Breier C, Lisch H J, Drexel H, Braunsteiner H
Atherosclerosis. 1984 Sep;52(3):317-27. doi: 10.1016/0021-9150(84)90062-5.
In order to study the effects of chronic alcoholism, 3 groups of patients were investigated and compared to 10 healthy controls. Group I consisted of 9 heavy drinkers, who exhibited type V hyperlipidemia (HLP) under alcohol intake. Group II consisted of 7 patients, who previously had type V HLP under the influence of alcohol. At the time of the investigation, however, they had ceased alcohol drinking for at least 6 months and were normolipidemic. Group III consisted of 7 heavy drinkers without hyperlipidemia. Compared to controls, group I had significantly decreased plasma concentrations of high density lipoproteins2 (HDL2) and HDL3 (both P less than 0.01); activities of post-heparin lipoprotein lipase (LPL) and hepatic lipase (HTGL) as well were excessively decreased (both P less than 0.01). In group III LPL was also decreased (P less than 0.01), but HTGL was distinctly (P less than 0.01) higher than in controls. No such differences could be demonstrated for the patients of group II. Acute alcohol withdrawal from a patient suffering from alcoholism with HLP led to a sharp increase of LPL with a simultaneous decrease of VLDL within 2 days and a more delayed increase of LDL, HDL2 and HTGL, all reaching normal values within 12 days after cessation of alcohol drinking. With respect to the apolipoprotein (apo) composition of HDL2, patients of group I and group III exhibited a significantly lower percentual content of apo C-I at the expense of a significantly higher content of apo A-II as compared to controls and patients of group II. In group I and II, the percentual content of apo D in HDL2 was significantly higher than in controls and in group III. It is concluded that severe alcohol intake strongly impairs LPL in patients with HLP. The pronounced increase of HTGL in some patients (group III) may protect these individuals from HLP. The increased content of apo D in HDL2 may be a possible primary trait for alcohol-inducible HLP.
为研究慢性酒精中毒的影响，对3组患者进行了调查，并与10名健康对照者进行比较。第一组由9名重度饮酒者组成，他们在饮酒时表现为V型高脂血症（HLP）。第二组由7名患者组成，他们以前在酒精影响下患有V型HLP。然而，在调查时，他们已戒酒至少6个月且血脂正常。第三组由7名无高脂血症的重度饮酒者组成。与对照组相比，第一组的高密度脂蛋白2（HDL2）和HDL3血浆浓度显著降低（均P<0.01）；肝素后脂蛋白脂肪酶（LPL）和肝脂肪酶（HTGL）的活性也过度降低（均P<0.01）。第三组的LPL也降低（P<0.01），但HTGL明显高于对照组（P<0.01）。第二组患者未显示出此类差异。患有HLP的酗酒患者急性戒酒导致LPL在2天内急剧增加，同时极低密度脂蛋白（VLDL）降低，低密度脂蛋白（LDL）、HDL2和HTGL的增加更为延迟，在戒酒12天内均达到正常水平。关于HDL2的载脂蛋白（apo）组成，与对照组和第二组患者相比，第一组和第三组患者的apo C-I百分比含量显著降低，而apo A-II含量显著升高。在第一组和第二组中，HDL2中apo D的百分比含量显著高于对照组和第三组。结论是，重度饮酒会严重损害HLP患者的LPL。一些患者（第三组）中HTGL的显著增加可能使这些个体免受HLP影响。HDL2中apo D含量的增加可能是酒精诱导性HLP的一个可能的主要特征。
