Gabazza E, Taguchi O, Yamakami T, Machishi M, Ibata H, Suzuki S
Mie University School of Medicine, Third Department of Internal Medicine, Tsu-City, Japan.
Cancer. 1993 Oct 1;72(7):2134-40. doi: 10.1002/1097-0142(19931001)72:7<2134::aid-cncr2820720712>3.0.co;2-8.
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.
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.
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.
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.
凝血病常与恶性肿瘤相关。癌症中这些并发症的发病机制尚不清楚。有研究提示，宿主炎症（单核细胞/巨噬细胞）细胞介导的凝血激活触发机制与之相关。
本研究的目的是评估中性粒细胞衍生的弹性蛋白酶在肺癌凝血和纤溶激活中的作用。研究对象为42例连续的肺癌患者（34例男性和8例女性）。13例为小细胞肺癌（SCLC），13例为肺鳞癌，16例为肺腺癌。通过检测D-二聚体（DD）、凝血酶-抗凝血酶III复合物（TAT）、纤溶酶-α2-抗纤溶酶复合物（PAP）、纤维蛋白降解产物（FDP）、纤维蛋白原、凝血酶原时间（PT）和活化部分凝血活酶时间（APTT）来评估止血功能。检测弹性蛋白酶-α1-蛋白酶抑制剂（EPI）复合物作为中性粒细胞激活的标志物。
与对照组相比，癌症患者的弹性蛋白酶血浆水平和凝血-纤溶参数显著升高。在所有患者中，EPI的血浆浓度与APTT、DD、TAT、PAP和纤维蛋白原显著相关。虽然在非小细胞肺癌（非SCLC）患者中，DD、TAT、PAP、APTT和纤维蛋白原与EPI显著相关，但在SCLC患者中未发现这种相关性。非SCLC患者中EPI与TAT、PAP和PT的相关性比疾病晚期患者更强。
肺癌中凝血-纤溶系统的激活可能至少部分是由中性粒细胞弹性蛋白酶释放增加所触发。这种机制与分期相关，且似乎主要在非SCLC中起作用。
