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. 2005 Aug 19;94(4):372–377. doi: 10.1111/j.1349-7006.2003.tb01449.x

Food/nutrient intake and risk of atrophic gastritis among the Helicobacter pylori‐infected population of northeastern Japan

Ai Montani 1,2, Shizuka Sasazuki 1, Manami Inoue 1, Kazuhide Higuchi 2, Tetsuo Arakawa 2, Shoichiro Tsugane 1,
PMCID: PMC11160215  PMID: 12824907

Abstract

Although Helicobacter pylori (H. pylori) infection is considered a key risk factor for atrophic gastritis, along with other environmental factors, it is still unclear which factor is involved in the development of atrophic gastritis among H. pylori‐infected subjects. In the present cross‐sectional study, therefore, we analyzed various dietary factors in relation to the presence of atrophic gastritis among H. pylori‐infected subjects who participated in a health check‐up program in a town in northeastern Japan. One thousand and seventy‐one subjects (362 males and 709 females) who provided both self‐administered validated food frequency questionnaires and blood samples were the basis for the study, and all of them were serologically positive for H. pylori immunoglobulin G (IgG) antibody. Among them, 663 (223 males and 440 females) were diagnosed as having atrophic gastritis on the basis of serum pepsinogen levels. Odds ratios (OR) and 95% confidence intervals (95% CI) were calculated based on tertile categories of subjects without atrophic gastritis, using logistic regression analysis. Among females, high consumptions of rice (OR=1.6, 95% CI: 1.1–2.3), cod roe (OR=1.5, 95% CI: 1.0–2.2) and cuttlefish (OR=1.5, 95% CI: 1.0–2.3) were associated with a moderately increased risk of atrophic gastritis after adjustment for age (P for trend=0.02 for these items). Among males, high consumptions of rice and miso soup showed a tendency toward an increased risk (P for trend=0.12 and 0.13, respectively). Vegetables and fruits showed no association among either males or females. From these results, it is suggested that the dietary habits of consumers of traditional Japanese foods may play a role in the development of atrophic gastritis after H. pylori infection. (Cancer Sci 2003; 94: 372–377)

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