肝性脑病发病机制的研究进展  

Research Progress on Pathogenesis of Hepatic Encephalopathy

作　　者：李梦羽 周希乔[1] LI Mengyu;ZHOU Xiqiao(Department of Gastroenterology, the First Affiliated Hospital of Nanjing Medical University, Nanjing ,210029)

机构地区：[1]南京医科大学第一附属医院消化内科,210029

出　　处：《胃肠病学》2020年第2期116-120,共5页Chinese Journal of Gastroenterology

基　　金：国家自然科学基金(81570522)。

摘　　要：肝性脑病(HE)是一种由急、慢性肝功能障碍或门体分流异常所引起,基于代谢紊乱的轻、重程度不等的神经精神异常综合征,是各种终末期肝病的常见并发症和死亡原因之一。其临床表现可从性格改变、行为异常到意识障碍、昏迷。HE发病机制复杂,经典的氨中毒学说、神经递质改变已被普遍接受,近年提出的炎症反应、肠道菌群、星形胶质细胞早衰、脑血流改变、半通道功能障碍、胆汁酸等学说也日益受到重视。本文就HE发病机制的研究进展作一综述。Hepatic encephalopathy(HE)is a kind of neuropsychiatric syndrome basing on metabolic disorder caused by acute or chronic liver dysfunction or abnormal portosystemic shunt.It is one of the common complications and causes of death in various end-stage liver diseases.The clinical manifestations of patients with HE can vary from personality changes,behavior abnormalities to disturbance of consciousness and coma.The pathogenesis of HE is complex.Theories about ammonia neurotoxicity and alterations in neurotransmitters have been widely accepted.Roles of inflammation,gut microbiota,premature astrocyte senescence,impaired cerebral microcirculation,hemichannel dysfunction,and bile acid also attract much attention.In this review article,the research progress on pathogenesis of HE was briefly summarized.

关 键 词：肝性脑病 氨中毒 星形细胞 胆汁酸和盐类 

分 类 号：R74[医药卫生—神经病学与精神病学]