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不同阶段HIV-1感染中脂蛋白(a)、前列腺素I(2)合成刺激血浆因子、前列腺素I(2)的生物半衰期与高密度脂蛋白的关联

Association of lipoprotein(a), prostaglandin I(2)--synthesis stimulating plasma factor, biological half-life of prostaglandin I(2)and high-density lipoproteins in HIV-1 infection of different stages.

作者信息

Kritz H, Efthimiou Y, Stamatopoulos J, Najemnik C, Sinzinger H

机构信息

Wilhelm Auerswald Atherosclerosis Research Group (ASF), Vienna, Austria.

出版信息

Prostaglandins Leukot Essent Fatty Acids. 2000 Nov;63(5):309-14. doi: 10.1054/plef.2000.0219.

DOI:10.1054/plef.2000.0219
PMID:11090258
Abstract

Patients with human immunodeficiency virus show increased atheroembolism and premature arterial events (stroke, myocardial infarction), but no increased venous thromboembolism. This paper describes an association of elevated lipoprotein(a), a decreased prostaglandin I(2)(PGI(2)) synthesis stimulating plasma factor, diminished PGI(2)-stability in plasma and decreased high-density lipoprotein-cholesterol and apolipoprotein A. It is unclear to what extent these biochemical findings represent an acute phase reaction only or a disturbance in the prostaglandin system. Definitely, they are resulting in severe hemostatic imbalance decreasing local PGI(2)-availability with a dramatic reduction in the cytoprotective capacity favouring the onset of premature arterial events seen in some of the patients.

摘要

人类免疫缺陷病毒感染者发生动脉粥样硬化栓塞和过早出现动脉事件(中风、心肌梗死)的风险增加,但静脉血栓栓塞风险并未增加。本文描述了脂蛋白(a)升高、刺激血浆因子的前列腺素I(2)(PGI(2))合成减少、血浆中PGI(2)稳定性降低以及高密度脂蛋白胆固醇和载脂蛋白A降低之间的关联。目前尚不清楚这些生化结果在何种程度上仅代表急性期反应或前列腺素系统的紊乱。可以肯定的是,它们导致了严重的止血失衡,降低了局部PGI(2)的可用性,同时细胞保护能力大幅下降,这有利于某些患者过早出现动脉事件。

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