Iijima K et al. – 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.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.
- 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.