Source: Annual Congress 2001 - Thoracoscopy
Disease area: Thoracic oncology

Abstract

According to previous studies from our group, fibrinolitic activity is associated with pleurodesis failure (Am J Respir Crit Care Med 1995; 151: 785-90). In order to assess which cells are associated with plasmin generation in malignant pleural effusions, thirty one patients who were submitted to thoracoscopic talc pleurodesis, were studied.
Plasmin-antiplasmin complex (PAP) was analyzed in serial samples of pleural fluid by ELISA (Behring Diagnostics, Marburg, Germany). Fibrinolysis markers expression was also studied in tissue (tumoral cells, fibroblasts, vascular endothelium and non tumoral mesothelium) using monoclonal antibodies against urokinase plasminogen activator (uPA), its receptor (uPAR), tisular plasminogen activator (tPA) and plasminogen activator inhibitor type-1 (PAI-1) by immunohistochemistry (American Diagnostica, Greenwich, Connecticut, USA) and ELISA. These samples were obtained under visual control by thoracoscopy.
RESULTS: Plasmin-antiplasmin complex in pleural fluid at baseline was associated with endothelial uPAR (r=0,99, p<0,001), mesothelial tPA (r=0,692, p<0,001) and fibroblasts PAI-1 expression (r=0,651, p<0,005).
CONCLUSION: Non tumoral tissue, especially vascular endothelial cells, plays an important role in the modulation of endopleural fibrinolysis in malignant pleural effusions.
Founded by F.I.S. 98/0419

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B. R. Romero, L. G. Izquierdo, L. D. Cañaveral, J. M. Juan, F. Rodríguez Panadero, J. C. Gómez (Sevilla, Spain). Intrapleural fibrinolysis modulation in malignant pleural effusions. Eur Respir J 2001; 16: Suppl. 31, 3485

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