急性肝脏衰竭(以下简称AHF)可致脑病,其生化机理与肝硬化性脑病不同。AHF时血脑屏障的通透性增高,以致加重生化异常的效应,可能也是脑水肿的重要因素。研究工作虽大多致力于正常时由肝脏代谢的“毒物”在血液中的积累,但迄今并未鉴定出单独能引起肝性脑病的一种毒物。过量的氨、硫醇、脂肪酸和异常的氨基酸分析谱均与其发病有关。不管哪一 Acute liver failure (hereinafter referred to as AHF) can cause encephalopathy, its biochemical mechanism and cirrhosis encephalopathy different. AHF increased permeability of the blood-brain barrier, resulting in increased biochemical abnormalities may also be an important factor in brain edema. Although most of the research work is devoted to the accumulation of “poison” normally metabolized by the liver in the blood, no toxicant has been identified to cause hepatic encephalopathy alone. Excess ammonia, thiols, fatty acids and abnormal amino acid profiles are associated with its pathogenesis. No matter which one