Data from The Role of Gastric Atrophy in the Association between Helicobacter pylori Infection and Esophageal Adenocarcinoma

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Abstract Background: The mechanisms underlying pathways linking Helicobacter pylori infection, gastric atrophy, and esophageal adenocarcinoma have yet to be quantitatively investigated. Methods: Four hundred thirty-five patients with esophageal adenocarcinoma and 1,298 cancer-free subjects were included from the International Barrett’s and Esophageal Adenocarcinoma Consortium (BEACON). Samples were collected from 1993 to 2004. Gastric atrophy was determined by serum pepsinogens. H. pylori infection was assessed by antibodies against 15 antigens. Logistic regression models were fitted to estimate odds ratio (OR) and quantify the association between antibodies and gastric atrophy. A 4-way decomposition of the overall effect into natural direct and indirect effects was used to measure the mediating effects of mediators between H. pylori and esophageal adenocarcinoma while also considering their role as effect modifiers. Results: Seropositivity for 15 H. pylori antigens was associated with a lower risk of esophageal adenocarcinoma; the ORs ranged from 0.44 (95% CI, 0.40–0.49) to 0.91 (95% CI, 0.84–0.98). Seropositivity for multiple antigens was also associated with a reduced risk of esophageal adenocarcinoma. The effect of H. pylori infection was not mediated through gastric atrophy, body mass index (BMI), and gastroesophageal reflux disease (GERD), whether these factors were examined individually or combined, as the estimates of natural indirect effects were close to 0. Conclusions: This study confirmed the inverse association between H. pylori and esophageal adenocarcinoma, which was not mediated by gastric atrophy or the combination with BMI and GERD. Impact: It suggests refining esophageal adenocarcinoma risk prediction models and exploring other potential mediators and pathways between H. pylori and esophageal adenocarcinoma.

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