Tumor Etiology and Screening Department of Cancer Institute and General Surgery, the First Affiliated Hospital of China Medical University, and Key Laboratory of Cancer Etiology and Prevention (China Medical University), Liaoning Provincial Education Department, Shenyang 110001, China.
BMC Infect Dis. 2013 Nov 20;13:555. doi: 10.1186/1471-2334-13-555.
There are increasing studies examining the relationship between the status of H. pylori oipA gene and peptic ulcer disease (PUD) and gastric cancer (GC) but the results turn out to be controversial. We attempted to clarify whether oipA gene status is linked with PUD and/or GC risks.
A systematically literature search was performed through four electronic databases. According to the specific inclusion and exclusion criteria, seven articles were ultimately available for the meta-analysis of oipA presence/absence with PUD and GC, and eleven articles were included for the meta-analysis of oipA on/off status with PUD and GC.
For the on/off functional status analysis of oipA gene, the "on" status showed significant associations with increased risks of PUD (OR = 3.97, 95% CI: 2.89, 5.45; P < 0.001) and GC (OR = 2.43, 95% CI: 1.45, 4.07; P = 0.001) compared with gastritis and functional dyspepsia controls. Results of the homogeneity test indicated different effects of oipA "on" status on PUD risk between children and adult subgroups and on GC risk between PCR-sequencing and immunoblot subgroups. For the presence/absence analysis of oipA gene, we found null association of the presence of oipA gene with the risks of PUD (OR = 1.93, 95% CI: 0.60, 6.25; P = 0.278) and GC (OR = 2.09, 95% CI: 0.51, 8.66; P = 0.308) compared with gastritis and functional dyspepsia controls.
To be concluded, when oipA exists, the functional "on" status of this gene showed association with increased risks for PUD and GC compared with gastritis and FD controls. However, merely investigating the presence/absence of oipA would overlook the importance of its functional on/off status and would not be reliable to predict risks of PUD and GC. Further large-scale and well-designed studies concerning on/off status of oipA are required to confirm our meta-analysis results.
越来越多的研究探讨了 H. pylori oipA 基因的状态与消化性溃疡病(PUD)和胃癌(GC)之间的关系,但结果存在争议。我们试图阐明 oipA 基因状态是否与 PUD 和/或 GC 风险有关。
通过四个电子数据库进行系统文献检索。根据具体的纳入和排除标准,最终有 7 篇文章可用于 oipA 存在/缺失与 PUD 和 GC 的荟萃分析,11 篇文章可用于 oipA 开/关状态与 PUD 和 GC 的荟萃分析。
对于 oipA 基因的开/关功能状态分析,与胃炎和功能性消化不良对照组相比,“开”状态与 PUD(OR = 3.97,95%CI:2.89,5.45;P < 0.001)和 GC(OR = 2.43,95%CI:1.45,4.07;P = 0.001)风险增加显著相关。同质性检验结果表明,oipA“开”状态对儿童和成人亚组 PUD 风险的影响不同,对 PCR 测序和免疫印迹亚组 GC 风险的影响也不同。对于 oipA 基因的存在/缺失分析,我们发现 oipA 基因的存在与 PUD(OR = 1.93,95%CI:0.60,6.25;P = 0.278)和 GC(OR = 2.09,95%CI:0.51,8.66;P = 0.308)风险之间无关联与胃炎和功能性消化不良对照组相比。
综上所述,当 oipA 存在时,与胃炎和 FD 对照组相比,该基因的功能“开”状态与 PUD 和 GC 风险增加相关。然而,仅仅研究 oipA 的存在/缺失会忽略其功能开/关状态的重要性,并且无法可靠地预测 PUD 和 GC 的风险。需要进一步进行大规模和精心设计的研究,以确认我们的荟萃分析结果。