Center for Clinical Management Research, Ann Arbor Veterans Affairs Medical Center, Ann Arbor, Michigan; Division of Gastroenterology, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, Michigan.
Division of Gastroenterology, Department of Internal Medicine, University of Washington Medical School, Seattle, Washington.
Clin Gastroenterol Hepatol. 2014 Feb;12(2):239-45. doi: 10.1016/j.cgh.2013.08.029. Epub 2013 Aug 27.
BACKGROUND & AIMS: Infection with Helicobacter pylori, particularly the cytotoxin-associated gene A (cagA)+ strain, is believed to protect against Barrett's esophagus, but it is not clear if it protects against gastroesophageal reflux disease (GERD). We aimed to determine whether H pylori infection is associated with GERD symptoms, erosive esophagitis, and Barrett's esophagus within the same cohort.
We analyzed data from a case-control study of 533 men (ages, 50-79 y) who underwent colorectal cancer screening at 2 tertiary medical centers in Michigan between 2008 and 2011 and who also were recruited to undergo upper endoscopy. We assessed 80 additional men found to have Barrett's esophagus during clinically indicated upper-endoscopy examinations. Logistic regression was used to estimate the associations between serum antibodies against H pylori or cagA and GERD symptoms, esophagitis, and Barrett's esophagus, compared with randomly selected men undergoing colorectal cancer screens (n = 177).
H pylori infection was associated inversely with Barrett's esophagus (odds ratio [OR], 0.53; 95% confidence interval [CI], 0.29-0.97), particularly the cagA+ strain (OR, 0.36; 95% CI, 0.14-0.90). There was a trend toward an inverse association with erosive esophagitis (H pylori OR, 0.63; 95% CI, 0.37-1.08; and cagA+ OR, 0.47; 95% CI, 0.21-1.03). However, GERD symptoms were not associated with H pylori infection (OR, 0.948; 95% CI, 0.548-1.64; and cagA+ OR, 0.967; 95% CI, 0.461-2.03).
Based on a case-control study, infection with H pylori, particularly the cagA+ strain, is associated inversely with Barrett's esophagus. We observed a trend toward an inverse association with esophagitis, but not with GERD symptoms.
幽门螺杆菌(H. pylori)感染,尤其是细胞毒素相关基因 A(cagA)+株,被认为可预防 Barrett 食管,但它是否能预防胃食管反流病(GERD)尚不清楚。我们旨在确定在同一队列中,H. pylori 感染是否与 GERD 症状、糜烂性食管炎和 Barrett 食管相关。
我们分析了密歇根州 2 家三级医疗中心在 2008 年至 2011 年间进行的结直肠癌筛查中招募的 533 名男性(年龄 50-79 岁)的病例对照研究的数据,这些男性还接受了上消化道内镜检查。我们评估了在临床上进行上消化道内镜检查时发现的 80 名患有 Barrett 食管的额外男性。使用逻辑回归来估计与随机选择的接受结直肠癌筛查的男性(n=177)相比,针对 H. pylori 或 cagA 的血清抗体与 GERD 症状、食管炎和 Barrett 食管之间的关联。
H. pylori 感染与 Barrett 食管呈负相关(比值比[OR],0.53;95%置信区间[CI],0.29-0.97),尤其是 cagA+株(OR,0.36;95%CI,0.14-0.90)。与糜烂性食管炎呈负相关的趋势(H. pylori OR,0.63;95%CI,0.37-1.08;和 cagA+OR,0.47;95%CI,0.21-1.03)。然而,GERD 症状与 H. pylori 感染无关(OR,0.948;95%CI,0.548-1.64;和 cagA+OR,0.967;95%CI,0.461-2.03)。
基于病例对照研究,H. pylori 感染,尤其是 cagA+株,与 Barrett 食管呈负相关。我们观察到与食管炎呈负相关的趋势,但与 GERD 症状无关。