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* From the Department of Chest Medicine (Dr. Chen), Taipei Medical University Hospital, Taipei, Taiwan; Graduate Institute of Medical Sciences (Drs. Chung and Sheu), College of Medicine, Taipei Medical University, Taipei, Taiwan; Chest Department (Ms. Chen), Taipei Veterans General Hospital, Taipei, Taiwan; and the School of Medicine (Dr. Chang), National Yang-Ming University, Taipei, Taiwan.
Correspondence to: Shi-Chuan Chang, MD, Chest Department, Taipei Veterans General Hospital, # 201, Sec. 2, Shih-Pai Road, Shih-Pai, Taipei, Taiwan, 112; e-mail: scchang{at}vghtpe.gov.tw
Study objectives: To measure tumor necrosis factor (TNF) 
, interleukin (IL) 1ß, and transforming growth factor (TGF) ß1 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-, IL-1ß, TGF-ß1, 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- (87.0 pg/mL), IL-1ß (13.8 pg/mL), TGF-ß1 (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-, 15.0 pg/mL; IL-1ß, 2.9 pg/mL; TGF-ß1, 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-ß1 correlated positively with those of TNF- (r = 0.51 and p < 0.001 vs r = 0.42 and p < 0.05, respectively) and IL-1ß (r = 0.52 and p < 0.001 vs r = 0.49 and p < 0.01, respectively), and the values of PAI-1 correlated positively with those of TNF- (r = 0.59 and p < 0.001 vs r = 0.55 and p < 0.001, respectively), IL-1ß (r = 0.35 and p < 0.05 vs r = 0.47 and p < 0.01, respectively), and TGF-ß1 (r = 0.53 and p < 0.001 vs r = 0.58 and p < 0.001, respectively). In contrast, the levels of tPA correlated negatively with those of TNF- (r = –0.37, p < 0.05) and IL-1ß (r =–0.56, p < 0.001) in loculated effusions. Twenty-seven of 42 patients with loculated effusions were classified into a secondary loculation group, which, compared with the primary loculation group, had significantly higher median levels of effusion TNF- (119.2 vs 14.2 pg/mL, respectively; p = 0.001), IL-1ß (33.3 vs 3.4 pg/mL, respectively; p < 0.001), TGF-ß1 (13,152.7 vs 7746.0 pg/mL, respectively; p = 0.041), and PAI-1 (114.9 vs 94.1 pg/mL, respectively; p = 0.019).
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-, IL-1ß, and TGF-ß1, 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.
Key Words: fibrinolysis • loculation • malignancy • pleural effusion • proinflammatory cytokines • tuberculosis
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