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 retrospective analysis was performed in patients with a transjugular intrahepatic portosystemic 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 than 3 months (mean follow-up: 15.5 +/- 10.8 months) the diagnosis of H. pylori infection was established by a specific and sensitive immunoblot assay for IgG- and IgA-antibodies. During follow-up, hepatic encephalopathy was assessed 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 transjugular intrahepatic portosystemic shunt, and shunt function. The ammonia concentrations of the patients without (group 1) and with antibodies against 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 correlates with plasma ammonia concentration nor with the incidence of hepatic encephalopathy in patients with cirrhosis of the liver and portosystemic shunt.