41.   That gastric metaplasia develops in response to acid hypersecretion has been found both experimentally and in human studies.

42.   In a limited number of patients, however, who were treated continuously with omeprazole, we found an appreciably reduced extent of gastric metaplasia.

43.   Gastric metaplasia is probably a non-specific response to injury.

44.   Even among subjects examined at least three years after successful treatment of H pylori infection, the extent of gastric metaplasia did not change significantly.

45.   We do realise that the large variability when estimating the extent of gastric metaplasia is one of the important limitations of any endoscopic study.

46.   So far, no prospective study has been performed to investigate the natural history of gastric metaplasia.

47.   Duodenitis and gastric metaplasia, which is often colonised by Helicobacter pylori, are increasingly recognised for their importance in the pathogenesis of duodenal ulcers.

48.   H pylori positive gastritis, and the combination of active duodenitis and gastric metaplasia were independent predictors of duodenal ulceration.

49.   The two groups were similar with respect to the number of smokers, patients with gastric H pylori, gastric metaplasia, and duodenal ulcers.

50.   Similar to patients with active chronic duodenitis, most of the patients with duodenal ulcers were also found to have gastric metaplasia.