BACKGROUND: The intrapleural hypofibrinolysis is caused by mainly excessive concentration of pleural plasminogen ogen activator inhibitor-1 antigen(PAI-1 Ag), which binds tissue type plasminogen activator. In pleural inflammation induced by sclerosing agents for pleurodesis, levels of pleural PAI-1 antigen increase in relation to decreing D-dimer levels. It has been known that the pleural mexothelial cells have the capability of secreting PAI-1 Ag in response to inflammation in vivo. Therefore, we estimated whether pleural inflammation changes the balance between fibrinolytic and coagulative properties in exudative pleural effusions. METHOD: The thirty cases was included in our study. We determined the pleural levels of glucose, lactic dehy-drogenase(LDH), pH and the counts of white blood cell(WBC), polymorpho leukocyte(PMN), lymphocyte as the parameters of pleural inflammation and cellular components of pleural fluid. The plasma level of fibrinogen in fluid and the neutrophil count in blood were determined. The levels of D-dimer, PAI-1 Ag and thrombin-antithrombin lll complex(TAT) were determined by ELISA(Behring, Marburg, Germany). RESULTS: The causes of pleural effusion were as following : tuberculous in 14 cases, malignant in 10 cases and parapneumonic in 6 cases. The levels of pleural D-dimer, PAI-1 Ag and TAT was significantly higher than that of plasma(p<0.001). The severity of pleural inflammation did not correlated with pleural D-dimer, PAI-1 Ag, TAT and their plaxma levels. But the level of pleural TAT correlated with pleural WBC and lymphocyte count. CONCLUSION: We found the the severity of pleural inflammations did not correlated with pleural D-dimer, PAI-1 Ag, TAT and the possibility of local production of PAI-1 antigen is present.