肝性脑病发病机制中的多器官交互作用
DOI: 10.12449/JCH260533
利益冲突声明:本文不存在任何利益冲突。
作者贡献声明:赵子昕负责拟定文章思路,并起草和修改文章的关键内容;祝叶青负责搜集参考文献;叶存心负责图片制作;宋卓芫负责文章格式修改与投稿;宋冬负责指导文章撰写以及最终定稿。
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摘要: 肝性脑病是肝硬化等终末期肝病常见且严重的并发症,其本质是由于急性或慢性肝功能严重障碍或门体分流引起的以代谢紊乱为基础的神经精神异常综合征。临床实践中,肝性脑病的发作与血氨水平并非完全线性相关,常由肝外因素诱发,提示其发病机制中存在多器官间的复杂交互。本文基于氨中毒、炎症、神经递质失衡及氧化/硝化应激4种主要发病机制,系统阐述肝性脑病中的多器官交互作用机制,并结合肌少症、糖尿病等新兴风险因素展开讨论,旨在为深入探究肝性脑病的病理生理机制及未来临床诊疗策略的制定提供新的理论依据。Abstract: Hepatic encephalopathy is a common and serious complication of end-stage liver diseases such as liver cirrhosis, and it is basically a neuropsychiatric syndrome resulting from metabolic disorders caused by severe acute or chronic liver dysfunction or portosystemic shunt. In clinical practice, the onset of hepatic encephalopathy does not completely correlate linearly with the level of blood ammonia and is often triggered by extrahepatic factors, suggesting the presence of complex multiorgan crosstalk in the pathogenesis of hepatic encephalopathy. Based on the four main pathogeneses of ammonia toxicity, inflammation, neurotransmitter imbalance, and oxidative/nitrosative stress, this article systematically elaborates on the mechanism of multiorgan crosstalk in hepatic encephalopathy and discusses the emerging risk factors such as sarcopenia and diabetes mellitus, in order to provide a novel theoretical framework for deepening the understanding of the pathophysiological mechanisms of hepatic encephalopathy and formulating clinical diagnosis and treatment strategies in the future.
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Key words:
- Hepatic Encephalopathy /
- Pathologic Processes /
- Multiorgan Crosstalk
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