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Japanese Journal of Cancer Research : Gann logoLink to Japanese Journal of Cancer Research : Gann
. 2000 Aug;91(8):774–779. doi: 10.1111/j.1349-7006.2000.tb01012.x

Effect of Age on the Relationship between Gastric Cancer and Helicobacter pylori

Shogo Kikuchi 1,†,✉, Toshifusa Nakajima 4, Osamu Kobayashi 5, Tatsuo Yamazaki 6, Masahiro Kikuichi 7, Kiyoshi Mori 8, Shinsuke Oura 2, Hideaki Watanabe 3, Hirokazu Nagawa 10, Reiji Otani 11,‡, Naoyuki Okamoto 13, Michiko Kurosawa 1, Haruyuki Anzai 6, Takuji Kubo 7, Toshiro Konishi 8, Shunji Futagawa 2, Noboru Mizobuchi 3, Oichiro Kobori 14, Ruriko Kaise 12, Tosiya Sato 15, Yutaka Inaba 1, Osamu Wada 9,§; for the Tokyo Research Group of Prevention for Gastric Cancer
PMCID: PMC5926433  PMID: 10965016

Abstract

Helicobacter pylori is thought to be involved in the pathogenesis of gastric cancer, but the time point at which it produces its effects (critical time) is unknown. We measured the serum level of H. pylori antibody in 787 gastric cancer patients and 1007 controls aged 20 to 69. Odds ratios for different gastric cancer types and stages were determined for each 10‐year age class. The overall odds ratio for gastric cancer decreased with age, being 7.0 for those aged 20–29, 14.5 for those aged 30–39, 9.1 for those aged 40–49, 3.5 for those aged 50–59, and 1.5 for those aged 60–69 (trend in odds ratios: P < 0.01). However, there was no such age‐dependent trend for early diffuse‐type cancer; the odds ratios were 12.6, 4.0, 7.2, 6.5, and 18.5 respectively (P=0.29). Early cancer tended to show higher seroprevalence than advanced cancer, especially in older subjects. No significant difference in seroprevalence was observed between diffuse and intestinal cancers within each age‐class. Seroreversion must have occurred in the time interval between the critical time and the diagnosis of the cancer, especially in older patients. The age‐dependent relationship between H. pylori and gastric cancer may be due to seroreversion, which itself may be independent of age. This age‐independence indicates that prolonged exposure to H. pylori does not increase the magnitude of its influence on gastric carcinogenesis. Possible mechanisms through which H. pylori exerts pathogenic effects are continuous inflammation in adulthood and/or irreversible damage to gastric mucosa in childhood or the teenage years.

Keywords: Gastric cancer, Helicobacter pylori, Age, Early diffuse‐type cancer

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