title: Biphasic effects of H. pylori infection on low-dose aspirin-induced gastropathy depending on the gastric acid secretion level.
abstract: 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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Division of Gastroenterology, Tohoku University Graduate School of Medicine, 1-1 Seiryo-machi, Aobaku, Sendai, Miyagi 980-8574, Japan. kiijima@med.tohoku.ac.jp
authors.forename: Katsunori
authors.initials: K
authors.lastname: Iijima
authors.forename: Nobuyuki
authors.initials: N
authors.lastname: Ara
authors.forename: Yasuhiko
authors.initials: Y
authors.lastname: Abe
authors.forename: Tomoyuki
authors.initials: T
authors.lastname: Koike
authors.forename: Toshimitsu
authors.initials: T
authors.lastname: Iwabuchi
authors.forename: Hirohiko
authors.initials: H
authors.lastname: Shinkai
authors.forename: Kaname
authors.initials: K
authors.lastname: Uno
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Endo
authors.forename: Naoki
authors.initials: N
authors.lastname: Asano
authors.forename: Tooru
authors.initials: T
authors.lastname: Shimosegawa
mesh_terms: D000368:Aged; D001241:Aspirin / Q000008:administration & dosage / Q000009:adverse effects*; D004334:Drug Administration Schedule; D005260:Female; D005343:Fibrinolytic Agents / Q000008:administration & dosage / Q000009:adverse effects*; D005744:Gastric Acid / Q000378:metabolism; D016481:Helicobacter Infections / Q000150:complications* / Q000378:metabolism; D016480:Helicobacter pylori / Q000302:isolation & purification*; D006801:Humans; D008297:Male; D008875:Middle Aged; D010418:Pentagastrin; D010975:Platelet Aggregation Inhibitors / Q000008:administration & dosage / Q000009:adverse effects; D011446:Prospective Studies; D013272:Stomach Diseases / Q000139:chemically induced* / Q000378:metabolism / Q000382:microbiology
chemical_list: D005343:Fibrinolytic Agents; D010975:Platelet Aggregation Inhibitors; D010418:Pentagastrin; D001241:Aspirin