MacDougall B R, Dordoni B, Thompson R P, Davis M, Williams R
Clin Chim Acta. 1978 May 16;86(1):121-7. doi: 10.1016/0009-8981(78)90466-7.
The activity of ethanol metabolising enzymes was assessed in 51 patients with alcoholic and non-alcoholic liver disease using tracer doses of [1-14C]ethanol and measuring 14CO2 excretion in the breath. Alcoholic patients with only fatty infiltration of the liver showed significantly increased activity compared with controls. Comparing alcoholic patients with cirrhosis and a serum albumin greater than 28 g/l, activity in those with a recent history of continued heavy drinking was significantly greater than in patients who had abstained from alcohol. In addition, both groups of alcoholic cirrhosis showed significantly more activity than patients with non-alcoholic cirrhosis. The activities of patients with acute alcoholic or viral hepatitis were normal when their prothrombin times were less than 7 sec prolonged, but were reduced when prolongation exceeded 7 sec. These results demonstrate that in chronic alcoholic liver disease, even with cirrhosis, alcohol can still increase the activity of ethanol oxidising enzymes provided hepatic function remains adequate. However, this response is lost in acute liver damage and in chronic alcoholic disease with severe hepatic dysfunction.
采用示踪剂量的[1-¹⁴C]乙醇并测量呼出气体中¹⁴CO₂的排泄量，对51例酒精性和非酒精性肝病患者的乙醇代谢酶活性进行了评估。仅患有肝脏脂肪浸润的酒精性患者与对照组相比，酶活性显著增加。比较血清白蛋白大于28 g/l的酒精性肝硬化患者，近期持续大量饮酒者的酶活性显著高于戒酒者。此外，两组酒精性肝硬化患者的酶活性均显著高于非酒精性肝硬化患者。急性酒精性或病毒性肝炎患者，当凝血酶原时间延长小于7秒时，酶活性正常，但当延长超过7秒时，酶活性降低。这些结果表明，在慢性酒精性肝病中，即使存在肝硬化，只要肝功能保持良好，酒精仍可增加乙醇氧化酶的活性。然而，在急性肝损伤和严重肝功能不全的慢性酒精性疾病中，这种反应消失。
