BACKGROUND: Coagulopathies often are associated with malignant tumors. The pathogenesis of these complications in cancer is not clear. Host inflammatory (monocyte/macrophage) cell-mediated triggering of clotting activation has been suggested. METHODS: The objective of this study was to evaluate the role of neutrophil-derived elastase in the activation of blood coagulation and fibrinolysis in lung cancer. The study population was 42 consecutive patients with lung cancer (34 men and 8 women). Thirteen patients had small cell lung cancer (SCLC), 13 had squamous cell lung cancer, and 16 had adenocarcinoma. Hemostatic function was assessed by measuring D-dimer (DD), thrombin-antithrombin III complex (TAT), plasmin-alpha 2-antiplasmin complex (PAP), fibrin degradation product (FDP), fibrinogen, prothrombin time (PT) and activated partial thromboplastin time (APTT). Elastase-alpha 1-protease inhibitor (EPI) complex was measured as a marker of neutrophil activation. RESULTS: Significant elevation of the elastase plasma levels and coagulation-fibrinolysis parameters was found in patients with cancer compared with control subjects. Among all patients, the plasma concentration of EPI was significantly correlated with APTT, DD, TAT, PAP, and fibrinogen. Although in patients with non-small cell lung cancer (non-SCLC), DD, TAT, PAP, APTT, and fibrinogen were significantly correlated with EPI, such a correlation was not found in patients with SCLC. Patients with non-SCLC had stronger correlation of EPI with TAT, PAP, and PT than did patients with advanced stages of disease. CONCLUSION: The activation of coagulation-fibrinolysis system in lung cancer may be triggered, at least in part, by an increased release of neutrophil elastase. This mechanism is stage related and seems to operate predominantly in non-SCLC.
BACKGROUND:Coagulopathies often are associated with malignant tumors. The pathogenesis of these complications in cancer is not clear. Host inflammatory (monocyte/macrophage) cell-mediated triggering of clotting activation has been suggested. METHODS: The objective of this study was to evaluate the role of neutrophil-derived elastase in the activation of blood coagulation and fibrinolysis in lung cancer. The study population was 42 consecutive patients with lung cancer (34 men and 8 women). Thirteen patients had small cell lung cancer (SCLC), 13 had squamous cell lung cancer, and 16 had adenocarcinoma. Hemostatic function was assessed by measuring D-dimer (DD), thrombin-antithrombin III complex (TAT), plasmin-alpha 2-antiplasmin complex (PAP), fibrin degradation product (FDP), fibrinogen, prothrombin time (PT) and activated partial thromboplastin time (APTT). Elastase-alpha 1-protease inhibitor (EPI) complex was measured as a marker of neutrophil activation. RESULTS: Significant elevation of the elastase plasma levels and coagulation-fibrinolysis parameters was found in patients with cancer compared with control subjects. Among all patients, the plasma concentration of EPI was significantly correlated with APTT, DD, TAT, PAP, and fibrinogen. Although in patients with non-small cell lung cancer (non-SCLC), DD, TAT, PAP, APTT, and fibrinogen were significantly correlated with EPI, such a correlation was not found in patients with SCLC. Patients with non-SCLC had stronger correlation of EPI with TAT, PAP, and PT than did patients with advanced stages of disease. CONCLUSION: The activation of coagulation-fibrinolysis system in lung cancer may be triggered, at least in part, by an increased release of neutrophil elastase. This mechanism is stage related and seems to operate predominantly in non-SCLC.