EFFECT OF HELICOBACTER-PYLORI ERADICATION ON GASTRIC METAPLASIA OF THE DUODENUM

Helicobacter pylori associated duodenal ulcers occur in patches of gas tric metaplasia. The pathogenesis of gastric metaplasia is unclear, bu t it has been produced in experimental animals by acute injury and has been shown to be present to a greater extent of H pylori positive sub jects. This study aimed to discover if gastric metaplasia regressed wi th eradication of H pylori or healing of duodenal ulcers, or both. Thi rty two duodenal ulcer patients with H pylori infection confirmed by b iopsy urease test and by antral histological examination were studied. Patients were treated with triple therapy (deNol 240 mg twice daily, amoxycillin 500 mg three times daily, and metronidazole 400 mg three t imes daily) for two weeks after the first endoscopy and were subsequen tly re-endoscoped. Three duodenal bulb biopsy specimens were obtained per patient at each endoscopy. Biopsy sections were stained with haema toxylin and eosin to determine the severity of duodenitis, and with di astase periodic acid-Schiff/alcian blue to assess the extent of gastri c metaplasia. Slides were assessed by two histopathologists unaware of treatment status. H pylori was eradicated in 63% of subjects and all ulcers were healed at follow up. The median extent of gastric metaplas ia at the start of treatment and 6-18 months (median 10) after treatme nt was compared in the two groups. Gastric metaplasia declined in erad icators from 16% to 8% (p<0.05) while in non-eradicators there was no significant change (25% initially and at follow up). A positive relati on between extent of gastric metaplasia and duodenal inflammation scor e was present before treatment (r(s)=0.74, p<0.001) and was unchanged after treatment in the non-eradicator group (r(s)=0.89, p<0.001). In t he eradicator group, however, the inflammation score had significantly declined (p<0.02) and the close relation with gastric metaplasia was no longer present. These results suggest that H pylori itself is at le ast in part responsible for producing gastric metaplasia of the duoden um.