Progression of chronic atrophic gastritis associated with Helicobacter pylori infection increases risk of gastric cancer
Progression of chronic atrophic gastritis associated with Helicobacter pylori infection increases risk of gastric cancer
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DOI：
10.1002/ijc.11680
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发表时间：
2004-03-10
影响因子：
6.4
通讯作者：
Ichinose, M
中科院分区：
文献类型：
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作者：
Ohata, H;Kitauchi, S;Ichinose, M
我们进行了一项纵向队列研究，以确定幽门螺杆菌感染与慢性萎缩性胃炎（CAG）与胃癌进展的关系。对4655名健康无症状受试者进行了平均7.7年的随访。血清特异性抗体确定幽门螺杆菌感染，血清胃蛋白酶原证实CAG存在。随访期间共发现胃癌45例（发病率126/10万人年）。年龄调整后的单因素分析显示，幽门螺杆菌和CAG与胃癌均显著相关。为了明确幽门螺杆菌和CAG之间的相互作用，我们进行了幽门螺杆菌和CAG状态的分层分析。在研究期间，幽门螺杆菌（-）ICAG（-）组未发生癌症。这支持了一种理论，即在没有幽门螺旋杆菌的健康胃中，任何类型的胃癌都是非常罕见的。随着幽门螺杆菌引起的胃炎的进展，胃癌的风险从无cag胃炎逐步增加[H]。幽门(+)ICAG(-)组)(HR = 7.13, 95% ci = 0.95 - -53.33) CAG (H。幽门螺杆菌(+)/CAG（+）组](HR= 14.85, 95%CI=1.96 ~ 107.7)，最终发展到严重CAG伴广泛肠化生[H。幽门螺杆菌(-)/ CAG（+）组](HR=61.85, 95%CI=5.6-682.64)，胃幽门螺杆菌消失。因此，幽门螺杆菌本身可能与胃癌的发生没有直接关系。相反，幽门螺杆菌似乎通过CAG的发展影响胃癌的发生。观察到幽门螺杆菌引起的胃炎的程度与癌症的发展有很强的正相关，特别是肠道型。这些结果令人信服地证明，严重胃炎伴广泛肠化生是胃癌的主要危险因素，并证实了先前描述的胃癌发生模型：胃炎-化生-癌序列。(C) 2003 Wiley-Liss, Inc。
We conducted a longitudinal cohort study to determine the association of Helicobacter pylori infection and the progression of chronic atrophic gastritis (CAG) with gastric cancer. A cohort of 4,655 healthy asymptomatic subjects was followed for a mean period of 7.7 years. H. pylori infection was established by serum specific antibodies and the presence of CAG was confirmed by serum pepsinogen. During the follow-up period, 45 gastric cancer cases were detected (incidence rate, 126/100,000 person-years). A univariate analysis after adjustment for age showed that both H. pylori and CAG were significantly associated with gastric cancer. To clarify the interaction between H. pylori and CAG, an analysis stratified by H. pylori- and CAG-status was performed. No cancer developed in the H. pylori(-)ICAG(-) group during the study period. This supports the theory that it is quite rare for any type of gastric cancer to develop in an H. pylori-free healthy stomach. With the progression of H. pylori-induced gastritis, the risk of gastric cancer increased in a stepwise fashion from CAG-free gastritis [H. pylori(+)ICAG(-) group] (HR=7.13, 95%CI=0.95-53.33) to CAG [H. pylori(+)/CAG(+) group] (HR= 14.85, 95%CI=1.96-107.7) and finally to severe CAG with extensive intestinal metaplasia [H. pylori(-)/ CAG(+) group] (HR=61.85, 95%CI=5.6-682.64) in which loss of H. pylori from the stomach is observed. Therefore, it is probable that H. pylori alone is not directly associated with stomach carcinogenesis. Instead, H. pylori appears to influence stomach carcinogenesis through the development of CAG. The observed positive correlation between the extent of H. pylori-induced gastritis and the development of cancer was strong, especially for the intestinal type. These results are compelling evidence that severe gastritis with extensive intestinal metaplasia is a major risk factor for gastric cancer, and they confirm the previously described model of stomach carcinogenesis: the gastritis-metaplasia-carcinoma sequence. (C) 2003 Wiley-Liss, Inc.