Jenkins W J, Cakebread K, Palmer K R
Lancet. 1984 May 12;1(8385):1048-9. doi: 10.1016/s0140-6736(84)91453-3.
Two liver biopsies were performed 6 months apart in each of 29 patients with alcoholic liver disease. Hepatic aldehyde dehydrogenase activity was measured on each occasion. The patients were seen regularly and their alcohol consumption was assessed independently. Hepatic aldehyde dehydrogenase activity was unchanged in 17 patients who continued to drink to excess; it rose in 10 patients who significantly reduced their alcohol intake; and it fell dramatically in 2 patients who were virtually abstinent initially, but then began drinking heavily. These results clearly demonstrate that alcohol consumption itself depresses hepatic aldehyde dehydrogenase activity. It is unlikely that the low hepatic aldehyde dehydrogenase activity reported in alcoholics represents a primary abnormality predisposing to alcoholism or alcoholic liver disease.
对29例酒精性肝病患者每隔6个月进行一次肝活检,每次均测定肝醛脱氢酶活性。定期对患者进行检查,并独立评估其酒精摄入量。17例继续过度饮酒的患者肝醛脱氢酶活性未发生变化;10例显著减少酒精摄入量的患者肝醛脱氢酶活性升高;2例最初几乎戒酒但后来开始大量饮酒的患者肝醛脱氢酶活性急剧下降。这些结果清楚地表明,饮酒本身会降低肝醛脱氢酶活性。酗酒者报告的低肝醛脱氢酶活性不太可能是导致酗酒或酒精性肝病的原发性异常。