Rickles F R, Falanga A
The Division of Hematology-Oncology, Department of Medicine, The George Washington University Medical Center, 2300 Eye Street NW, Washington, DC 20037, USA.
Thromb Res. 2001 Jun 15;102(6):V215-24. doi: 10.1016/s0049-3848(01)00285-7.
Cancer patients are highly susceptible to thromboembolic complications, which some have estimated accounts for a significant percentage of the morbidity and mortality of the disease. Not all of the mechanisms for the production of the hypercoagulable state characteristic of cancer are entirely understood. Those that are known seem to interdigitate the biology of cancer with the major regulatory pathways that mediate blood coagulation, platelet-vessel wall interaction, fibrinolysis and inflammatory cytokine production. In other words, the events responsible for thrombosis in cancer appears to be a result of an over exuberant host response in an attempt to delimit tumor growth. In this brief review, therefore, we attempt to put into the context of tumor growth, angiogenesis and metastasis the current information about the pathogenesis of venous thromboembolism (VTE).
癌症患者极易发生血栓栓塞并发症，据估计，这在该疾病的发病率和死亡率中占相当大的比例。并非所有导致癌症特征性高凝状态的机制都完全清楚。已知的机制似乎将癌症生物学与介导血液凝固、血小板-血管壁相互作用、纤维蛋白溶解和炎性细胞因子产生的主要调节途径相互交织。换句话说，癌症中导致血栓形成的事件似乎是宿主过度活跃反应以限制肿瘤生长的结果。因此，在这篇简短的综述中，我们试图将目前关于静脉血栓栓塞（VTE）发病机制的信息置于肿瘤生长、血管生成和转移的背景下。
