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Tuberculous effusion is a common disease entity with a spectrum of presentations from a largely benign effusion, which resolves completely, to a complicated effusion with loculations, pleural thickening and even frank empyema, all of which may have a lasting effect on lung function. The pathogenesis is a combination of true pleural infection and an effusive hypersensitivity reaction, compartmentalized within the pleural space. Diagnostic thoracentesis with thorough pleural fluid analysis including biomarkers such as adenosine deaminase and gamma interferon achieves high accuracy in the correct clinical context. Definitive diagnosis may require invasive procedures to demonstrate histological evidence of caseating granulomas or microbiological evidence of the organism on smear or culture. Drug resistance is an emerging problem that requires vigilance and extra effort to acquire a complete drug sensitivity profile for each tuberculous effusion treated. Nucleic acid amplification tests such as Xpert MTB/RIF can be invaluable in this instance; however, the yield is low in pleural fluid. Treatment consists of standard anti‐tuberculous therapy or a guideline‐based individualized regimen in the case of drug resistance. There is low‐quality evidence that suggests possible benefit from corticosteroids; however, they are not currently recommended due to concomitant increased risk of adverse effects. Small studies report some short‐ and long‐term benefit from interventions such as therapeutic thoracentesis, intrapleural fibrinolytics and surgery but many questions remain to be answered. [ABSTRACT FROM AUTHOR]

The possibility of tuberculous pleuritis should be considered in every patient with an undiagnosed pleural effusion, for if this diagnosis is not made the patient will recover only to have a high likelihood of subsequently developing pulmonary or extrapulmonary tuberculosis Between 3% and 25% of patients with tuberculosis will have tuberculous pleuritis. The incidence of pleural tuberculosis is higher in patients who are HIV positive. Tuberculous pleuritis usually presents as an acute illness with fever, cough and pleuritic chest pain. The pleural fluid is an exudate that usually has predominantly lymphocytes. Pleural fluid cultures are positive for Mycobacterium tuberculosis in less than 40% and smears are virtually always negative. The easiest way to establish the diagnosis of tuberculous pleuritis in a patient with a lymphocytic pleural effusion is to generally demonstrate a pleural fluid adenosine deaminase level above 40 U/L. Lymphocytic exudates not due to tuberculosis almost always have adenosine deaminase levels below 40 U/L. Elevated pleural fluid levels of γ-interferon also are virtually diagnostic of tuberculous pleuritis in patients with lymphocytic exudates. In questionable cases the diagnosis can be established by demonstrating granulomas or organisms on tissue specimens obtained via needle biopsy of the pleura or thoracoscopy. The chemotherapy for tuberculous pleuritis is the same as that for pulmonary tuberculosis. [ABSTRACT FROM AUTHOR]

Objectives and background: The determination of adenosine deaminase (ADA) activity in pleural fluid is important for differentiation of pleural effusions and diagnosing pleural tuberculosis. Although measurement of ADA is simple and inexpensive, controversies exist regarding potential errors caused by time elapsed between sample collection and analysis, storage temperature and the use of anticoagulants. The objective of this study was to evaluate the influence of storage time (1, 3, 7, 10 and 28 days) and temperature (4°C and −20°C) on the determination of ADA in pleural fluid samples collected in EDTA and sent at ambient temperature to the laboratory for initial processing within 1 h of collection. Methodology: Twenty-seven pleural exudates obtained from 20 patients with neoplastic disease and seven with tuberculosis were analysed. The ADA activity obtained within 1 h of collection was considered the gold standard and was compared with the other measurements. Results: The correlation between the initial measurement and all others was ≥0.90 for both temperatures up to the 10th day after thoracocentesis and tended to decrease by 28 days after collection, but this difference was not significant. Conclusions: Pleural fluid samples collected in EDTA and sent for analysis within 1 h after collection can be used to determine ADA up to 28 days after collection if stored at 4°C or −20°C, with no evidence of significant increases or decrease in enzyme activity that might distort the results. [ABSTRACT FROM AUTHOR]