Inflammation:A novel target of current therapies for hepatic encephalopathy in liver cirrhosis

Hepatic encephalopathy(HE) is a severe neuropsychiatric syndrome that most commonly occurs in decompensated liver cirrhosis and incorporates a spectrumof manifestations that ranges from mild cognitive impairment to coma. Although the etiology of HE is not completely understood, it is believed that m...

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Bibliographic Details
Published in:World journal of gastroenterology : WJG 2015-11, Vol.21 (41), p.11815-11824
Main Authors: Luo, Ming, Guo, Jian-Yang, Cao, Wu-Kui
Format: Article
Language:English
Subjects:
Animals
Anti-Inflammatory Agents - therapeutic use
encephalopathy
Pathogenesis
T
Hepatic Encephalopathy - diagnosis
Hepatic Encephalopathy - drug therapy
Hepatic Encephalopathy - etiology
Hepatic Encephalopathy - metabolism
Humans
Inflammation Mediators - antagonists & inhibitors
Inflammation Mediators - metabolism
Inflammation
Hepatic
Liver Cirrhosis - complications
Liver Cirrhosis - diagnosis
Review
Signal Transduction - drug effects
Treatment Outcome
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Summary:Hepatic encephalopathy(HE) is a severe neuropsychiatric syndrome that most commonly occurs in decompensated liver cirrhosis and incorporates a spectrumof manifestations that ranges from mild cognitive impairment to coma. Although the etiology of HE is not completely understood, it is believed that multiple underlying mechanisms are involved in the pathogenesis of HE, and one of the main factors is thought to be ammonia; however, the ammonia hypothesis in the pathogenesis of HE is incomplete. Recently, it has been increasingly demonstrated that inflammation, including systemic inflammation, neuroinflammation and endotoxemia, acts in concert with ammonia in the pathogenesis of HE in cirrhotic patients. Meanwhile, a good number of studies have found that current therapies for HE, such as lactulose, rifaximin, probiotics and the molecular adsorbent recirculating system, could inhibit different types of inflammation, thereby improving the neuropsychiatric manifestations and preventing the progression of HE in cirrhotic patients. The antiinflammatory effects of these current therapies provide a novel therapeutic approach for cirrhotic patients with HE. The purpose of this review is to describe the inflammatory mechanisms behind the etiology of HE in cirrhosis and discuss the current therapies that target the inflammatory pathogenesis of HE.
ISSN:1007-9327
2219-2840
DOI:10.3748/wjg.v21.i41.11815