Background and study aim: Ammonia plays a major role in hepatic encephalopathy pathogenesis. Most of ammonia is known to be produced by the action of colonic bacteria which possess a urease enzyme activity. H. pylori which infects the stomach possesses a stronger urease activity which produce a large amount of ammonia that may precipitate hepatic encephalopathy (HE). The aim of the present study is to determine the correlation between Helicobacter pylori infection and HE  in patients with liver cirrhosis.
Patients and Methods: One hundred patients (50 patients of liver cirrhosis with hepatic encephalopathy and 50 patients of liver cirrhosis without hepatic encephalo-pathy) were evaluated for presence of H. pylori by stool antigen test (ELISA method) and for blood ammonia level estimation.
Results: Pevalence of H. pylori infection in the study groups (patients of liver cirrhosis with and without hepatic encephalopathy) was 70% (liver cirrhosis with hepatic encephalopathy group (A) 80%, and liver cirrhosis without hepatic encephalopathy group (B) 60%). Mean blood ammonia levels were: 82.14± 47.9 mmol/l for group A (liver cirrhosis with hepatic encephalopathy) and 36.44± 17.9 mmol/l for group B (liver cirrhosis without hepatic encephalopathy). Prevalence of H. pylori and blood ammonia level were found significantly increasing with the severity and the degree of hepatic encephalopathy.
Conclusion: There is a significant association between H. pylori and hepatic encephalopathy in patients with liver cirrhosis. There may be a role of anti-H. pylori therapy in patients of hepatic encephalopathy and should be investigated further.