Original Article

Digestive Diseases and Sciences

, Volume 55, Issue 6, pp 1627-1636

First online:

Relationship Between Low-Dose Aspirin-Induced Gastric Mucosal Injury and Intragastric pH in Healthy Volunteers

  • Masafumi NishinoAffiliated withFirst Department of Medicine, Hamamatsu University School of Medicine
  • , Mitsushige SugimotoAffiliated withFirst Department of Medicine, Hamamatsu University School of Medicine
  • , Chise KodairaAffiliated withFirst Department of Medicine, Hamamatsu University School of Medicine
  • , Mihoko YamadeAffiliated withFirst Department of Medicine, Hamamatsu University School of Medicine
  • , Naohito ShiraiAffiliated withDepartment of Gastroenterology, Enshu General Hospital
  • , Mutsuhiro IkumaAffiliated withFirst Department of Medicine, Hamamatsu University School of Medicine
  • , Tatsuo TanakaAffiliated withDepartment of Endoscopic & Photodynamic Medicine, Hamamatsu University School of Medicine
  • , Haruhiko SugimuraAffiliated withFirst Department of Pathology, Hamamatsu University School of Medicine
  • , Akira HishidaAffiliated withFirst Department of Medicine, Hamamatsu University School of Medicine
    • , Takahisa FurutaAffiliated withCenter for Clinical Research, Hamamatsu University School of Medicine Email author 

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Abstract

Background and Aims

Gastric acid plays an important role in the pathogenesis of gastric mucosal lesions. We investigated whether aspirin-induced gastric mucosal injury might have any association with the intragastric pH.

Materials and Methods

Fifteen healthy, Helicobacter pylori-negative volunteers randomly underwent the four different 7-day regimens: (1) aspirin 100 mg, (2) rabeprazole 10 mg, (3) aspirin 100 mg + rabeprazole 10 mg, and (4) aspirin 100 mg + rabeprazole 40 mg. Gastric mucosal injury based on the modified Lanza score (MLS), 24-h intragastric pH, and histopathology of gastric mucosa were evaluated prior to the start and on day 7 of each regimen.

Results

The median MLSs were 0 in the baseline and the rabeprazole 10 mg regimen. The median MLS in the aspirin regimen was 3, while those in both aspirin + rabeprazole 10 mg and aspirin + rabeprazole 40 mg regimens were 0. Rabeprazole significantly prevented the gastric mucosal injury by aspirin (P = 0.001 for rabeprazole 10 mg and P = 0.005 for rabeprazole 40 mg). The MLSs were negatively correlated with the 24-h intragastric pH (P = −0.711, < 0.001), whereas aspirin had no effect on the intragastric pH. Aspirin expanded the mean diameter of the microvessels of the gastric mucosa, which, in turn, was negatively correlated with the intragastric pH.

Conclusions

Aspirin might induce gastric mucosal injury by affecting the mucosal microvessels in an acid-dependent manner. Sustained maintenance of the intragastric pH at an elevated value is necessary to prevent gastric mucosal damage induced by aspirin.

Keywords

Proton pump inhibitor Rabeprazole CYP2C19 Microvessel