Barrison I G, Viola L, Murray-Lyon I M
Prostaglandins Leukot Med. 1983 Mar;10(3):331-44. doi: 10.1016/0262-1746(82)90088-9.
Impaired platelet aggregation is a common finding in patients with alcoholic liver disease. This may be due to impairment of prostaglandin synthesis and alterations in the proportions of platelet membrane lipids secondary to changes in circulating lipids. Platelet prostaglandin synthesis was measured by the production of malonaldehyde (MDA), and was increased in patients with alcoholic cirrhosis compared with normal controls. Mean MDA production in cirrhotics was 3.37 nmoles MDA/10(9) platelets, and in controls 1.01 nmoles MDA/10(9) platelets (p less than 0.01). Platelet prostaglandin synthesis was significantly related to the serum cholesterol:triglyceride ratio (r = 0.73, p less than 0.005). Platelet aggregation was impaired in 12/14 cirrhotics. Five of the cirrhotics had a factor in their plasma which appeared to enhance the aggregation of normal platelets. Impaired platelet aggregation in patients with alcoholic liver disease appears to be due to a defect in intraplatelet metabolism.
血小板聚集功能受损是酒精性肝病患者的常见表现。这可能是由于前列腺素合成受损以及循环脂质变化继发的血小板膜脂质比例改变所致。通过丙二醛(MDA)的生成来测定血小板前列腺素合成,与正常对照组相比,酒精性肝硬化患者的该合成增加。肝硬化患者的平均MDA生成量为3.37纳摩尔MDA/10⁹血小板,而对照组为1.01纳摩尔MDA/10⁹血小板(p<0.01)。血小板前列腺素合成与血清胆固醇:甘油三酯比值显著相关(r = 0.73,p<0.005)。14例肝硬化患者中有12例血小板聚集功能受损。其中5例肝硬化患者的血浆中有一个因子,似乎可增强正常血小板的聚集。酒精性肝病患者血小板聚集功能受损似乎是由于血小板内代谢缺陷所致。