Aronson D L, Menache D
Dev Biol Stand. 1987;67:149-55.
Factor IX Complex therapy has been associated with thrombosis when used in patients with liver disease, hemophilia B and hemophilia A with inhibitors to Factor VIII when administered repetitively and in high doses. Three mechanisms for inducing thrombogenicity have been proposed: activated coagulants, coagulant-active phospholipid content and/or the high zymogen level attained in recipients. A new animal model using Russel Viper Venom (RVV) as an in vivo stimulus of coagulation has been used to investigate the role of high levels of zymogens in the induction of thrombosis. The quantity of RVV tolerated by rabbits infused with Factor IX Complex is reduced 100-fold. Infusion of Factor X or prothrombin also reduces the lethal dose of RVV. In contrast, Coagulation Factor IX devoid of other coagulants has little effect. However other animal data indicate that the amount of activated coagulants can play a role in the in vivo thrombogenicity of Factor IX Complex.
在肝病患者、B型血友病患者以及反复大剂量使用时对VIII因子产生抑制剂的A型血友病患者中，使用IX因子复合物治疗与血栓形成有关。已提出三种诱导血栓形成的机制：活化的凝血因子、具有凝血活性的磷脂含量和/或受体内达到的高酶原水平。一种使用罗素蝰蛇毒液（RVV）作为体内凝血刺激物的新动物模型已被用于研究高水平酶原在血栓形成诱导中的作用。输注IX因子复合物的兔子对RVV的耐受量降低了100倍。输注X因子或凝血酶原也会降低RVV的致死剂量。相比之下，不含其他凝血因子的凝血因子IX几乎没有作用。然而，其他动物数据表明，活化凝血因子的量可能在IX因子复合物的体内血栓形成性中起作用。
