Department of Gastroenterology, Beijing Friendship Hospital, Capital Medical University, National Clinical Research Center for Digestive Disease, Beijing Digestive Disease Center, Beijing Key Laboratory for Precancerous Lesion of Digestive Disease, Beijing, 100050, China.
Medicine (Baltimore). 2024 Feb 23;103(8):e37175. doi: 10.1097/MD.0000000000037175.
Recent epidemiological research suggests a possible negative correlation between Helicobacter pylori infection and inflammatory bowel disease (IBD). However, conflicting studies have provided unclear evidence regarding these causal relationships. Therefore, recommending specific prevention and treatment strategies for H. pylori infection and IBD is challenging. We used various antibodies (anti-H. pylori IgG, VacA, and GroEl) related to H. pylori infection as indicators. We acquired relevant genetic variants from public databases within the Genome-wide Association Studies (GWAS) dataset using IBDs tool variables from 2 different GWAS datasets. We thoroughly examined the data and screened for IVs that fulfilled these criteria. Subsequently, Bidirectional Mendelian randomization (MR) was conducted to predict the potential causality between the 2. To ensure the accuracy and robustness of our results, we conducted a series of sensitivity analyses. Based on our comprehensive MR analysis, no potential causal relationship was observed between H. pylori infection and IBD. Across various methodologies, including IVW, MR-Egger, and weighted median, our findings showed P values > .05. The only exception was observed in the reverse MR analysis using the MR-Egger method, which yielded a P value of < .05. However, because the IVW method is considered the most statistically significant method for MR, and its P value was > .05, we do not believe that a potential causal relationship exists between them. Our sensitivity analysis did not suggest significant horizontal pleiotropism. Although heterogeneity was detected in the analysis of IBD (IIBDGC source) versus H. pylori GroEL antibody levels (MR-Egger, Qp = 0.038; IVW, Qp = 0.043), the results remained reliable because we selected IVW as a random-effects model in our MR analysis method. Based on our MR research, no direct correlation was observed between H. pylori infection and IBD risk. This implies that eradicating H. pylori may not provide substantial benefits in preventing or treating regional IBD, and vice versa. Nevertheless, the use of H. pylori serological index substitution has limitations, and further research using histological diagnosis and additional MR studies is required to comprehensively assess the link between H. pylori infection and IBD.
最近的流行病学研究表明,幽门螺杆菌(H. pylori)感染与炎症性肠病(IBD)之间可能存在负相关关系。然而,存在相互矛盾的研究结果,使得这些因果关系的证据并不明确。因此,推荐针对 H. pylori 感染和 IBD 的具体预防和治疗策略具有挑战性。我们使用了与 H. pylori 感染相关的各种抗体(抗 H. pylori IgG、VacA 和 GroEl)作为指标。我们从两个不同的 GWAS 数据集的 IBDs 工具变量中从公共数据库中获取了相关的遗传变异。我们彻底检查了数据,并筛选出符合这些标准的 IVs。随后,进行了双向孟德尔随机化(MR)以预测两者之间的潜在因果关系。为了确保结果的准确性和稳健性,我们进行了一系列敏感性分析。基于我们全面的 MR 分析,没有观察到 H. pylori 感染与 IBD 之间存在潜在的因果关系。在各种方法中,包括 IVW、MR-Egger 和加权中位数,我们的发现均显示 P 值>0.05。唯一的例外是在使用 MR-Egger 方法的反向 MR 分析中观察到的 P 值<0.05。然而,由于 IVW 方法被认为是 MR 中最具统计学意义的方法,并且其 P 值>0.05,因此我们认为它们之间不存在潜在的因果关系。我们的敏感性分析并未提示存在明显的水平偏倚。尽管在 IBD(IIBDGC 来源)与 H. pylori GroEL 抗体水平的分析中存在异质性(MR-Egger,Qp=0.038;IVW,Qp=0.043),但由于我们在 MR 分析方法中选择了 IVW 作为随机效应模型,因此结果仍然可靠。基于我们的 MR 研究,没有观察到 H. pylori 感染与 IBD 风险之间的直接相关性。这意味着根除 H. pylori 可能不会在预防或治疗局部 IBD 方面带来实质性的益处,反之亦然。然而,H. pylori 血清学指标替代存在局限性,需要使用组织学诊断和其他 MR 研究进一步研究,以全面评估 H. pylori 感染与 IBD 之间的联系。