Published online Nov 7, 2015. doi: 10.3748/wjg.v21.i41.11815
Peer-review started: April 18, 2015
First decision: May 18, 2015
Revised: June 19, 2015
Accepted: September 14, 2015
Article in press: September 14, 2015
Published online: November 7, 2015
Hepatic encephalopathy (HE) is a severe neuropsychiatric syndrome that most commonly occurs in decompensated liver cirrhosis and incorporates a spectrum of 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 anti-inflammatory 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.
Core tip: Currently, inflammation appears to play a critical role in the pathogenesis of hepatic encephalopathy (HE) and is gradually being considered a critical therapeutic target for HE in patients with liver cirrhosis. Current therapies for HE, including lactulose, rifaximin, probiotics and the molecular adsorbent recirculating system, have been found to improve clinical manifestations and prevent the progression of HE by ameliorating inflammation in cirrhotic patients. This review will provide an overview of the inflammatory pathogenesis of HE, focusing on the recent findings on its therapeutic manipulation.