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Does disordered upper gastrointestinal motility predispose to Helicobacter pylori colonization of the stomach in
R Rintala1, M L Kokkonen, H Lindahl
1Department of Pediatric Surgery, Children's Hospital, University of Helsinki, Finland.
Insights
Helicobacter pylori colonization is common in children with gastroesophageal reflux and duodenal atresia. These conditions may increase H. pylori infection risk due to impaired motility.
Area of Science:
- Pediatric Gastroenterology
- Infectious Diseases
- Microbiology
Background:
- Helicobacter pylori is a key factor in chronic gastritis and ulcers.
- Mechanisms of H. pylori colonization in children remain unclear.
Purpose of the Study:
- To evaluate the prevalence of H. pylori colonization in pediatric patients undergoing upper gastrointestinal endoscopy.
- To identify patient groups with a higher risk of H. pylori infection.
Main Methods:
- A 12-month study of 266 children undergoing endoscopy.
- H. pylori detection using histology and rapid urease testing.
Main Results:
- Overall H. pylori prevalence was 11.6% (31/266).
- High prevalence observed in operated duodenal atresia (36%) and reflux esophagitis (47%) groups.
- Infection rates ranged from 2-14% in other groups.
Conclusions:
- Disturbed esophagogastroduodenal motility, linked to reflux and duodenal atresia, may predispose children to H. pylori infection.
- Highlights potential risk factors for H. pylori in pediatric populations.
Abstract:
Helicobacter pylori is an important factor in the pathogenesis of chronic gastritis and gastroduodenal ulcer disease. However, the basic causal mechanisms of H pylori colonization on the gastric mucosa are still unclear. The authors evaluated the prevalence of H pylori colonization in 266 children who underwent upper gastrointestinal endoscopy during a 12-month period. The indications for endoscopy were follow-up of esophagitis related to gastroesophageal reflux (n = 17), suspicion of gastroesophageal reflux (n = 51), abdominal pain (n = 28), vomiting (n = 30), follow-up of esophageal atresia (n = 46) and duodenal atresia (n = 28), inflammatory bowel disease (n = 28), and miscellaneous (n = 38). The methods used to detect H pylori colonization were histology and the rapid urease test. H pylori colonization was demonstrated in 31 (11.6%) of the 266 patients. In two patient groups, a high prevalence of colonization was identified. In patients with an operated duodenal atresia, 36% (10 of 28) had H pylori on the gastric mucosa. The organism was demonstrated on the gastric mucosa in 47% (8 of 17) of the patients with gastroesophageal reflux-related esophagitis; five of the eight patients had neurological impairment. In the other patient groups, the prevalence of H pylori infection ranged from 2% to 14%. The present study suggests that, in children, the disturbed esophagogastroduodenal motility, which is commonly associated with gastroesophageal reflux and duodenal atresia, predisposes to H pylori infection.