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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: Evidence suggests that the fibrinolysis system and peritumoral connective tissue play important roles in tumor spread., Methods: In this study, the authors evaluated the following parameters in 30 consecutive patients with lung cancer: thrombin-antithrombin complex (TAT), cross-linked fibrin split products D-dimer (DD), plasmin-alpha 2-antiplasmin inhibitor complex (PAP), and two antigens related to connective tissue, the aminoterminal propeptide of type III procollagen (PIIIP) and the 7S domain of type IV collagen (7S-collagen)., Results: Each parameter was increased significantly in the patients with cancer compared with the control subjects. Except for PIIIP, their concentration in blood was elevated to a significantly greater extent in the patients with distant metastases. The PAP concentration correlated well with the plasma concentration of TAT (r = 0.5; P < 0.01) and DD (r = 0.9; P < 0.0001). There was also a strong correlation between the serum concentrations of PIIIP and 7S-collagen (r = 0.7; P < 0.001). In patients with localized disease, DD levels were correlated significantly with those of PIIIP (Spearman rank-order correlation [rs] = 0.6; P < 0.025) and 7S-collagen (rs = 0.6; P < 0.01). In the group with disseminated metastases, there was a significant inverse relationship between serum PAP concentrations and serum concentrations of 7S-collagen (rs = -0.6; P < 0.025)., Conclusions: These results confirm the presence of a subclinical chronic activation of the parameters of intravascular clotting-fibrinolysis and alterations in the extracellular matrix of patients with lung cancer. These parameters may be useful as indicators of the clinical progression of malignant disease, particularly of lung cancer.