Gastroenterology

Gastroenterology

Volume 114, Issue 2, February 1998, Pages 245-255
Gastroenterology

Alimentary Tract
Infection of Helicobacter pylori in gastric adaptation to continued administration of aspirin in humans

https://doi.org/10.1016/S0016-5085(98)70474-3Get rights and content

Abstract

Background & Aims: Involvement of Helicobacter pylori in aspirin-induced gastropathy and adaptation to aspirin remains unclear. The aim of this study was to compare gastric damage and adaptation after repeated exposures to acetylsalicylic acid in the same subjects before and after eradication of H. pylori. Methods: Before and after H. pylori eradication, 8 volunteers were given aspirin, 2 g/day during 14 days. Mucosal damage was evaluated by endoscopy and histological analysis of biopsy samples. Gastric microbleeding, DNA synthesis, prostaglandin E2 generation, and luminal contents of transforming growth factor α and its immunohistochemical expression were determined on days 0, 3, 7, and 14 of aspirin course. Results: In all subjects, aspirin-induced gastric damage that reached maximum on day 3. In H. pylori–positive subjects, this damage was maintained at a similar level up to day 14. After H. pylori eradication, the damage was significantly lessened both in endoscopy and histology at day 14 and accompanied by increased mucosal expression and luminal release of transforming growth factor α. Prostaglandin E2 generation was significantly greater in H. pylori–positive subjects than after H. pylori eradication, but aspirin treatment resulted in >90% reduction of this generation independent of H. pylori status. Conclusions: Gastric adaptation to aspirin is impaired in H. pylori–positive subjects, but eradication of this bacterium restores this process.

GASTROENTEROLOGY 1998;114:245-255

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).

. Gastric microbleeding in 8

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].

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