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[目的]探讨幽门螺杆菌CagA感染与胃癌的关系,及其与代谢酶基因多态性的交互作用对胃癌易感性的影响。[方法]以社区为基础的病例对照研究。肠型胃癌病例经胃镜及病理确诊,有效分析样本包括:完成CagA抗体检测胃癌108例,对照217例;完成CagA抗原检测病例107例,对照284例。[结果]胃癌组H.PyloriCagA抗体阴性率为85.19%,显著高于对照组的49.31%,OR值为5.91(95%CI:3.26～10.71,P=0.001);在CagA抗体阴性时,胃癌组CagA抗原阳性率达12.50%,显著高于对照组的1.82%,OR值为7.71(95%CI:1.01～59.18,P=0.023),在CagA抗体阳性组则未见两者有显著性差异;调整混杂因素后,GSTM1缺失基因型与H.PyloriCagA抗原之间有明显的相乘交互作用,γ为19.58,交互作用OReg达10.49,与H.PyloriCagA抗体之间也有明显的交互作用。[结论]H.PyloriCagA毒株感染后产生的CagA抗体是保护性因素,而H.PyloriCagA抗原为胃癌的危险性指标;H.PyloriCagA感染与GSTM1缺失基因型对胃癌发生有明显的交互作用。
[Objective] To investigate the relationship between Helicobacter pylori CagA infection and gastric cancer and its interaction with metabolic enzyme gene polymorphism on gastric cancer susceptibility. [Methods] Community-based case-control study. The cases of enteric gastric cancer were diagnosed by endoscopy and pathology. The effective samples included: complete CagA antibody detection of gastric cancer in 108 cases and control of 217 cases; complete CagA antigen test in 107 cases and control in 284 cases. [Results] The negative rate of H. pyloriCagA antibody in gastric cancer group was 85.19%, significantly higher than that in control group (49.31%), OR was 5.91 (95% CI: 3.26-10.71, P = 0.001) The positive rate of CagA antigen was 12.50%, which was significantly higher than that of control group (1.82%), OR was 7.71 (95% CI: 1.01 ~ 59.18, P = 0.023). There was no significant difference between the two groups in CagA antibody positive group. After adjusting the confounding factors, the GSTM1 deletion genotype had a significant reciprocal interaction with the H. pyloriCagA antigen, with a γ of 19.58, an OR of 10.49 and a clear interaction with the H. pyloriCagA antibody. [Conclusion] The CagA antibody produced by H. pyloriCagA infection is a protective factor, while the H. pyloriCagA antigen is a risk indicator of gastric cancer. H. pyloriCagA infection has a significant interaction with GSTM1 deletion genotype on gastric cancer.