OBJECTIVES: To compare gastric secretory function in patients with duodenal ulcer and in healthy volunteers with and without Helicobacter pylori infection. METHODS: Basal acid output, peak acid output, meal-stimulated acid output, fasting and meal-stimulated serum gastrin concentrations were measured in 136 healthy volunteers (63 H. pylori positive, 73 H. pylori negative) and 52 duodenal ulcer patients, all but one of whom were H. pylori positive. RESULTS: By multivariate linear regression analysis, H. pylori infection was a significant negative predictor of basal acid output and a positive predictor of fasting and meal-stimulated gastrin concentrations. When compared to truly normal (i.e., H. pylori-negative) control subjects, duodenal ulcer patients had elevated basal acid output, peak acid output, fasting and meal-stimulated gastrin concentrations. CONCLUSIONS: Our results show that in patients with duodenal ulcer disease, hypergastrinemia is largely related to gastric H. pylori infection, whereas acid hypersecretion is due to factors other than H. pylori.
OBJECTIVES: To compare gastric secretory function in patients with duodenal ulcer and in healthy volunteers with and without Helicobacter pylori infection. METHODS:Basal acid output, peak acid output, meal-stimulated acid output, fasting and meal-stimulated serum gastrin concentrations were measured in 136 healthy volunteers (63 H. pylori positive, 73 H. pylori negative) and 52 duodenal ulcerpatients, all but one of whom were H. pylori positive. RESULTS: By multivariate linear regression analysis, H. pylori infection was a significant negative predictor of basal acid output and a positive predictor of fasting and meal-stimulated gastrin concentrations. When compared to truly normal (i.e., H. pylori-negative) control subjects, duodenal ulcerpatients had elevated basal acid output, peak acid output, fasting and meal-stimulated gastrin concentrations. CONCLUSIONS: Our results show that in patients with duodenal ulcer disease, hypergastrinemia is largely related to gastric H. pylori infection, whereas acid hypersecretion is due to factors other than H. pylori.
Authors: A B R Thomson; M Keelan; R Lastiwka; S Appelman-Eszczuk; L Zuk; L Drozdowski; A Prentice; P Sinclair Journal: Dig Dis Sci Date: 2003-10 Impact factor: 3.199
Authors: J P Gisbert; M Blanco; J M Mateos; L Fernández-Salazar; M Fernández-Bermejo; J Cantero; J M Pajares Journal: Dig Dis Sci Date: 1999-11 Impact factor: 3.199
Authors: T Jaworski; I Sarosiek; S Sostarich; K Roeser; M Connor; S Brotze; G Wallner; J Sarosiek Journal: Dig Dis Sci Date: 2005-02 Impact factor: 3.199
Authors: Yana Zavros; Sivaprakash Rathinavelu; John Y Kao; Andrea Todisco; John Del Valle; Joel V Weinstock; Malcolm J Low; Juanita L Merchant Journal: Proc Natl Acad Sci U S A Date: 2003-10-10 Impact factor: 11.205