Pathogenesis of duodenal ulcer disease: the rest of the story

Although several duodenal ulcer disease-specific abnormalities in gastric f unction have been described (e.g. exaggerated gastrin releasing peptide-sti mulated acid secretion and an abnormal sensitivity of the parietal cells to gastrin), none has withstood careful examination. We describe here the cri tical nature of the duodenal acid load in precipitating and washing out bil e salts, which inhibit the growth of Helicobacter pylori (H. pylori) in the development of duodenal ulcer disease. The risk of duodenal ulcer is enhan ced by infection with proinflammatory H. pylori (e.g. with an intact cog pa thogenicity island). Progressive damage to the duodenum promotes gastric me taplasia, resulting in sites for H. pylori growth and more inflammation. Th is cycle results in an increasing inability of the duodenal bulb to neutral ize acid entering from the stomach until changes in duodenal bulb structure and function are sufficient for an ulcer to develop. Cure of the H. pylori infection results in a sustained fall in duodenal acid load as well as a m arked (and continuing) reduction in inflammation, which results in the cure of chronic ulcer disease.