Gastric metaplasia in duodenal ulcer. Histochemical considerations of its pathophysiological significance.

Gastric metaplasia of the duodenal mucosa in biopsy specimens of healed duodenal ulcer and in surgical specimens of perforated duodenal ulcer was investigated using mucin histochemistry and the indirect immunoperoxidase method. Endoscopic methylene blue test was performed prior to biopsy. All specimens from areas showing no dye absorption revealed varying degrees of gastric metaplasia characterized by heterotopic occurrence of gastric-type foveolar cells mainly at the tips of stunted intestinal villi. On average, 31.8% of the total surface length of duodenal mucosa taken from areas showing no dye absorption was occupied by the metaplastic cells. They showed strong reactivities for periodic acid-Schiff (PAS) and galactose oxidase-Schiff sequences, while alcian blue and paradoxical concanavalin A staining, class III, were negative. Immunoperoxidase-PAS double staining revealed a few gastrin and somatostatin cells in foci of gastric metaplasia, but almost no cells containing motilin, secretin, cholecystokinin and gastric inhibitory peptide. Such endocrine cells were scattered in nonmetaplastic mucosa. While such metaplastic change has been regarded as a self-defence mechanism or adaptation of the duodenal mucosa against acid, a local decrease of normal endocrine cells, which allegedly function as acid receptors, may lead to alterations of gastroduodenal interaction. It is suggested that gastric metaplasia is important as one of the pathophysiological mechanisms involved in the recurrence of duodenal ulcer.