Role of Helicobacter pylori infection in the pathogenesis of minimal hepatic encephalopathy and effect of its eradication.

Background and Aim Helicobacter pylori (H. pylori) bacteria convert urea to ammonia, which has been implicated in causation of hepatic encephalopathy in patients with liver cirrhosis. The role of H. pylori infection in causation of minimal hepatic encephalopathy (MHE) has not been well studied. We looked at the relationship of H. pylori infection with MHE and hyperammonemia in patients with liver cirrhosis and the effects of anti-H. pylori treatment in patients with MHE and H. pylori infection. Methods Patients with liver cirrhosis underwent psychometric tests for detection ofMHE, rapid urease test to look for evidence of H. pylori infection and measurement of fasting blood ammonia levels. Patients with MHE were treated with triple-drug anti-H. pylori treatment for one week. Rapid urease test, blood ammonia levels, and psychometric tests were repeated four weeks after treatment. Results H. pylori infection was found more often in patients with MHE (63%) than in those without MHE (37%). Blood ammonia levels were significantly higher in patients with MHE than those without. After H. pylori treatment in patients with MHE, blood ammonia levels showed a significant decline and psychometric test results returned towards normal. Conclusion In patients with liver cirrhosis, there is a significant association between H. pylori infection and MHE. Anti-H. pylori therapy results in reduction in blood ammonia levels and improvement in MHE.