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Abstract Details
Pathophysiology of Hepatic Encephalopathy
Clin Liver Dis. 2020 May;24(2):175-188. doi: 10.1016/j.cld.2020.01.002.Epub 2020 Feb 19.
Ariel Jaffe1, Joseph K Lim2, Sofia Simona Jakab3
Author information
1Section of Digestive Diseases, Yale Liver Center, Yale University School of Medicine, 333 Cedar Street, LMP 1080, New Haven, CT 06520-8019, USA.
2Section of Digestive Diseases, Yale Liver Center, Yale University School of Medicine, 333 Cedar Street, LMP 1080, New Haven, CT 06520-8019, USA; VA Connecticut Healthcare System, West Haven, Connecticut, USA.
3Section of Digestive Diseases, Yale Liver Center, Yale University School of Medicine, 333 Cedar Street, LMP 1080, New Haven, CT 06520-8019, USA; VA Connecticut Healthcare System, West Haven, Connecticut, USA. Electronic address: simona.jakab@yale.edu.
Abstract
Hepatic encephalopathy (HE) is one of the major clinical decompensations of cirrhosis, with a high impact on health care resource utilization and cost. For an effective and comprehensive management of HE, the clinicians need to understand the pathophysiologic mechanisms of HE. This review describes the multiorgan processes involved in HE and how several HE precipitants and treatment strategies act on ammonia production, excretion, and neurotoxicity, including the impact of diabetes and use of cannabinoids. The authors also discuss the current and future role of gut microbiome, systemic/central inflammation, and various neurotransmitters for the pathogenesis and treatment of HE.