There is good evidence to suggest that gastric
metaplasia in the proximal duodenum and Helicobacter pylori
gastritis are essential requirements for the development of duodenal ulceration in most cases. Gastric
metaplasia is most likely to be a defence response or adaptation to excess
acid reaching the duodenum. The appearance of gastric-type epithelium over the duodenal villi probably results from substitution by cells migrating from Brunner's gland ducts. These metaplastic foci provide sites for colonization by H. pylori passing through the duodenum; the organisms do not attach to native duodenal epithelial cells. Having colonized the metaplastic areas, H. pylori provokes an active chronic inflammatory response akin to that seen in the gastric mucosa. Active chronic
duodenitis leads to a weakening of mucosal defence against
acid-peptic attack, and erosion and ulceration may ensue. Healing of
ulcers by conventional
acid-reducing treatments does not influence the extent of gastric
metaplasia, (although there may be some reduction with long-term
proton pump inhibitors); nor do such regimens affect the background
duodenitis. Only with eradication of H. pylori is there resolution of
inflammation, but studies to date indicate that eradication alone has no substantial effect on the prevalence or extent of gastric
metaplasia. Nevertheless the elimination of H. pylori appears to remove one of the essential co-factors for duodenal ulceration and the patient can be considered cured, despite the persistence of gastric
metaplasia.