Helicobacter pylori and perturbations in acid secretion: The end of the beginning
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Cited by (21)
Chromoendoscopy points the way to understanding recovery of gastric function after Helicobacter pylori eradication
2006, Gastrointestinal EndoscopyNoninvasive versus histologic detection of gastric atrophy in a hispanic population in North America
2006, Clinical Gastroenterology and HepatologyPathogenesis of duodenal ulcer disease: The rest of the story
2000, Bailliere's Best Practice and Research in Clinical GastroenterologyH. pylori in the pathogenesis of duodenal ulcer: Interaction between duodenal acid load, bile, and H. pylori
2000, American Journal of GastroenterologyCitation Excerpt :The duodenal acid load has at least two components: acid secretion by the stomach, and neutralization of acid in the duodenum (39–42). There are a number of factors that are reversed after cure of H. pylori infection and that promote an increase in duodenal acid load, such as an H. pylori-associated inhibition of the effect of antral distention on acid secretion and impaired duodenal bicarbonate secretion (43–45). Duodenal ulcer disease is also associated with a reduction in size and motility of the duodenal bulb, as well as replacement of normal villous architecture by gastric metaplasia; and areas of gastric metaplasia in the duodenal bulb have also been shown to be capable of local acid secretion (5, 46).
Relationship between antral lymphocyte density and basal gastrin levels in patients with Helicobacter pylori infection
2000, Digestive and Liver DiseaseThe role of the host versus the environment in duodenal ulcer disease
1999, Journal of Physiology Paris
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