Felaco F M, Pagliano P
Istituto di Malattie Tropicali e Subtropicali, II Universita degli Studi di Napoli.
Infez Med. 1997 Mar;5(1):14-9.
Hepatic encephalopathy is a frequent complication of cirrhosis. Portal-systemic shunts and depression of hepatic function are the primary underlying abnormalities. Arterial blood ammonia levels are frequently elevated during hepatic encephalopathy and are lower when a clinical improvement is established. Glutamine synthesis is part of the metabolic pathway for ammonia cerebral detoxification that induces ATP and glutamate (excitatory neurotransmitter) depletion. Plasma levels of branched chain amino acids are reduced in patients with cirrhosis, this event allows aromatic amino acids to cross the hemato-liquoral barrier through exchange with glutamine. Cerebral excess of aromatic amino acids promotes the synthesis of octopamine and feniletiletanolamine, weak neurotransmitters. Benzodiazepine-like substances may affect GABA-ergic transmission by interacting with their receptors on the GABA-benzodiazepine complex. Therapy is aimed at controlling the events that may precipitate the acute encephalopathy, at reducing the ammonia levels, and correcting the neurotransmission abnormalities.
肝性脑病是肝硬化常见的并发症。门体分流和肝功能减退是主要的潜在异常。肝性脑病时动脉血氨水平常升高，临床改善时则降低。谷氨酰胺合成是氨脑解毒代谢途径的一部分，该途径会导致三磷酸腺苷（ATP）和谷氨酸（兴奋性神经递质）耗竭。肝硬化患者血浆支链氨基酸水平降低，这使得芳香族氨基酸通过与谷氨酰胺交换穿过血脑屏障。脑内芳香族氨基酸过量会促进章鱼胺和苯乙醇胺的合成，这两种都是弱神经递质。苯二氮䓬类物质可能通过与γ-氨基丁酸（GABA）-苯二氮䓬复合物上的受体相互作用来影响GABA能传递。治疗旨在控制可能引发急性脑病的因素，降低血氨水平，并纠正神经传递异常。
