Monroe Dougald M
Division of Hematology/Oncology, Department of Medicine, Center for Thrombosis and Hemostasis, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599-7035, USA.
Semin Hematol. 2008 Apr;45(2 Suppl 1):S7-S11. doi: 10.1053/j.seminhematol.2008.03.013.
Recombinant activated factor VII (rFVIIa) is being increasingly used to treat bleeding associated with a variety of non-hemophilic coagulopathic indications, and its mechanism of action in these areas is under active investigation. Numerous studies have shown that FVIIa binds with low affinity to activated platelets; rFVIIa can subsequently enhance platelet-surface thrombin generation by activating factor (F) X and by contributing additional FIXa to the hemostatic process. This FIXa can rapidly activate additional FX, which may explain why non-hemophilic coagulopathic bleeds respond to lower doses of rFVIIa than do hemophilic bleeds. However, the platelet surface may be able to process only a limited amount of FXa, accounting for the observation that some models of non-hemophilic coagulopathy show a plateau in the effect of rFVIIa.
重组活化凝血因子 VII(rFVIIa)越来越多地用于治疗与多种非血友病性凝血病相关的出血,其在这些领域的作用机制正在积极研究中。大量研究表明,FVIIa 与活化血小板的亲和力较低;rFVIIa 随后可通过激活因子(F)X 并在止血过程中提供额外的 FIXa 来增强血小板表面凝血酶的生成。这种 FIXa 可迅速激活更多的 FX,这可能解释了为什么非血友病性凝血病出血对 rFVIIa 剂量的反应低于血友病性出血。然而,血小板表面可能只能处理有限量的 FXa,这就解释了为什么一些非血友病性凝血病模型显示 rFVIIa 的效果会达到平台期。