There is a scientific agreement that portal systemic encephalopathy (PSE) is caused morphologically by portal systemic shunts and biochemically by constituents of the portal venous blood. Ammonia has a key role in the pathogenesis of PSE. In PSE, ammonia is probably responsible for damage to astrocytic and neuronal cells. Ammonia toxic effect is due to the intracerbral glutamine synthesis. Although colonic bacteria are considered the main source of ammonia, the stomach in subjects with urease producing Helicobacter pylori (H. Pylori) is an alternative site. In addition to ammonia produced in the intestinal lumen, ammonia generated in the stomach by urease producing. H. pylori has recently been suggested to contribute substantially to blood ammonia levels and to precipitate or exacerbate hepatic encephalopathy in patients with cirrhosis. It was reported that eradication of gastric H.pylori infection in addition to the conventional treatment of hepatic encephalopathy can decrease hyperammonemia and thus improving hepatic encephalopathy.