J Clin Pathol 58:1189-1193 doi:10.1136/jcp.2005.026310
  • Original article

Atrophic gastritis in young children and adolescents

  1. O Ricuarte1,
  2. O Gutierrez1,
  3. H Cardona1,
  4. J G Kim2,
  5. D Y Graham3,
  6. H M T El-Zimaity4
  1. 1Department of Gastroenterology, National University of Colombia, Bogotá, Colombia
  2. 2Guro Hospital, Korea University College of Medicine, Seoul, Korea
  3. 3Department of Medicine VA Medical Center, and Baylor College of Medicine, Houston, Texas 77030, USA
  4. 4Department of Pathology VA Medical Center, and Baylor College of Medicine
  1. Correspondence to:
 Dr H M T El-Zimaity
 Gastrointestinal Mucosa Pathology Laboratory, Michael E DeBakey VA Medical Center (111-D), Room 3A-320, 2002 Holcombe Blvd, Houston, Texas 77030, USA;
  • Accepted 29 March 2005


Background:Helicobacter pylori associated gastric cancer arises via a multistage process, with atrophic gastritis being the precursor lesion. Helicobacter pylori is typically acquired in childhood, yet little is known of the prevalence of atrophic gastritis in childhood.

Aim: To study atrophic gastritis among children from countries with high gastric cancer incidence.

Methods: Sections from topographically mapped gastric biopsy specimens from children undergoing clinically indicated endoscopy in Korea and Colombia were evaluated using visual analogue scales. Atrophy was defined as loss of normal glandular components, including replacement with fibrosis, intestinal metaplasia (IM), and/or pseudopyloric metaplasia of the corpus (identified by the presence of pepsinogen I in mucosa that was topographically corpus but phenotypically antrum).

Results: One hundred and seventy three children, 58 from Korea (median age, 14 years) and 115 from Colombia (median age, 13 years), were studied. Helicobacter pylori was present in 85% of Colombian children versus 17% of Korean children (p<0.01). Atrophic mucosa near the antrum–corpus border was present in 16% of children, primarily as pseudopyloric metaplasia (31%, IM; 63%, pseudopyloric metaplasia; 6%, both). The median age of children with corpus atrophy was 15 (range, 7–17) years.

Conclusion: Gastric atrophy occurs in H pylori infected children living in countries with high gastric cancer incidence. Identification and characterisation of the natural history of H pylori gastritis requires targeted biopsies to include the lesser and greater curve of the corpus, starting just proximal to the anatomical antrum–corpus junction, in addition to biopsies targeting the antrum and cardia.