Francis R B, McGehee W G
Thromb Haemost. 1985 Apr 22;53(2):249-51.
A 57 year old man presented with apparently spontaneous lower extremity deep vein thrombosis and pulmonary embolism. He was treated in conventional fashion with intravenous heparin and oral warfarin. After 4 daily doses of warfarin the prothrombin and proconvertin (P+P) time was within therapeutic range, and heparin was stopped. Over the next six hours complete defibrination occurred, associated with severe bleeding complications. Functional protein C measured after normalization of routine coagulation tests averaged 40% of normal, and was only 3.5% of normal immediately prior to the episode of defibrination. We conclude that the very low functional protein C levels seen immediately prior to defibrination were caused by a combination of pre-existent protein C deficiency and warfarin therapy, and directly predisposed to defibrination once heparin was stopped, despite "therapeutic" warfarin anticoagulation. Exacerbation of intravascular coagulation should be considered a potential prothrombotic effect of warfarin therapy in protein C deficient individuals.
一名57岁男性出现明显自发性下肢深静脉血栓形成和肺栓塞。他接受了静脉注射肝素和口服华法林的常规治疗。在给予4剂华法林后,凝血酶原和凝血酶原转变加速因子(P+P)时间处于治疗范围内,肝素停用。在接下来的6小时内发生了完全性纤维蛋白溶解,并伴有严重出血并发症。常规凝血试验恢复正常后测得的功能性蛋白C平均为正常水平的40%,而在纤维蛋白溶解发作前即刻仅为正常水平的3.5%。我们得出结论,在纤维蛋白溶解发作前即刻所见的极低功能性蛋白C水平是由先前存在的蛋白C缺乏和华法林治疗共同导致的,并且尽管华法林抗凝处于“治疗”水平,但一旦停用肝素,就直接导致了纤维蛋白溶解。血管内凝血的加重应被视为华法林治疗在蛋白C缺乏个体中的潜在促血栓形成作用。