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Elevation of Meal-Stimulated Gastrin Release in Subjects with Helicobacter pylori Infection: Reversal by Low Intragastric pH
W. E. Karnes, Jr., G. V. Ohning, B. Sytnik, S. W. R. Kim and J. H. Walsh
Reviews of Infectious Diseases
Vol. 13, Supplement 8. Symposium on Helicobacter pylori: A Cause of Gastroduodenal Disease (Jul. - Aug., 1991), pp. S665-S670
Published by: Oxford University Press
Stable URL: http://www.jstor.org/stable/4456069
Page Count: 6
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The aim of the present study was to determine whether the association between Helicobacter pylori infection and increased concentrations of gastrin in serum is independent of chronic duodenal ulcer disease and whether the mechanism of this association involves a disturbance of feedback inhibition of gastrin release by intragastric acid. Of 48 subjects evaluated, 26 (54%) were seropositive for H. pylori by ELISA. Fasting and peptone meal-stimulated gastrin release at pH 2.5 and pH 5.5 as well as integrated 24-hour plasma gastrin concentrations were significantly higher in the seropositive group, even when subjects with a history of duodenal ulcer were excluded. The inhibitory effect of low pH on the release of gastrin was not attenuated in subjects with positive results in the ELISA. These data indicate that the association between seropositivity for H. pylori and enhanced release of gastrin is independent of a history of duodenal ulcer and is not caused by a disturbance of the normal feedback inhibition of gastrin release by intragastric acid.
Reviews of Infectious Diseases © 1991 Oxford University Press