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Biphasic effects of H. pylori infection on low-dose aspirin-induced gastropathy depending on the gastric acid secretion level
Background The association of Helicobacter pylori infection with aspirin-induced gastropathy is controversial. H. pylori infection exerts diverse effects on gastric acid secretion. In this study, the interaction between H. pylori infection and aspirin was investigated with reference to the individua...
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Published in: | Journal of gastroenterology 2012-12, Vol.47 (12), p.1290-1297 |
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Main Authors: | , , , , , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | Background
The association of
Helicobacter pylori
infection with aspirin-induced gastropathy is controversial.
H. pylori
infection exerts diverse effects on gastric acid secretion. In this study, the interaction between
H. pylori
infection and aspirin was investigated with reference to the individual gastric acid secretion level in
H. pylori
-positive subjects.
Methods
Ninety-three (81 men, mean age: 70 years) long-term low-dose aspirin takers were prospectively enrolled.
H. pylori
infection was evaluated by serum IgG antibody determination, and gastrin-stimulated acid output was assessed with the endoscopic gastrin test.
H. pylori
-positive aspirin-takers were classified into 2 subgroups (hyposecretors and non-hyposecretors). The grade of gastric mucosal injury was assessed endoscopically according to the modified Lanza score; intensive aspirin-induced gastropathy was defined as a modified Lanza score of ≥4. Multiple logistic regression analyses were used to adjust for potential confounders.
Results
With
H. pylori
-negative patients taken as the reference,
H. pylori
infection was found to be positively associated with intensive gastropathy among non-hyposecretors, with an odds ratio (OR) (95 % confidence interval [CI]) of 4.2 (1.1–17.1), while the infection was negatively associated with gastropathy among hyposecretors, with an OR (95 % CI) of 0.3 (0.08–0.9). Aspirin-induced gastropathy occurred preferentially in the antrum among
H. pylori
-positive non-hyposecretors, while it affected the fundus among
H. pylori
-positive hyposecretors.
Conclusion
The effect of
H. pylori
infection on the aspirin-induced gastropathy was biphasic depending on the individual gastric acid secretion level. In the presence of sufficient amounts of gastric acid,
H. pylori
infection and aspirin could synergistically damage gastric mucosal integrity, while in the absence of sufficient amounts of gastric acid, the synergistic effect could be completely counteracted and the infection could even suppress the aspirin-induced gastropathy. |
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ISSN: | 0944-1174 1435-5922 |
DOI: | 10.1007/s00535-012-0598-8 |