrolled 64 TB patients, including 40 having
*Corresponding author: Mailing address: Division of Chest
Medicine, Department of Internal Medicine, Taichung
Veterans General Hospital, No. 160, Sec. 3, Chung-Kang
Road, Taichung, Taiwan, ROC, 40705. Tel: ＋886-423592525 ext. 3201, Fax: ＋886-4-23500034, E-mail: 911b
＠vghtc.gov.tw
367
Treatment outcomes: The treatment outcomes of pulmonary TB group were evaluated every 3 months on the
basis of chest radiography, sputum acid-fast staining,
and Mycobacterium cultures according to the World
Health Organization/International Union against
Tuberculosis and Lung Disease (WHO/IUTLD) guidelines (10). Ultrasound was performed when patients
with tuberculous serositis visited the hospital for undergoing blood sampling for measuring the CA-125 serum
levels. The amount of pericardial effusion was recorded
as large, moderate, or mild according to the method described by Eisenberg et al. (11). The amount of ascites
was divided into four grades: grade 0, not visible on
ultrasound; grade 1, mild and only visible on
ultrasound; grade 2, detectable with flank bulging and
shifting dullness; and grade 3, directly visible and confirmed by fluid thrill test. Pleural effusion was quantified and recorded by measuring the thickness of the
pleural lamella (12).
Statistical analyses: CA-125 serum levels in the pulmonary TB group and tuberculous serositis group were
compared using Fisher's exact test. The Wilcoxon
signed rank test was performed to evaluate the differences among the pretreatment, initial treatment, and
continuation treatment phases. Data were expressed as
frequency (n), percentage (z), and mean ± standard
deviation (SD). A value of P º 0.05 was considered
statistically significant. All statistical analyses were performed using the Statistical Package for the Social
Sciences (version 12.0; SPSS, Chicago, Ill., USA).
active pulmonary TB without serositis (pulmonary TB
group; 23 men and 17 women; mean age, 59.6 ± 21.1
years) and 24 having extrapulmonary TB with tuberculous serositis and without any active pulmonary TB
(tuberculous serositis group; 15 men and 9 women;
mean age, 64.0 ± 16.0 years). The tuberculous serositis
group included 13 patients with tuberculous pleurisy, 8
with tuberculous pericarditis, and 3 with tuberculous
peritonitis.
Active pulmonary TB was diagnosed on the basis of
chest radiographic findings and presence of Mycobacterium tuberculosis in sputum cultures. The diagnostic
criteria for tuberculous pleurisy included the detection
of M. tuberculosis in either the pleural fluid culture or
biopsy samples, detection of acid-fast bacilli or a typical
granuloma on histopathological examination, or adenosine deaminase (ADA) level of À70 U/L in pleural effusion (7). The diagnosis of tuberculous pericarditis and
peritonitis was on the basis of the detection of M. tuberculosis in either the pericardial/peritoneal fluid culture
or biopsy samples, detection of acid-fast bacilli or a
typical granuloma on histopathological examination, or
ADA level of À40 U/L in pericardial/peritoneal fluid
(8,9). The patients received 6 months of anti-TB combination chemotherapy with isoniazid, rifampin, ethambutol, and pyrazinamide if they were aged º65 years,
or 9 months of anti-TB combination chemotherapy with
isoniazid, rifampin, and ethambutol if they were aged
Æ65 years. The patients were followed-up for 2 years
after they completed the anti-TB combination
chemotherapy. This study was approved by the Institutional Review Board and Ethics Committee of Taichung
Veterans General Hospital.
Blood sampling: All patients underwent blood sampling before receiving the treatment (pretreatment
phase). If the pretreatment CA-125 serum values were
Æ35 U/mL, then the blood sampling was repeated in
the second month of treatment (initial treatment phase),
the sixth month (continuation treatment phase), and
then every 6 months thereafter for 2 years.
CA-125 serum levels were determined using an immunoradiometric assay kit (CIS Biointernational,
Saclay, France) according to the manufacturer's instructions, and a value of À35 U/mL was considered
abnormal.
RESULTS
The demographic and clinical characteristics of
patients are reported in Table 1. The incidence of
chronic obstructive pulmonary disease (COPD) was significantly higher in the pulmonary TB group than in the
tuberculous serositis group. There were no differences
between these two groups in the incidence of other
comorbidities. The sensitivity of elevated CA-125 serum
levels for diagnosing disease activity in the tuberculous
serositis group was 100z, which was higher than that of
the pulmonary TB group (45z), when considering a
cut-off value of 35 U/mL.
In the pretreatment phase, the mean CA-125 serum
Table 1. Demographic characteristics of the enrolled 64 tuberculosis patients
Tuberculous serositis group
Variable
Pulmonary
TB group
Pleurisy
Pericarditis
Peritonitis
Total
Total no. (male/female)
Age
Comorbidity
DM
H/T
COPD
CAD
Asthma
40 (23/17)
59.6 ± 21.1
13 (9/4)
69.2 ± 13.8
8 (4/4)
62.0 ± 18.1
3 (2/1)
47.0 ± 5.3
24 (15/9)
64.0 ± 16.0
0
1 (7.7z)
0
0
0
0
0
0
1 (12.5z)
0
5
7
10
2
5
(12.5z)
(17.5z)
(25z)
(5z)
(12.5z)
0
0
0
0
0
0
1 (4.2z)
0
1 (4.2z)
0
P value
0.148
0.240
0.011)
1.0
0.148
Data are presented as mean ± standard deviation (SD) or number (z).
By Fisher's exact test.
1): P º 0.05.
DM, diabetes mellitus; H/T, hypertension; COPD, chronic obstructive pulmonary disease; CAD, coronary artery disease;
TB, tuberculosis.
368
Fig. 2. The change of CA-125 serum levels in different treatment
phases in pulmonary tuberculosis group and tuberculous serositis group.
CA-125 serum levels along with a serial improvement in
the follow-up chest radiographic findings in all 18
patients.
In the tuberculous serositis group, the CA-125 serum
levels decreased along with a decrease in the amounts of
pleural/pericardial/peritoneal effusion (determined by
ultrasound) during anti-TB treatment (Fig. 3). In the
tuberculous pleurisy subgroup (n ＝ 13), the thickness
of the pleural lamella was Æ15 mm in all patients during the pretreatment phase. In the initial treatment
phase, the thickness of the pleural lamella was º15 mm
in all patients (10 mm in 3 patients [23z], 5 mm in 4
patients [31z], and no detectable pleural effusion in 6
patients [46z]). In the continuation treatment phase,
the thickness of the pleural lamella was º10 mm in all
patients (5 mm in 3 patients [23z], and no detectable
pleural effusion in 10 patients [77z]) (Fig. 3A).
In the tuberculous pericarditis subgroup (n ＝ 8), 4
patients (50z) had large amounts of pericardial effusion, and 4 patients (50z) had moderate amounts of
pericardial effusion during the pretreatment phase. In
the initial treatment phase, 2 patients (25z) had mild
amounts of pericardial effusion and 6 patients (75z)
had no detectable pericardial effusion. No pericardial
effusion was detected in any patient during the continuation treatment phase (Fig. 3B).
In the tuberculous peritonitis subgroup (n ＝ 3), 2
patients (67z) had grade 2 ascites and 1 patient (33z)
had grade 1 ascites during the pretreatment phase. In
the initial treatment phase, 2 patients (67z) had no visible ascites (grade 0), and 1 patient (33z) had grade 1 ascites. All 3 patients (100z) were found to have grade 0
ascites during the continuation treatment phase (Fig.
3C).
In the tuberculous pleurisy subgroup, 1 patient who
initially responded to anti-TB treatment showed increased CA-125 serum levels at the 24th month of follow-up. The patient's chest radiograph showed a recurrent right-sided pleural effusion. This relapse of rightsided tuberculous pleurisy was diagnosed by an ADA
level of À70 U/L in the pleural effusion. The increase
in the CA-125 serum levels correlated with the clinical
relapse of pleurisy (Fig. 4). All other patients were successfully treated without any clinical relapse or increase
Fig. 1. (A) Distribution of CA-125 serum levels in the pulmonary
tuberculosis group and tuberculous serositis group, including
tuberculous pleurisy, tuberculous pericarditis, and tuberculous
peritonitis. (B) Distribution of CA-125 serum levels in the pulmonary tuberculosis group and tuberculous serositis group after exclusion of the tuberculous peritonitis subgroup.
levels of the tuberculous serositis group was 234.82 ±
279.25 U/mL, which was higher than that of the pulmonary TB group (48.26 ± 53.30 U/mL; P º 0.001) (Fig.
1A). Subgroup analyses showed that the tuberculous
peritonitis subgroup had the highest mean CA-125 serum levels (820.67 ± 419.22 U/mL). Moreover, the
mean CA-125 serum levels in the tuberculous serositis
group (151.13 ± 109.80 U/mL) was significantly higher
than that of the pulmonary TB group (48.26 ± 53.30
U/mL, P º 0.001) during in the pretreatment phase,
even after excluding the tuberculous peritonitis subgroup (Fig. 1B).
We observed that the CA-125 serum levels in the
different treatment phases gradually reduced after the
commencement of anti-TB treatment in both the pulmonary TB group and tuberculous serositis group (Fig. 2).
In the pulmonary TB group, 18 patients (45z) had a
CA-125 serum level À35 U/mL during the pretreatment
phase, and all patients showed conversion of the sputum
acid-fast stains and Mycobacterium cultures in the third
month of treatment. However, after commencing the
anti-TB treatment, we observed a serial decrease in the
369
Fig. 3. The relationship of CA-125 serum levels and sonographic findings in different treatment phases in (A) tuberculous pleurisy, (B) tuberculous pericarditis, and (C) tuberculous peritonitis subgroups.
the pretreatment phase. The mean CA-125 serum level
was highest in the tuberculous peritonitis subgroup and
lowest in the pulmonary TB group. The CA-125 serum
levels had decreased along with improvements in followup chest radiographs, conversion of sputum acid-fast
stains and Mycobacterium cultures in the pulmonary TB
group, and decreased amounts of effusion in the tuber-
in CA-125 serum levels during the 2-year follow-up.
DISCUSSION
In this study, all of the patients in the tuberculous
serositis group and only 45z of the patients in the pulmonary TB group had elevated CA-125 serum levels in
370
ed with pleural thickening after anti-TB treatment.
Tuberculous peritonitis, the most well-known type of
serositis associated with CA-125 serum levels, becomes
normal after anti-TB therapy in tuberculous peritonitis
patients (6,17–19). A positive correlation between the
amount of ascites and CA-125 serum levels was found in
patients with ovarian cancer (20). In our study, the
CA-125 serum levels of the tuberculous serositis group
in the pretreatment phase were significantly higher than
those of the pulmonary TB group, indicating that the
serosal involvement may be associated with higher
CA-125 serum levels. The CA-125 serum level in the
tuberculous peritonitis subgroup was higher than that in
the tuberculous pleurisy or pericarditis subgroups;
however, the result was not statistically significant, possibly because there were only 3 tuberculous peritonitis
patients. However, it is possible that the CA-125 serum
levels may increase with an increase in the area of
serosal involvement in tuberculous peritonitis.
To the best of our knowledge, the correlation of
CA-125 serum levels and the therapeutic responses in
tuberculous pericarditis patients have not been reported
in the literature. In our study, the CA-125 serum levels
decreased along with a decrease in the amounts of
pericardial fluid during anti-TB treatment. Although
the clinical response was the main method used for the
evaluation of the therapeutic effects, CA-125 serum levels could assist in the follow-up of therapeutic responses
in tuberculous pericarditis patients.
In addition to the CA-125 serum levels, the C-reactive
protein (CRP) serum levels, and erythrocyte sedimentation rate (ESR) were elevated in pulmonary TB patients
(72–87z and 75–87z, respectively) and had decreased
to a mean level close to that of the control group after
anti-TB treatment along with the sputum smear conversion (21–23). Therefore, the serum CRP levels, similar
to the CA-125 serum levels in the present study, could
assist in the evaluation of therapeutic responses of pulmonary TB. The changes in ESR were slower and hence
could not be a timely indicator of clinical improvement
or deterioration of pulmonary TB (24).
Among patients with lymphocytic pleural effusion,
pleural fluid and serum CRP levels were significantly
higher in patients in the tuberculous pleurisy group than
in patients with malignant lymphocytic pleural effusion.
The cut-off value for a serum CRP level of Æ60 mg/L
had a sensitivity of 71z and a specificity of 80z. A
pleural fluid CRP level of º30 mg/L can practically
rule out the possibility of TB as the cause of lymphocytic pleural effusion (72–95z sensitivity; À90z specificity) (25–27).
The CA-125 levels in serum and pleural effusion were
higher in malignant pleural effusion than in benign
pleural effusion. For differentiating malignant and benign pleural effusions, the CA-125 levels of the serum
and pleural effusion had a low sensitivity (43.8–50z
and 48.0–56.3z, respectively) and high specificity
(45.5–70z and 70–85.0z, respectively) (28–31). Measuring only the CA-125 level is insufficient to differentiate malignant from benign pleural effusion including
tuberculous pleurisy.
To the best of our knowledge, serum CRP concentrations and ESR have never been used as the treatment indicators in tuberculous serositis patients. From our per-
Fig. 4. The rebound of CA-125 serum levels in one tuberculous
pleurisy patient during the 2-year follow-up.
culous serositis group.
CA-125 serum levels have been used to evaluate the
activity of pulmonary TB with a sensitivity ranging
from 63.0z to 97.5z (13,14). However, only 45z of
the patients having active pulmonary TB without serositis had elevated CA-125 serum levels in our study.
Yatiraj et al. reported that pulmonary TB without the
involvement of the pleural epithelium did not evoke a
CA-125 release (15). Ozsahin et al. observed that several
diseases often mistaken for active pulmonary TB, such
as pneumonia, bronchiectasis, and interstitial lung diseases, were associated with increased CA-125 serum levels (14). However, neither of the aforementioned
authors reported whether the active pulmonary TB
patients in their studies had pleural involvement or
other pleuropulmonary diseases. This may explain why
the sensitivity for the discrimination of pulmonary TB
activity by CA-125 serum levels reported in our study
was lower than that reported in the studies by Yilmaz et
al. and Ozsahin et al. (13,14). We excluded patients with
both active pulmonary TB and lung diseases, such as
bronchiectasis and interstitial lung disease, and divided
the enrolled TB patients into groups with active pulmonary TB without serositis and with tuberculous serositis
without active pulmonary TB.
In our study, the CA-125 serum levels were elevated
in all 13 tuberculous pleurisy patients, and the serum
levels of CA-125 had rapidly decreased along with a
decrease in the amounts of pleural fluid rapidly after
anti-TB treatment. The rapid decrease after anti-TB
treatment is a result of the short CA-125 half-life (4–8
days). Chest radiography is a useful tool in the followup of the therapeutic responses of tuberculous pleurisy
patients. However, 50z of the tuberculous pleurisy
patients will develop pleural thickening after anti-TB
treatment (16), which makes it difficult for clinicians to
monitor their therapeutic responses. In our study, 3
tuberculous pleurisy patients (23z) had a residual
5-mm thick pleural lamella in the continuation treatment phase. However, no color signs were found in
color Doppler ultrasound analysis in these 3 patients;
this indicated that the residual pleural lamella showed
thickening. On the basis of our observations, the measurement of CA-125 serum levels combined with chest
radiography may offer better monitoring efficacy, particularly in patients with tuberculous pleurisy complicat371
spective, measurement of CA-125 serum levels has less
sensitivity (45z in the pulmonary TB group in the
present study). However, the measurement of CA-125
serum levels offers an alternative follow-up tool for the
pretreatment evaluation in anti-TB treatment, particularly in tuberculous serositis patients because of its high
sensitivity (100z), as observed in the tuberculous serositis group in the present study.
Our study has some limitations. We conducted an observational study, and we had not included patients with
serositis other than TB and those with extrapulmonary
TB with diseases other than serositis in the control
groups. Although there were only 3 tuberculous peritonitis patients in our study, our observational results
were similar to the results reported by Mas et al. (17)
and Kuno et al. (6). We enrolled a larger numbers of
patients with tuberculous pleurisy and pericarditis than
patients with tuberculous peritonitis and a small number
of patients with tuberculous serositis was noted. We did
not encounter drug resistances or poor drug compliances in the present study. Therefore, we could not conclude whether CA-125 serum levels increased because of
probable drug resistances or poor compliances. Because
we detected a clinical relapse in 1 patient with tuberculous pleurisy who presented with recurrent right-sided
pleural effusion by measuring the increase in CA-125 serum levels, we assume that CA-125 serum levels play a
role in patients with drug resistances or poor compliances, however, further studies on the long-term followup of TB are required.
In conclusion, measurement of CA-125 serum levels
in combination with analysis of clinical responses on the
basis of chest radiography and sputum staining and culturing offer a better monitoring of the therapeutic
responses of patients undergoing anti-TB treatment.
9. Makhlouf, N.A., Nassar, G., Makhlouf, M., et al. (1992):
Adenosine deaminase activity in various pathological effusions.
J. Med. Liban., 40, 142–144.
10. World Health Organization (2003): Treatment of Tuberculosis:
Guidelines for National Programmes. 3rd ed.
11. Eisenberg, M.J., Oken, K., Guerrero, S., et al. (1992): Prognostic
value of echocardiography in hospitalized patients with pericardial effusion. Am. J. Cardiol., 70, 934–939.
12. Eibenberger, K.L., Dock, W.I., Ammann, M.E., et al. (1994):
Quantification of pleural effusion: sonography versus radiography. Radiology, 191, 681–684.
13. Yilmaz, A., Ece, F., Bayramgurler, B., et al. (2001): The value of
CA-125 in the evaluation of tuberculosis activity. Respir. Med.,
95, 666–669.
14. Ozsahin, S.L., Turgut, B., Nur, N., et al. (2008): Validity of the
CA125 level in the differential diagnosis of pulmonary tuberculosis. Jpn. J. Infect. Dis., 61, 68–69.
15. Kalantri, Y., Naik, G., Joshi, S.P., et al. (2007): Role of cancer
antigen–125 from pleural & ascitic fluid samples in non malignant
conditions. Indian. J. Med. Res., 125, 25–30.
16. Sahn, S.A. (2002): Pleural thickening, trapped lung, and chronic
empyema as sequelae of tuberculous pleural effusion: don't sweat
the pleural thickening. Int. J. Tuberc. Lung Dis., 6, 461–464.
17. Mas, M.R., C äomert, B., Sa ²glamkaya, U., et al. (2000): CA-125; a
new marker for diagnosis and follow-up of patients with tuberculous peritonitis. Dig. Liver Dis., 32, 595–597.
18. Piura, B., Rabinovich, A., Leron, E., et al. (2002): Peritoneal
tuberculosis mimicking ovarian carcinoma with ascites and
elevated serum CA-125: case report and review of literature. Eur.
J. Gynaecol. Oncol., 23, 120–122.
19. Ofluoglu, R., G äuler, M., Unsal, E., et al. (2009): Malignity-like
peritoneal tuberculosis associated with abdominal mass, ascites
and elevated serum Ca125 level. Acta Chir. Belg., 109, 71–74.
20. Topalak, O., Saygili, U., Soyturk, M., et al. (2002): Serum,
pleural effusion, and ascites CA-125 levels in ovarian cancer and
nonovarian benign and malignant diseases: a comparative study.
Gynecol. Oncol., 85, 108–113.
21. Lawn, S.D., Obeng, J., Acheampong, J.W., et al. (2000): Resolution of the acute-phase response in West African patients receiving treatment for pulmonary tuberculosis. Int. J. Tuberc. Lung
Dis., 4, 340–344.
22. Peresi, E., Silva, S.M.U.R., Calvi, S.A., et al. (2008): Cytokines
and acute phase serum proteins as markers of inflammatory
regression during the treatment of pulmonary tuberculosis. J.
Bras. Pneumol., 34, 942–949.
23. Awodu, O.A., Ajayi, I.O. and Famodu, A.A. (2007): Haemorheological variables in Nigeria pulmonary tuberculosis
patients undergoing therapy. Clin. Hemorheol. Microcirc., 36,
267–275.
24. Scott, G.M., Murphy, P.G. and Gemidjioglu, M.E. (1990):
Predicting deterioration of treated tuberculosis by corticosteroid
reserve and C-reactive protein. J. Infect., 21, 61–69.
25. Kiropoulos, T.S., Kostikas, K., Oikonomidi, S., et al. (2007):
Acute phase markers for the differentiation of infectious and
malignant pleural effusions. Respir. Med., 101, 910–918.
26. Garcia-Pachon, E., Soler, M.J., Padilla-Navas, I., et al. (2005):
C-reactive protein in lymphocytic pleural effusions: a diagnostic
aid in tuberculous pleuritis. Respiration, 72, 486–489.
27. Chierakul, N., Kanitsap, A., Chaiprasert, A., et al. (2004): A
simple C-reactive protein measurement for the differentiation between tuberculous and malignant pleural effusion. Respirology,
9, 66–69.
28. Li, C.S., Cheng, B.C., Ge, W., et al. (2007): Clinical value of
CYFRA21-1, NSE, CA15-3, CA19-9 and CA125 assay in the
elderly patients with pleural effusions. Int. J. Clin. Pract., 61,
444–448.
29. Ghayumi, S.M., Mehrabi, S., Doroudchi, M., et al. (2005): Diagnostic value of tumor markers for differentiating malignant and
benign pleural effusions of Iranian patients. Pathol. Oncol. Res.,
11, 236–241.
30. Sthaneshwar, P., Yap, S.F. and Jayaram, G. (2002): The diagnostic usefulness of tumour markers CEA and CA-125 in pleural
effusion. Malays. J. Pathol., 24, 53–58.
31. Liang, Q.L., Shi, H.Z., Qin, X.J., et al. (2008): Diagnostic accuracy of tumour markers for malignant pleural effusion: a metaanalysis. Thorax, 63, 35–41.
Acknowledgments We thank the Biostatistics Task Force of
Taichung Veterans General Hospital, Taichung, Taiwan, ROC for
assistance with the statistical analyses.
Conflict of interest None to declare.
REFERENCES
1. Shin, S.S., Furin, J.J., Alc áantara, F., et al. (2006): Long-term
follow-up for multidrug-resistant tuberculosis. Emerg. Infect.
Dis., 12, 687–688.
2. Kabawat, S.E., Bast, R.C., Jr., Bhan, A.K., et al. (1983): Tissue
distribution of a coelomic-epithelium-related antigen recognized
by the monoclonal antibody OC125. Int. J. Gynecol. Pathol., 2,
275–285.
3. Bast, R.C., Jr., Xu, F.J., Yu, Y.H., et al. (1998): CA 125: the
past and the future. Int. J. Biol. Markers, 13, 179–187.
4. Hassan, R., Bera, T. and Pastan, I. (2004): Mesothelin: a new target for immunotherapy. Clin. Cancer Res., 10, 3937–3942.
5. Miralles, C., Orea, M., Espa ãna, P., et al. (2003): Cancer antigen
125 associated with multiple benign and malignant pathologies.
Ann. Surg. Oncol., 10, 150–154.
6. Kuno, Y., Iyoda, M., Aoshima, Y., et al. (2010): A case of tuberculous peritonitis in a hemodialysis patient with high serum soluble interleukin-2 receptor and CA-125 levels. Intern. Med., 49,
1783–1786.
7. Oca ãna, I., Martinez-Vazquez, J.M., Segura, R.M., et al. (1983):
Adenosine deaminase in pleural fluids. Test for diagnosis of
tuberculous pleural effusion. Chest, 84, 51–53.
8. Koh, K.K., Kim, E.J., Cho, C.H., et al. (1994): Adenosine
deaminase and carcinoembryonic antigen in pericardial effusion
diagnosis, especially in suspected tuberculous pericarditis. Circulation, 89, 2728–2735.
372