Y Elitsur1, W E Triest. 1. Department of Pediatrics, Cabell Huntington Hospital, Marshall University School of Medicine, Huntington, West Virginia 25701-0195, USA.
Abstract
BACKGROUND: Duodenal gastric metaplasia (DGM) is commonly found in association with Helicobacter pylori (Hp)-associated gastritis in adults. DGM is also considered a risk factor for duodenal ulcer development. The prevalence of DGM in children and its association with gastritis, duodenitis, or the presence of Hp organisms is not clear. We investigated the prevalence of DGM in children and explore its association with several possible risk factors, including age, gender, gastritis, duodenitis, or Hp presence in the gastric antrum. METHODS: A retrospective analysis of 173 upper endoscopy procedures performed between 1993 and 1995 at Cabell Huntington Hospital, Huntington, WV, was done. Gastric and duodenal biopsies were stained with Giemsa for Hp detection, periodic acid-Schiff for DGM, and hematoxylin and eosin for histologic assessment. Gastric mucosal inflammation was graded according to Sydney criteria. RESULTS: Duodenal gastric metaplasia was identified in 23 of 173 (13%) patients. Duodenitis but not age, gender, gastritis, or the presence of Hp in the gastric antrum was associated with DGM development. In 4 of 23 DGM foci, Hp was identified. CONCLUSIONS: In children, DGM is not the consequence of Hp infection.
BACKGROUND: Duodenal gastric metaplasia (DGM) is commonly found in association with Helicobacter pylori (Hp)-associated gastritis in adults. DGM is also considered a risk factor for duodenal ulcer development. The prevalence of DGM in children and its association with gastritis, duodenitis, or the presence of Hp organisms is not clear. We investigated the prevalence of DGM in children and explore its association with several possible risk factors, including age, gender, gastritis, duodenitis, or Hp presence in the gastric antrum. METHODS: A retrospective analysis of 173 upper endoscopy procedures performed between 1993 and 1995 at Cabell Huntington Hospital, Huntington, WV, was done. Gastric and duodenal biopsies were stained with Giemsa for Hp detection, periodic acid-Schiff for DGM, and hematoxylin and eosin for histologic assessment. Gastric mucosal inflammation was graded according to Sydney criteria. RESULTS: Duodenal gastric metaplasia was identified in 23 of 173 (13%) patients. Duodenitis but not age, gender, gastritis, or the presence of Hp in the gastric antrum was associated with DGM development. In 4 of 23 DGM foci, Hp was identified. CONCLUSIONS: In children, DGM is not the consequence of Hp infection.