Section of Epidemiology and Population Sciences, Department of Medicine, Baylor College of Medicine, Houston, TX, USA. Division of Gastroenterology and Hepatology, University of North Carolina School of Medicine, Chapel Hill, NC, USA. QIMR Berghofer Medical Research Institute, Brisbane, QLD, Australia. Centre for Public Health, Queen's University Belfast, Belfast, Northern Ireland. Program in Epidemiology, Fred Hutchinson Cancer Research Center, Seattle, WA, USA. Division of Research, Kaiser Permanente Northern California, Oakland, CA, USA. San Francisco Medical Center, Kaiser Permanente Northern California, San Francisco, CA, USA. Section of Gastroenterology and Hepatology, Department of Medicine, Baylor College of Medicine, Houston, TX, USA. Center for Innovations in Quality, Effectiveness and Safety (IQuESt), Michael E DeBakey Veterans Affairs Medical Center, Houston, TX, USA. Center for Clinical Management Research, Ann Arbor Veterans Affairs Medical Center, Ann Arbor, MI, USA. Barrett's Esophagus Program, Division of Gastroenterology Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, MI, USA. Dan L Duncan Comprehensive Cancer Center, Baylor College of Medicine, Houston, TX, USA.
Am J Gastroenterol. 2018 Aug;113(8):1148-1155. doi: 10.1038/s41395-018-0070-3. Epub 2018 Jun 8.
Epidemiological studies of Helicobacter pylori infection and risk of Barrett's esophagus (BE) have reported conflicting results. We examined the association between H. pylori infection and BE and sought to determine whether the association is mediated by gastroesophageal reflux disease (GERD) and to identify potential effect modifiers.
We used individual level data from 1308 patients with BE (cases), 1388 population-based controls, and 1775 GERD controls in the Barrett's and Esophageal Adenocarcinoma Consortium (BEACON). We estimated study-specific odds ratios (ORs) and 95% CIs using multivariable logistic regression models and obtained summary risk estimates using a random-effects meta-analytic approach. We examined potential effect modification by waist-to-hip ratio (WHR), body mass index (BMI), and smoking status by conducting stratified analyses.
For comparisons with population-based controls, H. pylori infection was inversely associated with the risk of BE (adjusted OR = 0.44, 95% CI = 0.36-0.55), with no evidence of between-study heterogeneity (I = 0%). A stronger inverse association between H. pylori and BE was observed among individuals with the CagA-positive strain (P for interaction = 0.017). We found no evidence of interaction between WHR, BMI, smoking status, and H. pylori infection on the risk of BE. There was no association between H. pylori infection and BE for comparisons with GERD controls (OR = 0.96, 95% CI = 0.67-1.37; I = 48%).
This study provides the strongest evidence yet that H. pylori infection is strongly inversely associated with BE. This effect is probably mediated by a decrease in GERD in infected patients, since the protective effect disappears in patients with GERD symptoms.
幽门螺杆菌（H. pylori）感染与巴雷特食管（BE）风险的流行病学研究结果存在矛盾。我们检验了 H. pylori 感染与 BE 之间的关联性，并试图确定这种关联是否由胃食管反流病（GERD）介导，并确定潜在的效应修饰因子。
我们使用了 Barrett 和食管腺癌联合会（BEACON）中 1308 名 BE 患者（病例）、1388 名基于人群的对照者和 1775 名 GERD 对照者的个体水平数据。我们使用多变量逻辑回归模型估计了研究特异性比值比（OR）和 95%置信区间（CI），并使用随机效应荟萃分析方法获得了汇总风险估计值。我们通过分层分析检验了腰臀比（WHR）、体重指数（BMI）和吸烟状况的潜在效应修饰作用。
与基于人群的对照者相比，H. pylori 感染与 BE 的风险呈负相关（调整后的 OR=0.44，95%CI=0.36-0.55），且无研究间异质性（I=0%）。在 CagA 阳性菌株的个体中，H. pylori 与 BE 之间的负相关关系更强（交互作用检验 P=0.017）。我们没有发现 WHR、BMI、吸烟状况与 H. pylori 感染之间对 BE 风险的相互作用。与 GERD 对照者相比，H. pylori 感染与 BE 之间无关联（OR=0.96，95%CI=0.67-1.37；I=48%）。
本研究提供了迄今为止最强的证据表明，H. pylori 感染与 BE 呈强烈负相关。这种效应可能是通过感染患者中 GERD 的减少介导的，因为在有 GERD 症状的患者中，这种保护作用消失了。
