EFFECT OF HELICOBACTER PYLORI INFECTION OF GASTRIC MUCOSA ON BLOOD AMMONLA LEVEL IN HEALTHY PERSONS AND IN PATIENTS WITH DECOMPENSATED LIVER CIRRHOSIS

Abstract

Hepatic encephalopathy is a common complication affecting patients with cirrhosis although its pathogenesis and selective occurrence are not fully explained, ammonia toxicity is strongly incriminated. Encephalopathy is precipitated by compounds such as urea, which can contribute to the elevated blood ammonia levels frequently present in symptomatic patients. Bacterial urease contributes significantly to absorbed ammonia. Although this activity is usually attributed to fecal bacteria, the stomach, which possesses strong activity when infected with H. pylori is an alternative site. Urea readily diffuses from blood to the gastric lumen where, in the presence of H. pylori, it is hydrolised to ammonia, which is then rapidly absorbed. As a result H. pylori infection could potentially contribute to the development and severity of encephalopathy. In the present study we assessed the urease activity, lg against H. pylori infection together with intragastric and blood ammonia levels in 40 patients with advanced liver cirrhosis and in 20 healthy controls. Furthermore, patients were furtherly divided according to presence or absence ofH.E. symptoms.