Nilius R, Zipprich B, Krabbe S
Hepatogastroenterology. 1983 Aug;30(4):134-6.
Acetaldehyde dehydrogenase (ALDH) activity in liver biopsy specimens was considerably reduced in alcoholic cirrhosis (n = 5), elevated in alcoholic fatty liver (n = 11)--probably due to enzyme induction--only slightly elevated in alcoholic hepatitis (n = 6), but unaffected in non-alcoholic liver diseases (n = 23) in comparison with specimens obtained from patients with minimal liver lesions. We will argue as a working hypothesis that alcoholics with induced ALDH activity will mainly develop fatty liver, whereas reduced hepatic ALDH appears to be a reason for elevated acetaldehyde levels followed by additional liver injury and progression at least for alcoholic cirrhosis.
与肝损伤最小的患者的活检样本相比,酒精性肝硬化患者(n = 5)肝活检样本中的乙醛脱氢酶(ALDH)活性显著降低,酒精性脂肪肝患者(n = 11)的该活性升高——可能是由于酶诱导——酒精性肝炎患者(n = 6)的该活性仅略有升高,而非酒精性肝病患者(n = 23)的该活性未受影响。我们将提出一个工作假设,即ALDH活性被诱导的酗酒者主要会发展为脂肪肝,而肝脏ALDH活性降低似乎是乙醛水平升高的一个原因,进而导致额外的肝损伤,并至少会促使酒精性肝硬化病情进展。