Ammonia is considered to play a central role in the pathogenesis of (minimal) hepatic encephalopathy ((M)HE). Bacterial urease activity is the regulatory enzyme, and bacteria colonizing the colon were originally assumed to be the main source of urease activity. Current concepts of the pathogenesis of (M)HE focus, among other things, on ammonia, which is generated both by urease activity of intestinal bacteria and by Helicobacter pylori in the stomach.Aim:
The aim of this study was to provide a systematic review of the role of H. pylori in the pathogenesis of HE.Methods:
A systematic review was conducted following the recommendations in the Preferred Reporting Items for Systematic reviews and Meta-Analysis (PRISMA) statement with a database search in PubMed, Scopus, and the Cochrane Database for all original contributions published from January 1950 to December 2013. As search terms in title and abstract, the following combinations were used: hepatic encephalopathy AND Helicobacter pylori, HE AND Helicobacter pylori, MHE AND Helicobacter pylori, hyperammonemia AND Helicobacter pylori, and minimal hepatic encephalopathy AND Helicobacter pylori, with a language restriction to English and German.Results:
Observational studies revealed conflicting results concerning a possible role of H. pylori infection in the pathogenesis of HE. Thirteen prospective clinical trials assessed the effect of H. pylori eradication in patients with HE and liver cirrhosis. Seven of these showed a beneficial effect of eradication therapy on (M)HE. All of these studies were highly diverse in design and methodology.Conclusions:
Eradication therapy in H. pylori-positive cirrhotic patients may have a beneficial influence on hyperammonemia and (M)HE, but evidence from well-designed clinical studies is weak.