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Recurrence of duodenal ulcer after Helicobacter pylori eradication is related to high acid output
Author(s) -
HARRIS A. W.,
GUMMETT P. A.,
PHULL P. S.,
JACYNA M. R.,
MISIEWICZ J. J.,
BARON J. H.
Publication year - 1997
Publication title -
alimentary pharmacology and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.308
H-Index - 177
eISSN - 1365-2036
pISSN - 0269-2813
DOI - 10.1046/j.1365-2036.1997.146322000.x
Subject(s) - helicobacter pylori , gastroenterology , pentagastrin , medicine , duodenal ulcer , basal (medicine) , spirillaceae , gastrin , gastric acid , gastritis , stomach , secretion , insulin
Background : Helicobacter pylori eradication reduces the recurrence of duodenal ulcers. It is unclear why duodenal ulcers rarely recur in the absence of reinfection with H. pylori or NSAID treatment. Methods : Basal, gastrin‐releasing peptide‐ and pentagastrin‐stimulated peak acid outputs in patients with ulcer relapse after H. pylori eradication were measured, and compared with patients without ulcer relapse after H. pylori eradication. Results : Pentagastrin‐stimulated peak acid output was significantly higher in H. pylori ‐positive patients with duodenal ulcers than in H. pylori ‐negative controls, and fell significantly after H. pylori eradication. In H. pylori ‐negative patients with recurrent duodenal ulcers, pentagastrin‐stimulated peak acid output was significantly higher than in controls and similar to H. pylori ‐positive patients with duodenal ulcers. Conclusions : These findings suggest that duodenal ulcer relapse after eradication of H. pylori may be related to high pentagastrin‐stimulated peak acid output. In this subset of patients with duodenal ulcers, maintenance anti‐secretory treatment may be necessary to prevent relapse.