Sitemap | Policies | Feedback    
 About the Journal
Editorial Board
Journal Subscription
Instructions for Authors
E-mail Alerts
Forthcoming Events
Advertise with Us
Contact Us
 
Article Options
FULL TEXT
ABSTRACT
PDF
Printer Friendly Version
Search Pubmed for
Search Google Scholar for
Article Statistics
Bookmark and Share
 
Gastric atrophy and Helicobacter pylori infection in children
 
S Boukthir, 1S Mazigh Mrad, 1 N Kalach, A Sammoud1
Service de Médecine Infantile C Hôpital d’Enfants,
Bab Saadoun 1007 Tunis Jebbari,
Tunisia.1
Clinique de Pédiatrie Saint Antoine Hôpital Saint Vincent de Paul Université Catholique,
Bd de Belfort 59020 Lille,
France2


Corresponding Author
: Dr. Samir Boukthir
Email: aboukthir@yahoo.fr


Abstract

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 andwas significantly associated with H. pylori infection and nodular gastritis.