文章摘要
马山蕊,马箐,李纪宾,魏文强.幽门螺旋杆菌感染与食管-胃交界部肿瘤关联的Meta分析[J].中华流行病学杂志,2016,37(3):418-424
幽门螺旋杆菌感染与食管-胃交界部肿瘤关联的Meta分析
Meta-analysis on relationship between Helicobacter pylori infection and esophagogastric junction adenocarcinoma
收稿日期:2015-08-28  出版日期:2016-03-15
DOI:10.3760/cma.j.issn.0254-6450.2016.03.027
中文关键词: 幽门螺旋杆菌感染;食管胃交界部肿瘤;Meta分析
英文关键词: Helicobacter pylori infection;Esophagogastric junction adenocarcinoma;Meta- analysis
基金项目:国家自然科学基金(81241091)
作者单位E-mail
马山蕊 100021 北京, 中国医学科学院肿瘤医院流行病学教研室  
马箐 100021 北京, 中国医学科学院肿瘤医院流行病学教研室  
李纪宾 100021 北京, 中国癌症基金会  
魏文强 100021 北京, 中国医学科学院肿瘤医院流行病学教研室 weiwq@cicams.ac.cn 
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中文摘要:
      目的 探讨幽门螺旋杆菌(Hp)感染与食管-胃交界部肿瘤的病因学关联及感染者中Cag致病岛的致病性。方法 系统检索中国期刊全文数据库(CNKI)、万方数据资源系统(Wanfang data)、维普数据库(VIP)、The Cochrane Library、PubMed、EMBase等中外数据库中1980年1月至2015年4月所有Hp感染与食管-胃交界部肿瘤研究的文献。按照纳入与排除标准,获取所需文献,并采用NOS 量表对纳入的文献进行质量评价,运用Review Manager 5.3软件计算异质性检验以及合并OR值和95%CI。结果 共纳入5 547例研究对象,食管-胃交界部肿瘤1 446例,Hp感染阳性837例;对照组4 101例,Hp感染阳性2 056例; 13项研究合并OR=0.95(95%CI:0.66~1.36),P=0.71。高发地区OR=1.66(95%CI:1.33~2.08),P<0.001,高于低发地区(OR=0.68,95%CI:0.49~0.94),P=0.020。此外,6项研究数据显示,Cag致病岛在病例组和对照组的合并检出率分别为80.50%、79.80%,合并OR=1.24(95%CI:0.96~1.60),两组差异无统计学意义 (P=0.090)。敏感性与发表偏倚分析均表明研究结果比较稳定、可靠。结论 Hp感染与食管-胃交界部肿瘤无明显关联,但在高发与低发地区的关联截然相反,存在明显的地域分布;Cag致病岛在Hp感染者中检出率较高,但其与食管-胃交界部肿瘤关系有待进一步研究。
英文摘要:
      Objective To systematically evaluate the etiological association between esophagogastric junction adenocarcinoma and Helicobacter pylori (Hp) infection and the pathogenicity of Cag pathogenic island in Hp infection cases. Methods Literatures about Hp infection and esophagogastric junction adenocarcinoma published from January 1980 to April 2015 were retrieved from CNKI, Wanfang data, VIP, the Cochrane Library, PubMed, EMBase databases. The literatures which met the inclusion criteria were collected and evaluated by using Newcastle-Ottawa Scale, then the heterogeneity was analyzed with Review Manager 5.3, and the pooled OR value and 95% confidence interval were calculated. Results A total of 5 547 study subjects were recruited in 13 studies, including 1 446 esophagogastric junction adenocarcinoma cases and 4 101 controls. The combined OR for Hp infection was 0.95 (95%CI: 0.66-1.36), P=0.71; The OR in high risk areas was 1.66 (95%CI:1.33-2.08, P<0.001), higher than that in low-risk areas (0.68, 95%CI: 0.49-0.94, P=0.020). In addition, six studies found that the combined detection rates of Cag pathogenic island in esophagogastric junction adenocarcinoma cases and controls were 80.50% and 79.80%, respectively. There was no significant difference between two group, the combined OR was 1.24 (95%CI: 0.96-1.60). Conclusion The association between Hp infection and esophagogastric junction adenocarcinoma was not significant, however, the significant difference was observed between high risk area and low risk area; the detection rate of Gag pathogenic island in Hp infection cases was high, but the pathogenicity for esophagogastric junction adenocarcinoma needs further study.
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