Liver cirrhosis patients often have gastric mucosal lesions of various types, but the pathogenesis has been unclear. The present study was performed to examine whether Helicobacter pylori (Hp) act as an aggressive factor by investigating whether an increase of blood ammonia concentration is reflected in the gastric juice. The subjects examined included were 28 normal, healthy, age-matched controls, 20 patients with chronic hepatitis, and 17 patients with liver cirrhosis. Acidity in gastric juice, serum gastrin, serum pepsinogen (PG) I, II and I/II ratio, and ammonia in blood and gastric juice were determined. Hp was examined through four tests; i.e., serum anti-Hp IgG, CLO test, culture, and pathological study. Through the frequency of gastric mucosal lesions was high in the hepatic cirrhosis group, the positive rates of Hp were lower in this group (53%) than in the normal healthy controls (71%). The ammonia concentration in gastric juice was high in the Hp-positive group (p<0.05), but slightly correlation with blood ammonia concentration was observed. The serum PGI/II ratio was low in all Hp-positive groups and even lower in the Hp-positive hepatic disease groups. The ammonia concentration in gastric juice was considered to be less influenced by blood ammonia concentration than by Hp infection. The positive rate of Hp infection was low even in the hepatic disease group with high blood ammonia concentration, and are believed to play a more primary role than Hp infection in the development of gastric mucosal lesions which complicate hepatic function disorders factors such as mucosal blood flow
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