幽门螺杆菌感染不会影响从胃食管反流病到巴雷特食管再到食管腺癌的进展。

IF 1.9 Q3 GASTROENTEROLOGY & HEPATOLOGY
Minerva gastroenterology Pub Date : 2024-12-01 Epub Date: 2024-05-10 DOI:10.23736/S2724-5985.24.03609-X
Ahmed Edhi, Manesh K Gangwani, Muhammad Aziz, Fouad Jaber, Zubair Khan, Sumant Inamdar, Aaron P Thrift, Tusar K Desai
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引用次数: 0

摘要

简介我们进行了一项荟萃分析,评估幽门螺杆菌感染者罹患食管腺癌(EAC)的总体风险,并进行了一项网络荟萃分析,评估幽门螺杆菌感染在巴雷特食管(BE)发展为EAC过程中的作用:1988年至2023年6月期间,在MEDLINE、EMBASE和Cochrane数据库中检索了有关幽门螺杆菌感染和EAC风险的观察性研究。采用DerSimonian-Laird方法计算了总的几率比(OR)和95%置信区间(95% CI)。计算I2统计量以检查异质性:13项研究被纳入荟萃分析,另有3项研究被纳入网络荟萃分析。在与对照组的比较中,幽门螺杆菌感染者患 EAC 的几率比未感染幽门螺杆菌者低 46%(OR,0.54;95% CI:0.46,0.64),研究间的异质性较低(I2=4.4%)。与 11 项病例对照研究(OR=0.55)相比,两项大型队列研究(OR=0.31)的逆相关性更强。与对照组相比,6 项研究的网络荟萃分析表明,幽门螺杆菌感染与较低的胃食管反流病(OR=0.68)或 BE(OR=0.59)或 EAC(OR=0.54)风险相关;然而,幽门螺杆菌感染与 BE 患者的 EAC 风险无关(OR=0.91;95% CI:0.68, 1.21):这项荟萃分析提供了迄今为止最有力的证据,证明幽门螺杆菌感染与 EAC 呈反比关系。幽门螺杆菌似乎与 BE 进展为 EAC 无关。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Helicobacter pylori infection does not influence the progression from gastroesophageal reflux disease to Barrett's esophagus to esophageal adenocarcinoma.

Introduction: We conducted a meta-analysis evaluating the overall risk of esophageal adenocarcinoma (EAC) in individuals with Helicobacter pylori infection, and a network meta-analysis to assess the role of H. pylori infection in the progression from Barrett's esophagus (BE) to EAC.

Evidence acquisition: The MEDLINE, EMBASE and Cochrane databases were searched between 1988 and June 2023 for observational studies of H. pylori infection and the risk of EAC. Summary odds ratios (OR) and 95% confidence intervals (95% CI) were calculated using the DerSimonian-Laird method. I2 statistics were calculated to examine heterogeneity.

Evidence synthesis: Thirteen studies were included in the meta-analysis and 3 additional studies were included in the network meta-analysis. For comparisons with controls, individuals with H. pylori infection were 46% less likely to develop EAC than individuals without H. pylori infection (OR, 0.54; 95% CI: 0.46, 0.64), with low heterogeneity between studies (I2=4.4%). The magnitude of the inverse association was stronger in the two large cohort studies (OR=0.31) than in the 11 case-control studies (OR=0.55). When comparing to controls, the network meta-analysis of 6 studies showed that H. pylori infection was associated with a lower risk of GERD (OR=0.68) or BE (OR=0.59) or EAC (OR=0.54); however, H. pylori infection was not associated with risk of EAC in patients with BE (OR=0.91; 95% CI: 0.68, 1.21).

Conclusions: This meta-analysis provides the strongest evidence yet that H. pylori infection is inversely associated with EAC. H. pylori does not appear to be associated with BE progression to EAC.

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