Digestive Diseases and Sciences

, Volume 55, Issue 6, pp 1627–1636

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

Authors

  • Masafumi Nishino
    • First Department of MedicineHamamatsu University School of Medicine
  • Mitsushige Sugimoto
    • First Department of MedicineHamamatsu University School of Medicine
  • Chise Kodaira
    • First Department of MedicineHamamatsu University School of Medicine
  • Mihoko Yamade
    • First Department of MedicineHamamatsu University School of Medicine
  • Naohito Shirai
    • Department of GastroenterologyEnshu General Hospital
  • Mutsuhiro Ikuma
    • First Department of MedicineHamamatsu University School of Medicine
  • Tatsuo Tanaka
    • Department of Endoscopic & Photodynamic MedicineHamamatsu University School of Medicine
  • Haruhiko Sugimura
    • First Department of PathologyHamamatsu University School of Medicine
  • Akira Hishida
    • First Department of MedicineHamamatsu University School of Medicine
    • Center for Clinical ResearchHamamatsu University School of Medicine
Original Article

DOI: 10.1007/s10620-009-0920-3

Cite this article as:
Nishino, M., Sugimoto, M., Kodaira, C. et al. Dig Dis Sci (2010) 55: 1627. doi:10.1007/s10620-009-0920-3

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 inhibitorRabeprazoleCYP2C19Microvessel

Abbreviations

COX

Cyclooxygenase

CYP2C19

Cytochrome P450 2C19

H. pylori

Helicobacter pylori

IM

Intermediate metabolizer

MLS

Modified Lanza score

NSAID

Non-steroidal anti-inflammatory drug

PG

Prostaglandin

PM

Poor metabolizer

RM

Rapid metabolizer

Copyright information

© Springer Science+Business Media, LLC 2009