1996
DOI: 10.3109/00365529609031624
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Gastric Bicarbonate Secretion and Release of Prostaglandin E2Are Increased in Duodenal Ulcer Patients But Not inHelicobacter pylori-Positive Healthy Subjects

Abstract: Increased mucosal production of PGE2 may be responsible for the abnormally high gastric secretion of bicarbonate in inactive DU patients. The defective duodenal secretion of bicarbonate observed in these patients may be a consequence of previous ulceration rather than the mere presence of H. pylori infection.

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Cited by 24 publications
(16 citation statements)
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“…Their effects on gastrin release are controversial; they have been variously reported to decrease [24] or have no effect on [25] serum gastrin concentration.…”
Section: Discussionmentioning
confidence: 99%
“…Their effects on gastrin release are controversial; they have been variously reported to decrease [24] or have no effect on [25] serum gastrin concentration.…”
Section: Discussionmentioning
confidence: 99%
“…Recent studies demonstrate that there is impaired bicarbonate production in the proximal duodenum of H pylori-infected adult patients with duodenal ulcers (13). Additional studies of gastric acid production and duodenal bicarbonate secretion in H pylori-infected and uninfected children are needed to establish more directed and efficacious therapeutic strategies.…”
Section: Pathogenesis Of Ulcersmentioning
confidence: 99%
“…A recent trial investigated the effect of a clarithromycin and omeprazole combination therapy in 73 patients with H pylori-associated gastroduodenal pathology (69). A negative 13 C-urea breath test determined that H pylori was cleared after two weeks of treatment in 95.9% of the patients and eradicated in 78.1%.…”
Section: H Pylori Treatment Regimens Combination Therapiesmentioning
confidence: 99%
“…This secretion is controlled through central and peripheral neuroendocrine mechanisms. It is a main mechanism of duodenal mucosal defense against acid discharged from the stomach (11) and is deficient in patients with chronic and acute duodenal ulcer disease (16,19,29).…”
mentioning
confidence: 99%
“…This secretion is controlled through central and peripheral neuroendocrine mechanisms. It is a main mechanism of duodenal mucosal defense against acid discharged from the stomach (11) and is deficient in patients with chronic and acute duodenal ulcer disease (16,19,29).Melatonin influences a variety of biological processes, including behavior, and enterochromaffin cells in the gastrointestinal tract have been identified to be a major source of melatonin production (5). The total amount of melatonin present in the intestine is thus ϳ400ϫ larger than in the central nervous system (5,17,34).…”
mentioning
confidence: 99%