Alimentary TractInfection of Helicobacter pylori in gastric adaptation to continued administration of aspirin in humans☆
Section snippets
Subjects
Twenty-four healthy volunteers, 12 men and 12 women, aged between 18 and 28 years and weighing 67–80 kg, entered the study. All subjects were examined for the presence of H. pylori infection as determined by 13C-urea breath test33 and endoscopy with mucosal biopsy combined with rapid urease test (HUT-test; Astra, Wedel, Germany) and histological analysis. In all subjects, the presence of immunoglobulin G antibodies to H. pylori was determined by enzyme-linked immunosorbant assay using EIAGEN H.
Gastric microbleeding
All subjects in group B without H. pylori infection and those in group C before and after H. pylori eradication completed aspirin treatment. Subjects in group A completed placebo treatment at the same time schedule as those in groups B and C. In H. pylori–infected subjects (group C), the pretreatment value of gastric microbleeding was 1.2 ± 0.6 mL/day and was not significantly different from the value recorded in H. pylori–negative subjects (groups A and B; Figure 1).
Discussion
This study confirms earlier findings that aspirin has a deleterious effect on the gastric mucosa2, 3, 4, 5, 7, 26, 27, 28, 29, 30, 31, 32 and that this occurs independently of H. pylori status.20, 27 The dramatic increase in macroscopic damage of gastric mucosa reached its maximum on day 3 of aspirin treatment and was accompanied by a marked mucosal blood loss.12, 34 These mucosal lesions caused by aspirin and other NSAIDs were reported to resolve along with the course of treatment,12, 30, 31,
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Address requests for reprints to: Jan W. Konturek, M.D., Ph.D., Department of Medicine B, University of Münster, Albert-Schweitzer-Straße 33, D-48129 Münster, Germany. Fax: (49) 251-834-7576. e-mail: [email protected].