Baumgartner H P, Filippini L
Schweiz Med Wochenschr. 1977 Oct 8;107(40):1406-11.
Tests on 100 alcoholic patients revealed increased lipoprotein levels in 24%. Type IV was the most frequently ecountered (80%), followed by type II or V. The average plasma triglyceride level of the alcoholic group was significantly increased in comparison with a control population. The causal mechanism of alcoholic hyperlipoproteinemia remains poorly understood. The combination of a genetic defect of lipid metabolism, nutritional factors and acute alcohol excess may have an essential bearing on the incidence of hyperlipoproteinemia. Acute excessive intake of alcohol was significantly increased in comparison with alcoholic subjects wihtout hyperlipoproteinemia. The critical dose may be a daily ethanol consumption of about 200 gm. There appeared to be no correlation between acute pancreatic injury or active liver disease and serum lipid elevation. On the other hand, the observation was confirmed that alcoholic patients with hepatic cirrhosis usually do not develop hyperlipoproteinemia. Ethanol-induced hyperlipoproteinemia may be a risk factor for the development of atherosclerosis and pancreatitis.
对100名酒精性肝病患者的检测显示，24%的患者脂蛋白水平升高。IV型最为常见（80%），其次是II型或V型。与对照组相比，酒精性肝病组的平均血浆甘油三酯水平显著升高。酒精性高脂血症的发病机制仍知之甚少。脂质代谢的遗传缺陷、营养因素和急性酒精摄入过多共同作用，可能是高脂血症发病的关键因素。与无高脂血症的酒精性肝病患者相比，急性酒精摄入过多的情况显著增加。临界剂量可能是每日乙醇摄入量约200克。急性胰腺损伤或活动性肝病与血脂升高之间似乎没有关联。另一方面，有观察证实，肝硬化酒精性肝病患者通常不会发生高脂血症。乙醇诱导的高脂血症可能是动脉粥样硬化和胰腺炎发生的危险因素。
