Kikuchi S, Nakajima T, Kobayashi O, Yamazaki T, Kikuichi M, Mori K, Oura S, Watanabe H, Nagawa H, Otani R, Okamoto N, Kurosawa M, Anzai H, Kubo T, Konishi T, Futagawa S, Mizobuchi N, Kobori O, Kaise R, Sato T, Inaba Y, Wada O
Department of Epidemiology and Environmental Health, Juntendo University School of Medicine, Tokyo, Japan.
Jpn J Cancer Res. 2000 Aug;91(8):774-9. doi: 10.1111/j.1349-7006.2000.tb01012.x.
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.
幽门螺杆菌被认为与胃癌的发病机制有关，但其产生影响的时间点（关键时间）尚不清楚。我们测量了787例20至69岁胃癌患者和1007例对照者的血清幽门螺杆菌抗体水平。确定了每个10岁年龄组不同胃癌类型和分期的比值比。胃癌的总体比值比随年龄下降，20 - 29岁者为7.0，30 - 39岁者为14.5，40 - 49岁者为9.1，50 - 59岁者为3.5，60 - 69岁者为1.5（比值比趋势：P < 0.01）。然而，早期弥漫型癌症不存在这种年龄依赖性趋势；比值比分别为12.6、4.0、7.2、6.5和18.5（P = 0.29）。早期癌症的血清阳性率往往高于进展期癌症，尤其是在老年受试者中。在每个年龄组内，弥漫型和肠型癌症的血清阳性率未观察到显著差异。在关键时间与癌症诊断之间的时间间隔内一定发生了血清学逆转，尤其是在老年患者中。幽门螺杆菌与胃癌之间的年龄依赖性关系可能是由于血清学逆转，而血清学逆转本身可能与年龄无关。这种与年龄无关表明，长期接触幽门螺杆菌不会增加其对胃癌发生的影响程度。幽门螺杆菌发挥致病作用的可能机制是成年期的持续炎症和/或儿童期或青少年期胃黏膜的不可逆损伤。
