BACKGROUND: Conventional tests for tuberculous pleuritis have several limitations. A variety of new, rapid tests such as nucleic acid amplification tests--including polymerase chain reaction--have been evaluated in recent times. We conducted a systematic review to determine the accuracy of nucleic acid amplification (NAA) tests in the diagnosis of tuberculous pleuritis. METHODS: A systematic review and meta-analysis of 38 English and Spanish articles (with 40 studies), identified via searches of six electronic databases, hand searching of selected journals, and contact with authors, experts, and test manufacturers. Sensitivity, specificity, and other measures of accuracy were pooled using random effects models. Summary receiver operating characteristic curves were used to summarize overall test performance. Heterogeneity in study results was formally explored using subgroup analyses. RESULTS: Of the 40 studies included, 26 used in-house ("home-brew") tests, and 14 used commercial tests. Commercial tests had a low overall sensitivity (0.62; 95% confidence interval [CI] 0.43, 0.77), and high specificity (0.98; 95% CI 0.96, 0.98). The positive and negative likelihood ratios for commercial tests were 25.4 (95% CI 16.2, 40.0) and 0.40 (95% CI 0.24, 0.67), respectively. All commercial tests had consistently high specificity estimates; the sensitivity estimates, however, were heterogeneous across studies. With the in-house tests, both sensitivity and specificity estimates were significantly heterogeneous. Clinically meaningful summary estimates could not be determined for in-house tests. CONCLUSIONS: Our results suggest that commercial NAA tests may have a potential role in confirming (ruling in) tuberculous pleuritis. However, these tests have low and variable sensitivity and, therefore, may not be useful in excluding (ruling out) the disease. NAA test results, therefore, cannot replace conventional tests; they need to be interpreted in parallel with clinical findings and results of conventional tests. The accuracy of in-house nucleic acid amplification tests is poorly defined because of heterogeneity in study results. The clinical applicability of in-house NAA tests remains unclear.

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Adenosine deaminase (ADA) activity and tuberculostearic acid (TSA) levels in pleural effusions were measured in 18 patients with active tuberculous pleuritis, 16 patients suspected of having tuberculous pleuritis, 14 patients with carcinomatous pleuritis, and 19 patients suffering from pleuritis of non-malignant and non-tuberculous etiology. In the patients with active tuberculous pleuritis, ADA was elevated in 56% and TSA was positive in 78%. In 83% of these patients, either ADA was elevated or TSA was positive. ADA was elevated together with a positive TSA in 50%. In contrast, TSA was positive in only 6% and ADA was elevated in 24% of the patients with non-tuberculous pleuritis, and none of these patients showed the combination of an elevation of ADA and a positive TSA. These results suggest that simultaneous measurements of both ADA and TSA in pleural effusions are useful for the diagnosis of tuberculous pleuritis.

BACKGROUND: Adenosine Deaminase Activity (ADA) is a commonly used marker for the diagnosis of tuberculous pleural effusion. There has been concern about its usefulness in immunocompromised patients, especially HIV positive patients with very low CD4 counts. The objective of this study was to evaluate the sensitivity of ADA in pleural fluid in patients with low CD4 counts. MATERIALS AND METHODS: This was a retrospective case control study. Medical files of patients with tuberculous pleuritis and non-tuberculous pleuritis were reviewed. Clinical characteristics, CD4 cell counts in blood and biochemical markers in pleural fluid, including ADA were recorded. RESULTS: One ninety seven tuberculous pleuritis and 40 non-tuberculous pleuritis patients were evaluated. Using the cut-off value of 30 U/L, the overall sensitivity, specificity, positive likelihood ratio, and negative likelihood ratio of ADA was 94%, 95%, 19, and 0.06 respectively. The mean CD4 cell counts among TB pleuritis patients was 29 and 153 cells/microL in patients with CD4 <50 cells/microL and >50 cells/microL, (p<0.05) respectively. The corresponding mean ADA values for these patients were 76 U/L and 72 U/L respectively (p>0.5). There was no correlation between ADA values and CD4 cell counts (r = -0.120, p = 0.369). CONCLUSION: ADA analysis is a sensitive marker of tuberculous pleuritis even in HIV patients with very low CD4 counts in a high TB endemic region. The ADA assay is inexpensive, rapid, and simple to perform and is of great value for the immediate diagnosis of tuberculous pleuritis while waiting for culture result and this has a positive impact on patient outcome.

OBJECTIVE: To assess the clinical significance of the Amplicor Mycobacterium system for the diagnosis of mycobacterial infection in patients with pleural fluid, and to compare its usefulness with that of conventional smear and culture methods. DESIGN: Pleural fluid specimens were obtained randomly from in-patients admitted to National Tokyo Hospital between January and December 1996. All the patients were diagnosed with bacterial, histopathological and clinical gold standard. The sensitivity and specificity for diagnosis of mycobacterial infection were evaluated. RESULTS: Seventy-five pleural fluid specimens were obtained. Conventional methods demonstrated a sensitivity of 30.6% and a specificity of 100%, while the Amplicor Mycobacterium demonstrated a sensitivity and specificity of 27.3% and 97.6% respectively. Lactic dehydrogenase, carcinoembryonic antigen, red blood cell, protein, glucose and types of inflammatory cells were not different in Amplicor positive and negative pleural fluid with mycobacterial infection. CONCLUSION: There was not much improvement in the accuracy of diagnosis when Amplicor Mycobacterium was used to diagnose mycobacterial pleuritis among various diseases with pleural fluid; however, the assay time was dramatically reduced with the use of Amplicor Mycobacterium.

We have used polymerase chain reaction (PCR) with IS6110 and a new set of primers from an insertion element like repetitive sequence, (TRC4) to detect Mycobacterium tuberculosis in pleural effusion samples from 50 patients having pleuritis. The results of PCR were compared with the results of conventional methods like smear, culture and adenosine deaminase activity. Thirty six specimens were positive and 14 were negative by PCR. Among the 36 samples, 33 were from patients with clinical evidence of tuberculosis including response to anti-tuberculosis therapy. Only six samples were positive by the gold standard which is culture, and three were positive by smear. The measurement of adenosine deaminase activity classified 19 samples as positives. The overall sensitivity and specificity of PCR was 100 and 85 per cent respectively. PCR using IS6110 and TRC4 primers is a sensitive test as compared to conventional tests for detection of M. tuberculosis from pleural fluid samples of patients with tubercular pleuritis.

OBJECTIVES: To evaluate the diagnostic use of pleural fluid adenosine deaminase (ADAPF) levels in tuberculous pleuritis (TBpl), with a special reference to HIV coinfection and a Bayesian analysis. METHODS: We investigated a total of 216 patients with pleural effusion, including 100 with TBpl, 68 with malignant effusion, 6 with transudates, 19 with empyema, 15 with miscellaneous diseases, and 8 with diseases of unknown etiology. RESULTS: The mean values (SE) of ADAPF were 110 (4.5) U/L in patients with TBpl vs 28 (5.3) U/L in patients with a malignancy, 18 (5.7) U/L in patients with transudates, 13 (2.1) U/L in patients with diseases of unknown etiology, 22 (5.1) U/L in patients with miscellaneous diseases, and 191 (26.3) U/L in patients with empyema (Kruskal-Wallis test, p < 0.001). The ADAPF level was 110 (4.5) U/L in 37 HIV-positive patients with TBpl vs 114 (4.1) U/L in 52 HIV-negative patients with TBpl (Mann-Whitney U test, p > 0.05). A receiver operating characteristic curve identified the best cutoff at 60 U/L, yielding measures for sensitivity (0.95), specificity (0.96), positive predictive values (PPVs; 0.96), and negative predictive values (0.95). A Bayesian analysis showed a posttest probability of PPV ranging from 0.5 to 0.99, resulting from a pretest probability of 0.05 to 0.9. CONCLUSIONS: ADAPF is diagnostically useful across the various prevalences of TBpl, and its best diagnostic utility is in areas of intermediate prevalence of the disease. Moreover, the diagnostic value of ADAPF is independent of HIV serologic status.

AIM: The aim of the study was to evaluate the diagnostic potential of immunohistochemistry using an antibody to the secreted mycobacterial antigen MPT64, specific for Mycobacterium tuberculosis complex organisms, on formalin-fixed biopsies from patients with pleural tuberculosis (TB) from a high TB and HIV endemic area. METHODS AND RESULTS: Pleural biopsies from 25 TB cases and 11 non-TB cases were studied. Ziehl-Neelsen staining for acid-fast bacilli and immunohistochemistry with anti-MPT64 and anti-Bacille Calmette-Guérin (BCG) antibodies was performed. Nested polymerase chain reaction (N-PCR) for IS6110 was performed for comparison. Acid-fast bacilli were detected in only 2 cases and 3 biopsies showed granulomas with caseous necrosis. Immunostaining with anti-MPT64, anti-BCG, and N-PCR were positive in 20 (80%), 12 (48%), and 16 (64%) of the cases, and 0, 3 (27%), and 2 (18%) of the non-TB controls, respectively. The diagnostic validity of immunohistochemistry was calculated by comparison with N-PCR-positive TB cases and N-PCR-negative non-TB controls. The sensitivity of immunohistochemistry with anti-MPT64 and anti-BCG were 81% and 56% respectively, and the corresponding specificities were 100% and 78%. CONCLUSIONS: Detection of the MPT64 antigen by immunohistochemistry improves the diagnosis of TB pleuritis caused by M. tuberculosis complex organisms in patients living in HIV-endemic areas with atypical histology and negative staining for acid-fast bacilli.

The most used standard therapy for malignant pleural effusion(MPE)is tube thoracostomy drainage, except in cases where there are few pleural effusions or no symptoms. It has been reported that instilling an intrapleural agent is necessary for producing pleurodesis after tube thoracostomy drainage. To date, numerous chemical agents for the treatment of MPE have been studied. These include antibiotics, antineoplastic agents, biological response modifiers and others, that showed various degrees of chemical sclerosis. It was entered on a randomized comparison of tetracycline and bleomycin for treatment of MPE. The rate and time to recurrence were both significantly greater with bleomycin. In comparison, Talc was superior to bleomycin for control of MPE. Therefore, thoracoscopic pleurodesis with talc is now considered to be the gold standard treatment for MPE. However, talc has not been commercially available in Japan. We sought to evaluate the efficacy and toxicity of three intrapleural therapy regimens consisting of bleomycin, OK-432 or cisplatin plus etoposide(PE), for the management of malignant pleural effusion in previously untreated non-small cell lung cancer. The primary endpoint, pleural progression-free survival did not differ significantly between groups. Intrapleural treatment using OK-432 in the management of MPE was selected because it had the highest 4-week pleural progression-free survival rate and toxicity was tolerable. At present, OK- 432 is the standard agent used in Japan.

The diagnosis of pulmonary thromboembolism (PE) is often delayed because it is usually misdiagnosed as pneumonia or deep vein thrombosis. We report an unusual case of PE misdiagnosed as viral pleuritis on the first arrival at the emergency department (ED) in our hospital. A 14-year-old girl with no previous significant medical history was referred to the ED with pleuritic and chest pain with low-grade fever 4 days before admission. Echography showed a small amount of left pleural effusion. A 12-lead electrocardiogram was normal. She received a diagnosis of viral pleuritis. Two days before admission, she revisited ED with dyspnea and exacerbated pain. Echography showed slight increase in left pleural effusion. She had the same diagnosis. The chest pain remained at the same level. On the day of admission, she presented to ED with vomiting, watery diarrhea, abdominal pain, chest pain, and respiratory distress. Laboratory findings showed hypoalbuminemia and proteinuria. Echography showed a moderate amount of pleural effusion on both sides and no dilatation of the right cardiac ventricle. Contrast-enhanced chest computed tomography was performed to search the cause of the respiratory distress, which showed filling defects with contrast material in pulmonary arteries. A 12-lead electrocardiogram showed an S1Q3T3 pattern. She received a diagnosis of PE caused by nephrotic syndrome. Pulmonary thromboembolism can mimic infectious pleuritis and lead to misdiagnosis and/or delayed diagnosis. Thus, risk factors of PE should be considered in pediatric patients presenting with symptoms suggesting infectious pleuritis.