Proinflammatory Cytokines, Transforming Growth Factor-β1, and Fibrinolytic Enzymes in Loculated and Free-Flowing Pleural Exudates

Abstract

Study objectives To measure tumor necrosis factor (TNF) α, interleukin (IL) 1β, and transforming growth factor (TGF) β1 in loculated and free-flowing pleural effusions caused by malignancy, tuberculosis (TB), and pneumonia and their relationship with plasminogen activator inhibitor-type 1 (PAI-1) and tissue-type plasminogen activator (tPA) and to compare the differences between loculated and free-flowing effusions Design A prospective study Patients and methods The effusion levels of TNF-α, IL-1β, TGF-β1, PAI-1, and tPA were measured in 29 patients with malignant effusions, 19 patients with TB, and 30 patients with parapneumonic effusions. Pleural effusions were divided into loculated and free-flowing groups by imaging studies. A group of 42 patients with loculated effusions was subdivided into primary and secondary loculation groups by chest ultrasonography Results The median levels of TNF-α (87.0 pg/mL), IL-1β (13.8 pg/mL), TGF-β1 (10,952.9 pg/mL), PAI-1 (111.2 ng/mL), and lactate dehydrogenase (LDH) [498 IU/dL] in the loculated group were significantly higher than those in the free-flowing group (TNF-α, 15.0 pg/mL; IL-1β, 2.9 pg/mL; TGF-β1, 6,117.3 pg/mL; PAI-1, 61.5 ng/mL, and LDH, 266 IU/dL). In both the loculated and free-flowing effusions, the levels of TGF-β1 correlated positively with those of TNF-α ( r = 0.51 and p r = 0.42 and p r = 0.52 and p r = 0.49 and p r = 0.59 and p r = 0.55 and p r = 0.35 and p r = 0.47 and p r = 0.53 and p r = 0.58 and p r = −0.37, p r =−0.56, p Conclusion Compared with free-flowing effusions, fibrinolytic activity was depressed in loculated effusions. A higher intensity of pleural inflammation in loculated effusions may enhance the release of TNF-α, IL-1β, and TGF-β1, which may subsequently increase the levels of PAI-1. The imbalance of PAI-1 and tPA in pleural spaces may lead to fibrin deposition and loculation of pleural effusions