الفهرس 
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Abstract
Pleural effusion is not pathognomonic. Distinguishing between transudates and exudates often presents a diagnostic dilemma. Exudative processes always require extensive diagnostic workup while transudates mandate appropriate treatment of heart failure, liver and renal failure.
Exudates can result from a variety of causes. They often reflect the presence of pleural inflammation, infection or neoplasm. Transudates are not associated with pleural disease and are considered to be the result of systemic abnormalities that create an imbalance of hydrostatic and osmotic forces, which, in turn, leads to the accumulation of pleural fluid.
The finding of an exudative effusion usually requires an extensive diagnostic workup.
Thus a diagnostic dilemma in patients with exudative pleural effusions and clinical heart failure might result, leading to an unnecessary exposure to invasive and expensive diagnostic procedures.
Moreover, thoracentesis itself presents considerable risk of complications and is associated with discomfort to the patient.
Thus identifying transudate from exudate pleural effusions and possibly avoiding unnecessary diagnostic thoracenteses and/or further diagnostic procedures would be an attractive and potentially beneficial approach.
The criteria established by Light et al. for differentiating exudates from transudates have been widely accepted. Pleural fluid is considered an exudate if one of the following three criteria is met:
(1) pleural fluid to serum protein ratio is greater than 0.5
(2) pleural fluid to serum lactate dehydrogenase (LDH) ratio is greater than 0.6
(3) pleural fluid LDH level is greater than two-thirds of the upper limit of normal for serum LDH.
However, in some prospective studies applying the criteria of light, sensitivity remained high while specificity did not.
Treatment of congestive heart failure in patients with transudates may convert the effusion into a pseudoexudate’ with the elevation of pleural protein and LDH levels, as well as that of protein ratio as a result of aggressive diuretic therapy.
B-type natriuretic peptide (BNP) and aminoterminal pro-B-type natriuretic peptide (NT-proBNP) are cleavage products of a precursor protein released by myocytes in the cardiac ventricles in response to volume expansion and pressure overload.