Helicobacter pylori infection does not correlate with plasma ammonia concentration and hepatic encephalopathy in patients with cirrhosis

Background/Aims: In patients with cirrhosis, infection of the stomach with Helicobacter pylori may increase ammonia production and, consequently, the incidence of hepatic encephalopathy. To test this hypothesis a retrospectiv e analysis was performed in patients with a transjugular intrahepatic porto systemic shunt. These patients are regarded to be ideal candidates for such a study since they have a high bioavailability of gut-derived ammonia and many of them develop spontaneous hepatic encephalopathy. Methodology: In 132 patients (Child-Pugh class A: 24%, B: 49%, C: 27%) with stable transjugular intrahepatic portosystemic shunt function for more tha n 3 months (mean follow-up: 15.5 +/- 10.8 months) the diagnosis of H. pylor i infection was established by a specific and sensitive immunoblot assay fo r IgG- and IgA-antibodies. During follow-up, hepatic encephalopathy was ass essed by clinical examination and a structured questionnaire. Venous plasma ammonia concentration was measured at the time of antibody determination ( end of study period). Results: Eighty-four patients (64%) had negative and 48 patients (36%) had positive immunoblots for H.pylori. The groups were comparable with respect to age, gender, etiology of cirrhosis, Child-Pugh class, follow-up after tr ansjugular intrahepatic portosystemic shunt, and shunt function. The ammoni a concentrations of the patients without (group 1) and with antibodies agai nst H. pylori (group 2) were 73 +/- 27 and 69 +/- 28 mu mol/L (mean +/- SD) , respectively. Hepatic encephalopathy occurred in 23 of 84 patients (27%) of group 1 and in 11 of 48 patients (23%) of group 2. Conclusions: A positive immunoblot for H. pylori antibodies neither correla tes with plasma ammonia concentration nor with the incidence of hepatic enc ephalopathy in patients with cirrhosis of the liver and portosystemic shunt .