Related Experiment Videos
Helicobacter pylori-dependent intragastric urea biodegradation in children: diagnostic and pathogenetic importance
1Children's Republican Hospital, Bashkortostan, Ufa, Russia.
Insights
Helicobacter pylori infection in children causes gastritis by increasing gastric ammonia. This ammonia is a key factor in childhood acid-peptic disease, impacting urea levels in the stomach.
Area of Science:
- Pediatric Gastroenterology
- Microbiology
- Pathogenesis Research
Background:
- Helicobacter pylori (H. pylori) infection is prevalent in children with abdominal complaints.
- Urease activity of H. pylori contributes to gastric pathology.
- The role of H. pylori urease in childhood acid-peptic disease requires further elucidation.
Purpose of the Study:
- To investigate the link between intragastric urea hydrolysis by H. pylori urease and acid-peptic disease in pediatric patients.
- To assess the relationship between H. pylori infection, urease activity, and gastritis severity in children.
Main Methods:
- Analysis of urea and ammonia concentrations in gastric juice from 91 children with upper abdominal pain.
- Detection of H. pylori infection using standard diagnostic methods.
- Correlation of gastritis scores with gastric juice urea and ammonia levels, and H. pylori dissemination.
Main Results:
- H. pylori infection was identified in 76.9% of patients, including all with peptic ulcer disease.
- H. pylori-positive children showed decreased gastric urea and increased ammonia compared to H. pylori-negative children (P < 0.001).
- Gastritis severity and H. pylori dissemination correlated significantly with gastric ammonia levels.
Conclusions:
- H. pylori plays a critical role in the pathogenesis of childhood gastritis.
- Elevated gastric ammonia, resulting from H. pylori urease activity, is a significant pathogenic factor in childhood acid-peptic disease.
Abstract:
The objective of the present work was to study the relationship between intragastric urea hydrolysis generated by Helicobacter pylori urease and acid-peptic disease in childhood. Intragastric urease activity was examined by urea and ammonia concentration measurement in gastric juice in 91 children with upper abdominal complaints. Helicobacter pylori infection was detected from 70 (76.9%) of 91 patients, including all of the 15 subjects with peptic ulcer disease. Helicobacter pylori-related gastritis in children was associated with a decrease of urea and an increase of ammonia in gastric juice (P < 0.001) in comparison with H. pylori-negative children. The gastritis score was correlated with the concentrations of urea and ammonia in the gastric juice of patients infected with H. pylori. There was a significant correlation between the histologically detected dissemination of organisms and gastric ammonia levels. Similar results were obtained concerning correlation between gastric juice ammonia and anti-H. pylori specific immunoglobulin G versus highly purified antigen of H. pylori containing urease. Present findings prove that H. pylori plays an essential role in the pathogenesis of gastritis and that ammonia is one of the main pathogenic factors of acid-peptic disease.