Gastric atrophy and intestinal metaplasia in Helicobacter pylori infection.

To the Editor: We read with great interest the article by Guarner et al. (1), in which the relationship between gastric mucosal atrophy, intestinal metaplasia of the stomach and Helicobacter pylori, was evaluated in children. They observed atrophy and/or intestinal metaplasia in 12 of 19 (63%) children with H. pylori infection (mean age, 8.9 years). Atrophy alone was observed in 8, intestinal metaplasia alone in 2, and atrophy plus intestinal metaplasia in 2 patients. All patients with intestinal metaplasia were older than 9 years. Atrophy was seen in 10 of 45 (22%) control patients, and none of the controls had intestinal metaplasia. In our clinic, we encountered 175 patients with H. pyloriassociated chronic gastritis between April 2002 and October 2003 (91 females and 84 males; mean age 11.8 years; range, 4–17 years). All underwent upper gastrointestinal endoscopy because of persistent upper gastrointestinal symptoms and gastric biopsies were obtained from antrum and corpus. One antral biopsy was used for a rapid urease test. Patients with other diagnoses, including celiac disease, inflammatory bowel disease, and portal hypertension, were excluded from the study. Biopsy specimens were stained with hematoxylin and eosin. H. pylori-associated chronic gastritis was histologically documented in all patients and graded using the Sydney system (7). Atrophy and/or intestinal metaplasia were detected in only 5 (2.8%) patients. Atrophy and intestinal metaplasia were observed in 1 (15 years, male), atrophy alone in 3 (8.6, 10 and 13.9 years; all female), and intestinal metaplasia alone in 1 (15 years, female). The reported incidence of atrophy and/or intestinal metaplasia with H.pylori infection ranges from 0% to 77.7% in children (1–3). Cohen et al. (2) found no atrophy or metaplasia in 79 biopsy specimens from 15 children (mean age, 10.8 years) with H. pylori infection. In contrast, Ozturk et al. (3) found glandular atrophy and/or intestinal metaplasia in 14 of 18 (77.7%) children with H. pylori infection (mean age, 12.2 years) finding glandular atrophy in 13 and intestinal metaplasia in 14. Our rate of atrophy and/or metaplasia was lower than this but the number of patients included in these studies was lower than ours. Atrophy and/or intestinal metaplasia are frequently observed in gastric biopsy specimens of adults with H. pylori, and both are considered preneoplastic lesions (4,5). This relationship is still controversial in the pediatric population, and the incidence of atrophy and/or intestinal metaplasia is not consistent among published studies (1–3,6). The diagnosis of atrophy is difficult because it requires an adequate number of properly oriented gastric biopsy specimens. Intestinal metaplasia in the stomach has a patchy distribution. Interobserver agreement is poor especially in the evaluation of atrophy (7–9). At present, diagnostic criteria for atrophy and metaplasia in children are not established and are urgently needed. The duration of infection is probably important in this relationship, but the duration of childhood infections is often not known. We wonder whether genetic and/or environmental factors may affect the development of atrophy and/or intestinal metaplasia. The study of Ozturk et al. (3) involves Turkish children as does ours so we can assume that genetic/environmental differences are negligible even though the geographic regions of the studies are different. In conclusion, the relationship between these lesions and H. pylori infection in children is not as strong as it is in adults. Many factors may be responsible for this difference, such as the type of H. pylori, host immunologic response, genetic and environmental factors, interpretational variability, stains used, and adequacy of biopsy specimen orientation. Additional studies are needed to evaluate this relationship more precisely and the Sydney system needs to be improved in children.