Effect of Helicobacter pylori on gastric somatostatin in duodenal ulcer disease

doi:10.1016/0140-6736(92)92816-X

The Lancet

Volume 340, Issue 8825, 17 October 1992, Pages 930-932

https://doi.org/10.1016/0140-6736(92)92816-X Get rights and content

Abstract

Infection of the gastric antrum by Helicobacter pylori is associated with recurrent duodenal ulcer disease but the mechanism of ulcerogenesis is unclear. Since pathways inhibiting gastric secretion are defective in patients with duodenal ulcers, we investigated whether H pylori interferes with the normal gastric inhibition that is mediated by somatostatin. We studied 28 patients with active duodenal ulcers in whom H pylori was eradicated successfully. In 18 patients, we measured the density of antral somatostatin-immunoreactive cells and in a further 10 subjects, the amount of somatostatin mRNA before and after eradication of H pylori was determined. After eradication, the median density of somatostatin-immunoreactive cells increased significantly from 9 (range 3-47) to 19 (6-57) cells per mm muscularis mucosa (p=0·025). The median somatostatin mRNA/rRNA ratio increased from 50 (25-160) to 95 (40-180) (p=0·01). The number of gastrin cells and quantity of gastrin mRNA did not change significantly. Our results suggest that in duodenal ulcer disease, gastric secretory function is disinhibited through the suppression of mucosal somatostatin.

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ORIGINAL ARTICLESEffect of Helicobacter pylori on gastric somatostatin in duodenal ulcer disease

Abstract

Gastroenterology

Gastroenterology

Lancet

Gastroenterology

Gastroenterology

Analyt Biochem

Biochem Biophys Res Commun

Lancet

pH dependence of acid secretion and gastrin release in normal and ulcer subjects

J Clin Invest

Detailed composition of basal and food-stimulated gastric add secretion and serum gastrin concentrations in duodenal ulcer patients and normal subjects

J Clin Invest

Antral Campylobacter pylori, hypergastrinaemia, and duodenal ulcers: effect of eradicating the organism

BMJ

ORIGINAL ARTICLES
Effect of Helicobacter pylori on gastric somatostatin in duodenal ulcer disease