The role of ADAMTS-13 and von Willebrand factor in venous thromboembolism.

静脉血栓栓塞症是一种严重的循环障碍，通过深静脉血栓闭塞肺动脉而发展起来。一些临床研究表明，抗血小板药物在预防静脉血栓形成方面有很好的效果。然而，血小板和静脉血栓的参与尚不清楚。本研究探讨了对血小板功能表达起重要作用的血管性血友病因子(VWF)及其控制蛋白。深静脉血栓的免疫组织化学研究表明，静脉血栓呈纤维蛋白、血小板、VWF和第VIII因子阳性。抗FVIII抗体(中和抗体)减少了血小板在流动腔系统上的聚集，但不影响抗VWF抗体和抗ADAMTS-13。在兔静脉血栓模型中，FVIII促进静脉血栓大小，增加血小板和纤维蛋白的阳性面积。

Venous thromboembolism is a severe circulatory disorder that develops by occlusion of the pulmonary artery via deep venous thrombosis. The efficacy of anti-platelet agents is shown in the prevention of venous thromboembolism in some clinical studies. However, involvement of platelet and venous thrombosis is not clear. The present study investigates the von Willebrand factor (VWF), which is important to functional expression of platelet, and their control protein. Immunohistochemical study of deep venous thrombosis shows that venous thrombi is positive for fibrin, platelet, VWF and Factor VIII. Anti-FVIII antibody (Neutralizing antibody) reduced the platelet aggregation on flow chamber system, but not Anti-VWF antibody or Anti-ADAMTS-13.In rabbit venous thrombosis model, FVIII promoted the venous thrombus size, and increased the positive area of the platelet and fibrin.