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Background: Pleural effusion is not a pathognomonic sign and distinguishing between transudates and exudates often presents a diagnostic dilemma., Objective: To examine whether the NT pro-brain natriuretic peptide (NT-proBNP) in pleural fluid is a diagnostic tool for determining the cardiac etiology of pleural effusions., Methods: We measured pleural fluid and serum NT-proBNP levels in a consecutive series of 98 patients with heart failure and in 142 patients with other causes., Results: The median pleural fluid NT-proBNP levels among the heart failure patients were significantly higher (3,310 pg/mL) than hepatic hydrothorax (16 patients, 531 pg/mL), malignant pleural effusion (38 patients, 733 pg/mL), parapneumonic pleural effusion (40 patients, 294 pg/mL), and tuberculous pleural effusion (64 patients, 214 pg/mL) (p<0.001). At a cut-off point of > or = 1,714 pg/mL, the test had a sensitivity of 99%, a specificity of 99 % for the diagnosis of heart failure. There were 28 patients with pleural effusion due to heart failure misclassified as exudates by Light's criteria. Ten cases of misclassified heart failure (36% of 28 patients) showed serum-effusion protein gradient less than 3.1 g/dL; 26 of them exhibited pleural fluid NT-proBNP levels of > or = 1,714 pg/mL. The 26 patients of misclassified heart failure received diuretics before thoracentesis. Pleural fluid NT-proBNP levels were correlated with serum NT-proBNP levels (R(2)=0.928, p<0.001)., Conclusion: Pleural fluid NT-proBNP may be useful in the diagnosis of pleural effusion resulting from heart failure. The test may be especially useful in heart failure patients with exudates who have been treated with diuretics.

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.

We have found that natural killer (NK) cells were very active in pleural effusions containing Mycobacterium tuberculosis. Cytotoxicity against K562 and Raji was augmented when the mononuclear cells were cocultured for 18 hr with purified protein derivative (PPD) derived from M. tuberculosis culture supernatants. In pleural effusions of cancer patients, PPD-activated mononuclear cells were less cytotoxic than their counterparts in peripheral blood. However, in the same patients, interferon and interleukin-2 production was greater in pleural effusions than in peripheral blood. On the other hand, in tuberculosis patients there was no significant difference in cytotoxicity between peripheral blood and pleural effusion mononuclear cells, but the production of interferon and interleukin-2 was higher in pleural effusions than in peripheral blood. Neither group of patients consistently demonstrated a correlation between production of interferon or interleukin-2 in peripheral blood and cytotoxicity. Both PPD-induced cytotoxicity and the production of interferon and interleukin-2 were lower in mononuclear cells of carcinomatous than tuberculous pleural effusion. These results indicate that peripheral blood and pleural effusion mononuclear cells differ in cytotoxicity as well as in interferon and interleukin-2 production. Further, these activities also differ in tuberculous and carcinomatous pleural effusions.