Tytgat G N, Rauws E A
Department of Gastroenterology, University of Amsterdam, The Netherlands.
Gastroenterol Clin North Am. 1990 Mar;19(1):183-96.
In almost all patients with genuine nondrug-induced duodenal or gastric ulcer there is evidence of gastric Campylobacter pylori colonization and concomitant inflammation. C. pylori is only demonstrable in the duodenal cap when there is "gastric mucus metaplasia." Suppression or eradication of C. pylori with antibiotic therapy may accelerate duodenal ulcer healing. The relapse rate of duodenal ulcer is less after temporary clearing or permanent eradication of C. pylori. As eradication of C. pylori reduces or eliminates gastric (and duodenal) inflammation, this renders the gastroduodenal mucosa less susceptible to reulceration. Interference with C. pylori status presumably explains the retardation of relapse of duodenal ulcer healing with colloidal bismuth subcitrate.
