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血小板在糖尿病相关血管并发症中的作用。

The role of platelets in diabetes-related vascular complications.

作者信息

Sobol A B, Watala C

机构信息

Laboratory of Haemostatic Disorders, Medical University of Lodz, 96 Narutowicz Street, 90 141 Lodz, Poland.

出版信息

Diabetes Res Clin Pract. 2000 Sep;50(1):1-16. doi: 10.1016/s0168-8227(00)00160-1.

DOI:10.1016/s0168-8227(00)00160-1
PMID:10936664
Abstract

The contribution of platelets to the pathogenesis and progression of vascular complications in diabetes is supported by several studies. In general, platelets obtained from diabetic subjects show increased adhesiveness and an exaggerated aggregation, both spontaneous and in response to stimulating agents. The causes for this activation are multifold: altered exposure and/or abundance of glycoprotein receptors for agonists and adhesive proteins on the platelet surface, increased binding of fibrinogen, decreased membrane fluidity, altered platelet metabolism and changes in intraplatelet signalling pathways. The altered biophysical state of platelet membrane components in diabetes mellitus may be one of the major determinants of platelet hypersensitivity and hyperfunction and may contribute to impairments in various metabolic pathways, like intensified calcium mobilisation and accentuated thromboxane synthesis and release. Activated platelets interact with other cells, such as endothelial cells and leukocytes as well with the coagulation system in the process of atherosclerosis. Some studies indicated that platelet dysfunction was especially apparent in diabetic subjects with macro- or microangiopathy, while others showed that it may be related to the presence of diabetes mellitus per se. Several pharmaceutical compounds have been developed for the inhibition of platelet activation. However, aspirin treatment is cheap and effective, and aspirin remains to be the drug of choice for diabetic patients. It should be prescribed widely for patients who are at high risk of cardiovascular events.

摘要

多项研究证实了血小板在糖尿病血管并发症发病机制及进展中的作用。总体而言,糖尿病患者的血小板表现出更强的黏附性以及更易出现过度聚集,包括自发聚集以及对刺激剂的反应性聚集。这种激活的原因是多方面的:血小板表面激动剂和黏附蛋白的糖蛋白受体暴露和/或数量改变、纤维蛋白原结合增加、膜流动性降低、血小板代谢改变以及血小板内信号通路变化。糖尿病患者血小板膜成分的生物物理状态改变可能是血小板超敏反应和功能亢进的主要决定因素之一,可能导致各种代谢途径受损,如强化钙动员以及加剧血栓素的合成与释放。在动脉粥样硬化过程中,活化的血小板与其他细胞相互作用,如内皮细胞和白细胞,也与凝血系统相互作用。一些研究表明,血小板功能障碍在患有大血管或微血管病变的糖尿病患者中尤为明显,而其他研究则表明,这可能与糖尿病本身的存在有关。已经开发了几种抑制血小板活化的药物化合物。然而,阿司匹林治疗既便宜又有效,阿司匹林仍然是糖尿病患者的首选药物。对于心血管事件高危患者,应广泛开具此药。

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