Pathogenesis of the coagulation defect developing during pathological plasma proteolytic ("fibrinolytic") states. II. The significance, mechanism and consequences of defective fibrin polymerization.
Pathogenesis of the coagulation defect developing during pathological plasma proteolytic ("fibrinolytic") states. II. The significance, mechanism and consequences of defective fibrin polymerization.
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病理性血浆蛋白水解（“纤维蛋白溶解”）状态期间发生的凝血缺陷的发病机制。
DOI：
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发表时间：
1962
影响因子：
15.9
通讯作者：
S. Sherry
中科院分区：
文献类型：
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作者：
N. Alkjaersig;A. Fletcher;S. Sherry
一种以凝血缺陷、低纤维蛋白原血症为特征的临床综合征，通常伴随着出血性素质和全血或血浆“纤溶”(全血或血浆凝块的自发溶解)的表现，早已被认识到。它通常发生在手术创伤后或与某些产科并发症有关，也可能表现为一种慢性综合征，使长期内科疾病的病程复杂化(参考文献1，2中提到的综述)。此外，该综合征的医源性诱发，通常是一种轻微的形式，经常伴随着用酶方法治疗血管疾病的急性血栓栓塞性并发症(3-6)。
A clinical syndrome characterized by a coagulation defect, hypofibrinogenemia, often an associated hemorrhagic diathesis and manifestations of whole blood or plasma "fibrinolysis" (spontaneous lysis of whole blood or plasma clots), has long been recognized. Usually developing acutely after the trauma of surgery or in association with certain obstetric complications, it may also present as a chronic syndrome complicating the course of long-term medical disease (reviews noted in References 1, 2). Moreover, the iatrogenic induction of the syndrome, usually in a mild form, frequently accompanies the treatment of the acute thromboembolic complications of vascular disease by enzymatic means (3-6).