ABO blood type, Lewis and Secretor genotypes, and chronic atrophic gastritis: A cross-sectional study in Japan

Abstract

Background. The H type I structure, synthesized by the secretor (Se) enzyme in gastric foveolar cells, and its metabolite, Lewis b (Leb) antigen, mediate the adhesion of Helicobacter pylori (H. pylori) to the gastric epithelium, whereas H. pylori does not bind to modified forms of Leb specific for blood types A and B. Such host factors as Le and Se genotypes and ABO blood type may affect the establishment of H. pylori infection and, once infected, the risk of chronic atrophic gastritis. Methods. We investigated the cross-sectional relation of ABO blood type and Le and Se genotypes to gastric atrophy, assessed by serum pepsinogen levels, in Japanese residents from two sources. Results. Among the 151 H. pylori-positive participants of the H. pylori eradication program, odds ratios (ORs) for gastric atrophy, adjusted for age, sex, and smoking, were elevated for blood types A (OR = 5.35; 95% confidence interval (CI), 2.11-13.58) and B (OR = 4.79; 95% CI, 1.77-12.93) relative to type O. ORs for blood types A and B were also elevated in H. pylori-negative subjects. These associations were not observed among 250 H. pylori-positive health check-up examinees. The Le genotype was not associated with gastric atrophy in either study population. The se/se genotype was associated with statistically nonsignificant elevation of gastric atrophy risk in both populations. Conclusions. The present data showed a strong association of blood types A and B with gastric atrophy in one, but not the other, study population. Discrepant results between the two populations warrant further investigation.