Plasminogen Activator Inhibitor-1 (PAI-1) Levels in Loculated and Non-Loculated Infectious Pleural Effusions: A Comparative Cross-Sectional Study

Abstract

Infectious pleural effusion may progress to loculation through impaired fibrinolysis, causing prolonged hospitalization. Plasminogen activator inhibitor-1 (PAI-1), a fibrinolysis inhibitor, may reflect the antifibrinolytic process associated with pleural loculation. This study compared pleural fluid PAI-1 levels in loculated and non-loculated infectious pleural effusions and evaluated associations with loculation, hospital stay, and microbiological profile in 61 patients treated at Dr. Wahidin Sudirohusodo Hospital and teaching hospitals, Makassar, Indonesia. Pleural fluid PAI-1 concentrations were measured using enzyme-linked immunosorbent assay (ELISA), loculation was assessed using ultrasonography and/or computed tomography, and analyses included Spearman correlation, ROC analysis, and multivariable logistic regression. Patients with loculated effusions had higher PAI-1 concentrations than those with non-loculated effusions (median, 120.62 vs. 5.83 ng/mL; p=0.007), and concentrations correlated with loculation degree (Spearman's rho=0.521; p=0.002). ROC analysis identified a PAI-1 cut-off of 46.525 ng/mL, with area under the curve 0.703, sensitivity 73.3%, and specificity 61.3%. After adjustment, elevated PAI-1 remained independently associated with pleural loculation (adjusted odds ratio, 4.12; 95% confidence interval, 1.18–14.41; p=0.027). Streptococcus spp. predominated, but loculated effusions and Gram-negative organisms were associated with longer hospitalization, and PAI-1 weakly correlated with hospital stay (Spearman's rho=0.275; p=0.044). Elevated pleural fluid PAI-1 was associated with pleural loculation and greater septation and may serve as an adjunctive biomarker interpreted with imaging and microbiological findings and other clinical parameters.