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Prevalence of Helicobacter pylori Infection in Patients with Minimal Hepatic Encephalopathy
Christian Schulz1, Kerstin Schütte2, Nino Reisener1
1Department of Gastroenterology, Hepatology and Infectious Diseases, Otto von Guericke University of Magdeburg, Magdeburg, Germany.
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.
Insights
Helicobacter pylori (H. pylori) infection does not significantly impact ammonia levels in liver cirrhosis patients. Eradicating H. pylori is unlikely to benefit minimal hepatic encephalopathy (MHE) treatment.
Area of Science:
- Hepatology
- Gastroenterology
- Microbiology
Background:
- Ammonia is a key factor in minimal hepatic encephalopathy (MHE) pathogenesis, primarily from gut bacteria.
- Current treatments for MHE focus on reducing ammonia via non-absorbable antibiotics and disaccharides.
- The role of ammonia produced by Helicobacter pylori (H. pylori) in MHE remains under investigation.
Purpose of the Study:
- To investigate the association between H. pylori infection and MHE in patients with liver cirrhosis (LC).
- To determine if H. pylori contributes to elevated blood ammonia levels in LC patients with MHE.
Main Methods:
- Prospective clinical trial involving 84 liver cirrhosis patients.
- Assessed H. pylori serological status, MHE using critical flicker frequency (CFF) and NCT-A tests, and blood ammonia levels.
- Collected clinical and demographic data.
Main Results:
- 29% of LC patients had MHE (positive CFF).
- H. pylori prevalence was 21%; 17-22% of infected patients had MHE.
- MHE prevalence was 30% in H. pylori-negative patients.
- 19% of MHE patients had elevated blood ammonia.
Conclusions:
- H. pylori infection does not significantly increase venous ammonia levels in LC patients.
- H. pylori eradication is unlikely to provide additional therapeutic benefit for hepatic encephalopathy in this population.
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