Diabetes mellitus - A hypercoagulable state

Diabetes mellitus - A hypercoagulable state
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DOI:
10.1016/s1056-8727(00)00132-x
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发表时间:
2001-01-01
影响因子:
3
通讯作者:
Carr, ME
Carr, ME
中科院分区:
医学3区
文献类型:
--
作者:
Carr, ME

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80%的糖尿病患者死于血栓性死亡。这些死亡中有75%是由于心血管并发症,其余是由于脑血管事件和外周血管并发症。糖尿病患者的血管内皮细胞异常,血管内皮细胞是对抗血栓形成的主要防御系统。内皮异常无疑在糖尿病中观察到的血小板和克隆因子的增强活化中起作用。凝血激活标志物,如凝血酶原激活片段1+2和凝血酶-抗凝血酶复合物,在糖尿病中升高。许多凝血因子的血浆水平,包括纤维蛋白原,因子VII,因子VIII,因子SI。因子XII、激肽释放酶和血管性血友病因子在糖尿病中升高。相反,抗凝蛋白C(PC)的水平降低。纤维蛋白溶解系统是清除凝块的主要手段,在糖尿病中由于异常凝块结构而受到相对抑制,这些结构更耐降解和纤溶酶原激活物抑制剂1型(派-1)增加。增加的循环血小板聚集体、响应于血小板激动剂的增加的血小板聚集体、增加的血小板收缩力(PCF)和存在较高血浆水平的血小板释放产物(例如β-血栓球蛋白、血小板因子4和血栓烷β(2)),表明糖尿病中的血小板过度活跃。这些发现支持了糖尿病是一种高凝状态的临床观察。本文简要回顾了已发表的证据,这一结论和假定的作用所发挥的高血糖症和高胰岛素血症在其发展。(C)2001 Elsevier Science Inc. All rights reserved.
Eighty percent of patients with diabetes mellitus die a thrombotic death. Seventy-five percent of these deaths is due to cardiovascular complications, and the remainder is due to cerebrovascular events and peripheral vascular complications. Vascular endothelium, the primary defense against thrombosis, is abnormal in diabetes. Endothelial abnormalities undoubtedly play a role in the enhanced activation of platelets and cloning factors seen in diabetes. Coagulation activation markers, such as prothrombin activation fragment 1+2 and thrombin-antithrombin complexes, are elevated in diabetes. The plasma levels of many clotting factors including fibrinogen, factor VII, factor VIII, factor SI. factor XII, kallikrein, and von Willebrand factor are elevated in diabetes. Conversely, the level of the anticoagulant protein C (PC) is decreased. The fibrinolytic system, the primary means of removing clots, is relatively inhibited in diabetes due to abnormal clot structures that are more resistant to degradation and an increase in plasminogen activator inhibitor type 1 (PAI-1). Increased circulating platelet aggregates, increased platelet aggregation in response to platelet agonists, increased platelet contractile Force (PCF), and the presence of higher plasma levels of platelet release products, such as beta -thromboglobulin, platelet factor 4, and thromboxane beta (2), demonstrate platelet hyperactivity in diabetes. This constellation of findings supports the clinical observation that diabetes is a hypercoagulable state. This article briefly reviews the published evidence for this conclusion and the putative roles played by hyperglycemia and hyperinsulinemia in its development. (C) 2001 Elsevier Science Inc. All rights reserved.