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[纤维蛋白溶解与血管疾病]

[Fibrinolysis and vascular diseases].

作者信息

Udvardy M, Boda Z

机构信息

Debreceni Orvostudományi Egyetem, II. Belgyógyászati Klinika.

出版信息

Orv Hetil. 1996 Aug 25;137(34):1851-5.

PMID:8927337
Abstract

A wide array of in vitro fibrinolysis tests had been performed for a long period, suggesting defective fibrinolysis, mainly impaired tPA response and reserve as major, frequent abnormality, predecessor or causative factor of venous thromboembolism. However, these abnormalities were troublesome to reproduce, and more recently fibrinolytic activators and inhibitors received growing attention as rather atherogenic and less thrombogenic risk factors. Even if it is still not settled, lipoprotein(a) may interfere with fibrinolysis, and seems to carry atherogenic risk, too. The genetic polymorphism of fibrinogen, plasminogen, PAI-1 and some other compounds modifying circulating fibrinogen levels are also discussed in this review.

摘要

长期以来已经进行了大量的体外纤维蛋白溶解试验,提示存在纤维蛋白溶解缺陷,主要表现为组织型纤溶酶原激活物(tPA)反应和储备受损,这是静脉血栓栓塞的主要且常见的异常、先兆或致病因素。然而,这些异常难以重现,最近,纤维蛋白溶解激活剂和抑制剂作为动脉粥样硬化风险因素和血栓形成风险较低的因素受到越来越多的关注。即使尚未定论,脂蛋白(a)可能会干扰纤维蛋白溶解,似乎也具有动脉粥样硬化风险。本文还讨论了纤维蛋白原、纤溶酶原、纤溶酶原激活物抑制剂-1(PAI-1)以及其他一些可改变循环纤维蛋白原水平的化合物的基因多态性。

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