Atrophic gastritis in young children and adolescents

Abstract

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.

Figure 1

Mucosal biopsy specimens were obtained from five to six (median, five) predetermined locations. A special effort was made to examine five predetermined sites in all patients, namely: A2, A3, B2, B3, and B4. Grey circles correspond to those recommended by the updated Sydney system. Corpus atrophy, when present, was identified just proximal to the normal antrum–corpus junction (dashed line).

Figure 2

Pseudopyloric metaplasia (arrow) in a 9 year old child as identified by the presence of mucosa that was phenotypically antrum, stained positive for pepsinogen I (PGI), and was anatomically in a region where corpus would be expected. Replacement of oxyntic mucosa with mucous type glands starts as early as 9 years in Colombia. (A) El-Zimaity triple stain; original magnification, ×10. (B) El-Zimaity triple stain; original magnification, ×40. (C) Anti-PGI immunohistochemistry; original magnification, ×10.

Figure 3

The atrophic border location differs between different countries and between different groups within a country (it is more proximal in countries/ethnic groups with a higher risk of gastric carcinoma).