Progress in pathogenesis and treatment of type A hepatic encephalopathy in acute liver failure:a comprehensive review
作者机构：Key Lab of Drug Metabolism&PharmacokineticsState Key Laboratory of Natural MedicinesChina Pharmaceutical UniversityNanjing 210009China
出 版 物：《Pharmacology Discovery》
年 卷 期：2024年第4卷第1期
页 面：1-11页
学科分类：1002[医学-临床医学] 100201[医学-内科学(含：心血管病、血液病、呼吸系病、消化系病、内分泌与代谢病、肾病、风湿病、传染病)] 10[医学]
基 金：supported by the National Nature Science Foundation of China(Grants 81974533 81530098)
主 题：type A hepatic encephalopathy ammonia glutamine lactate,inflammation,blood-brain barrier,neurotransmission
摘 要：Hepatic encephalopathy is a serious neuropsychiatric complication caused by liver failure,which is characterized by the development of cognitive and motor disorders into ***,hepatic encephalopathy can be divided into three types(A,B,and C)according to the *** A hepatic encephalopathy(AHE)caused by acute liver failure seriously affects the prognosis of patients,ranging from mild neuropsychological changes to coma,brain edema,and even *** far,the research on the pathogenesis of AHE has focused on the toxic effects of ammonia on the central nervous system,metabolic disorders(glutamine and lactate accumulation),neurotransmission alteration,systemic inflammation,especially *** these mechanisms are not independent,but mutually have synergistic *** clinic,treatment of AHE based on only one mechanism is often *** clarify the pathogenesis and the interaction among the mechanisms will be beneficial to the effective treatment of AHE and reduce the *** aim of this review is to provide comprehensive scientific evidence for the clinical treatment of AHE via collecting and analyzing the latest mechanism of AHE,and clarifying the relationship among these mechanisms combing the investigation of the latest research progress of drug treatment of acute liver ***,we find that the pathogenesis of AHE is a complex neurocognitive disorder shaped by interactions among hyperammonemia,inflammation,and changes in neurotransmission,the signaling pathways thereby integrating the inflammatory and neurological inputs to impact pathophysiological or neurobehavioral outcomes.
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