Gastric atrophy and Helicobacter pylori infection in children
S Boukthir1, S Mazigh Mrad, N Kalach
1Service de Médecine Infantile C, Hôpital d'Enfants, Bab Saadoun, 1007 Tunis Jebbari, Tunisia. aboukthir@yahoo.fr
Insights
Gastric atrophy (GA) affects 9.3% of Tunisian children, strongly linked to Helicobacter pylori infection. This study details GA
Area of Science:
- Pediatric Gastroenterology
- Hepatology
- Microbiology
Background:
- Helicobacter pylori is prevalent in Tunisia.
- Gastric atrophy (GA) is a significant precursor to gastric cancer.
- Pediatric GA data is limited, especially in high-prevalence regions.
Purpose of the Study:
- To determine the prevalence of GA in Tunisian children.
- To describe the histological, clinical, and endoscopic characteristics of pediatric GA.
- To investigate the association between GA, H. pylori infection, and endoscopic findings in children.
Main Methods:
- Upper gastrointestinal (UGI) endoscopy with gastric biopsies was performed on 345 children.
- Biopsies were analyzed for histology (updated Sydney classification) and H. pylori culture.
- Children presented with recurrent abdominal pain, vomiting, or gastrointestinal bleeding.
Main Results:
- Gastric atrophy (GA) was identified in 9.3% of children.
- GA was significantly associated with H. pylori infection (93.7% of GA cases).
- Nodular gastritis was a common endoscopic finding in children with GA.
Conclusions:
- Gastric atrophy (GA) is present in 9.3% of Tunisian children undergoing UGI endoscopy.
- GA in children is strongly associated with H. pylori infection.
- Endoscopic findings like nodular gastritis correlate with GA in this pediatric cohort.
Aim:
To assess the prevalence of gastric atrophy (GA) in Tunisia (a high prevalence region for Helicobacter pylori), and describe its histological, clinical and endoscopic features in children.
Methods:
345 children, 151 male and 194 female, mean age 8.6 +/- 3.7 years, underwent upper gastrointestinal (UGI) endoscopy with gastric biopsies for recurrent abdominal pain (n=232, 67.2%), vomiting (n=72, 20%) associated with or without upper gastrointestinal bleeding (n=59, 17.1%) and miscellaneous causes (n=53, 15.4 %). Biopsies performed both in the gastric antrum (n=2) and corpus (n=2) were analysed for histological assessment according to the updated Sydney classification system and bacterial culture. A positive result was recorded where histology and/or culture were positive, confirming the presence of H. pylori infection (H. pylori +ve). A negative result was recorded when both tests were concomitantly negative (H. pylori -ve).
Results:
9.3% (32/345) of the total population, and 14.5% (32/221) of chronic gastritis patients exhibited GA, M/F: 16/16, mean age (SD) 9.4 (3.4) years. Amongst the 32 children with GA, 30 (93.7%) were H. pylori +ve and 2 (6.3%) were H. pylori -ve. GA was localised in the antrum (n=26, 81.2%), the fundus (n=2, 6.3%) and was also seen in both (n=4, 12.5%). GA was categorised as mild, grade 1 (n=18, 56.3%); moderate, grade 2 (n=13, 46.6%); and severe, grade 3 (n=1, 3.1%). GA was associated with mild active gastritis in 18 cases (56.3%). The prevalence of moderate or severe antral GA was detected in 9/26 (34.6%) of H. pylori +ve vs. any of H. pylori -ve (p=0.4), whereas GA in the corpus was detected in 1/2 (50%) vs. none, respectively. None exhibited intestinal metaplasia. There were no clinical features specific to this pathology. UGI endoscopy in GA patients showed nodular gastritis (n=17, 53.1%), congestive gastritis (n=9, 28.1%), and normal tissue (n=6, 18.8%). GA was significantly associated with H. pylori infection (p<0.0001) and nodular gastritis (p<0.005).
Conclusion:
GA was found in 9.3% of Tunisian children undergoing UGI endoscopy and was significantly associated with H. pylori infection and nodular gastritis.
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