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      Tuberculous pleural effusion.

      Lung
      Adenosine Deaminase, analysis, Antitubercular Agents, therapeutic use, Biological Markers, Biopsy, Drug Resistance, Bacterial, Drug Therapy, Combination, Exudates and Transudates, enzymology, immunology, microbiology, Humans, Interferon-gamma, Microbial Sensitivity Tests, Mycobacterium, isolation & purification, Paracentesis, Pleural Effusion, drug therapy, Predictive Value of Tests, Sputum, Tuberculosis, Pleural, diagnosis

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          Abstract

          Tuberculous pleural effusion is one of the most common forms of extrapulmonary tuberculosis (TB). The immediate cause of the effusion is a delayed hypersensitivity response to mycobacterial antigens in the pleural space. For this reason microbiological analyses are often negative and limited by the lengthy delay in obtaining results. In areas with high TB prevalence, pleural fluid adenosine deaminase (ADA) levels greater than 40 U/l argue strongly for TB; in contrast, low levels of pleural ADA have high negative predictive value in low-prevalence countries. The specificity of this enzyme increases if only lymphocytic exudates are considered. The shortcoming of the ADA test is its inability to provide culture and drug sensitivity information, which is paramount in countries with a high degree of resistance to anti-TB drugs. Sputum induction (in addition to pleural fluid) for acid-fast bacilli and culture is a recommended procedure in all patients with TB pleurisy. The microscopic-observation drug-susceptibility assay performed on pleural fluid or pleural tissue increases by two to three times the detection of TB over conventional cultures, and it allows for the identification of multidrug-resistant TB. A reasonable management strategy for pleural TB would be to initiate a four-drug regimen and perform a therapeutic thoracentesis in patients with large, symptomatic effusions.

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