Christian Schulz1, Kerstin Schütte1,2, Nino Reisener1, Julia Voss1, Peter Malfertheiner1
1) Department of Gastroenterology, Hepatology and Infectious Diseases,
Otto von Guericke University of Magdeburg, Magdeburg
2) Department of Internal Medicine and Gastroenterology, Niels-Stensen-Kliniken, Marienhospital Osnabrück, Osnabrück, Germany
ABSTRACT Background: Ammonia is a critical factor in the pathogenesis of minimal hepatic encephalopathy (MHE). Most of the ammonia is from bacterial production in the intestinal tract. Non-absorbable antibiotics and non-absorbable disaccharides are therefore the therapy of choice. A few studies have addressed the effect of ammonia produced by H. pylori in the pathogenesis of MHE.
Methods: In this prospective clinical trial, 84 consecutive patients with liver cirrhosis (LC) underwent laboratory, psychometric und neurophysiological testing to determine serological H. pylori status, MHE and blood ammonia levels. Relevant clinical and demographic characteristics were documented.
Results: Out of 84 LC patients (83% male), 29% presented with MHE as assessed by critical flicker frequency analysis (CFF). The prevalence of H. pylori infection in the cohort was 21%; 22% of H. pylori-infected patients presented with MHE according to the criterion of a positive CFF result. If the criterion for MHE was a positive CFF and a positive NCT-A result, then 17% of H. pylori positive patients suffered from MHE. The prevalence of MHE in H. pylori-negative patients, based on CFF alone and on the combination, was 30%. A proportion of 19% of the patients with MHE had increased blood ammonia levels.
Conclusion: The amount of ammonia produced by H. pylori does not affect venous ammonia levels. Therefore, an additional benefit of H. pylori eradication in the treatment of hepatic encephalopathy in patients with LC is unlikely to occur.