GASTRIC METAPLASIA AND DUODENAL-ULCER DISEASE IN CHILDREN INFECTED BYHELICOBACTER-PYLORI

Background-Helicobacter pylori infection of the gastric mucosa is vita l in the pathogenesis of duodenal ulcer disease. H pylori will only co lonise gastric epithelium and its association with duodenal disease is therefore not easily explained. Aims-To determine if gastric metaplas ia in the duodenum increases the risk of duodenal ulcer disease in chi ldren infected with H pylori. Patients-All children undergoing upper e ndoscopy over a 20 month period in a children's hospital in Ireland. M ethods-Two biopsy specimens were obtained from the antral mucosa and t wo from the first part of the duodenum. One antral biopsy specimen was used in a rapid urease test (Clo Test). Biopsy sections were stained with haematoxylin and eosin and also with cresyl violet for identifica tion of H pylori. Periodic acid Schiff (PAS) stain was performed to id entify areas of gastric metaplasia. Results-Gastric and duodenal biops y specimens were obtained from 148 patients (M:F 1 . 2:1). Twenty five children (17%) had H pylori positive gastritis. Thirty four children (23%) had gastric metaplasia in the duodenum. Nine per cent of childre n under the age of 8 years had gastric metaplasia compared with 38% in those 12 years of age or over (p<0.005). Seven children had duodenal ulcer disease. Gastric metaplasia was present in six of seven (86%) ch ildren with duodenal ulcer disease compared with 28 of 141 (20%) witho ut ulceration (p<0.001). While both H pylori and gastric metaplasia we re each significant risk factors for duodenal ulcer disease, the combi ned presence of both factors was associated with a pronounced increase in duodenal ulcer disease. Duodenal ulcer disease occurred in over 50 % of children with both H pylori infection and gastric metaplasia. In contrast duodenal disease did not occur in children (0 of 100) when bo th were absent. Conclusion-The presence of gastric metaplasia in the d uodenum is the major risk factor for duodenal ulcer disease in patient s colonised by H pylori.