Abstract

INTRODUCTION: The prevalence of H Pylori (HP) is known to be reduced in patients with GERD and Barrett’s Esophagus (BE) compared to population controls without GERD. However, the prevalence of HP does not differ between GERD patients and BE patients, implying that H Pylori does not influence progression of GERD to BE. We have conducted a systematic review and meta-analysis of the prevalence of HP in population controls compared to patients with Esophageal Adenocarcinoma (EAC). Additionally, we have compared HP prevalence in population controls compared to BE patients to EAC patients. METHODS: The MEDLINE, Ovid and Web of Science databases were searched starting in 1988 to 2019. The literature search was conducted using the terms “helicobacter pylori” or “h pylori” or “HP” and “esophageal neoplasms or adenocarcinoma” or “EAC” or “esophageal adenocarcinoma or cancer” or “esophageal tumour.” RESULTS: Literature search revealed 3045 studies, and 284 abstracts were reviewed based on the title. Based on the abstract review 35 full text articles were reviewed and 14 studies were selected for the analysis of HP in controls vs EAC patients. Eleven studies used serology to classify patients as HP positive or negative. Three studies used biopsy to classify patients as HP positive or negative. The 2 cohort studies which were the largest studies in this meta-analysis, included 10158 patients seronegative for HP and 11342 patients seropositive for HP. Patients in these cohort studies were followed for more than 15 years. The pooled odd ratio for EAC in patients with HP positive infection was 0.559 (95% CI 0.466–0.670, P Value 0.00). Thus, HP positivity decreases the risk of EAC by 45%. Additionally, we identified 5 studies that compared prevalence of HP in controls and BE patients and EAC patients. There was no difference in prevalence of HP between patients with BE and EAC. CONCLUSION: We report a lower prevalence of HP infection in EAC patients compared to population controls, but no difference in HP prevalence between patients with BE and EAC. This implies that HP infection seems to protect against the development of BE or EAC, but does not influence the progression of BE to EAC. Widespread antibiotic use may lead to changes in the bacterial microbiome other than eradication of HP. Further studies are needed to delineate non-HP related changes in the bacterial microbiome contributing to the increasing incidence of EAC.Figure 1Figure 2.: Forrest Plot of Pooled Odds ratio of BE & EAC in H. Pylori Positive with GERD as Control.

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