Is There a Difference in the Prevalence of Helicobacter pylori Infection between Short-Segment and Long-Segment Barrettʼs Esophagus?

Abstract

Purpose: Recent studies suggest that the length of Barrett's esophagus (BE) is a risk factor for neoplastic progression. Patients with long-segment Barrett's esophagus (LSBE) are at higher risk for development of dysplasia and adenocarcinoma of the esophagus when compared with short-segment Barrett's esophagus (SSBE), which suggests that different pathophysiological mechanisms may be involved in SSBE and LSBE. To date, the role of H. pylori infection in the development of BE is still unclear. We aimed to investigate by meta-analysis if any difference exists in the prevalence of H. pylori infection between SSBE and LSBE. Methods: Observational studies comparing the prevalence of H. pylori infection or cagA+ H. pylori strains in patients with SSBE (length < 3 cm) and LSBE (length ≥ 3 cm) conducted in adult populations and published in all languages were identified through MEDLINE, EMBASE and Cochrane database searches until week 21, 2007. H. pylori infection required confirmation by histology and/or serology and/or RUT and/or culture. Primary outcome was the prevalence of H. pylori infection in SSBE and LSBE. Secondary outcome was the prevalence of cagA+ H. pylori strains in SSBE and LSBE. Studies were excluded if lacking raw data for outcome of interest or were duplicate publications. Summary effect size was calculated as odds ratios (OR) and 95% confidence intervals (CI) by the random-effects model using Review Manager 4.2.8. Results: Of 458 citations, 13 studies met inclusion criteria. 825 patients with SSBE and 470 with LSBE were included for analysis. The prevalence of H. pylori infection was significantly higher in SSBE than in LSBE [39.6% (327/825) and 29.6% (139/470) respectively, OR = 1.49, 95% CI 1.02–2.18, P= 0.04], and homogeneity was seen between studies (P= 0.14). The results from 4 studies in H. pylori positive patients showed no difference in cagA+ H. pylori strains between SSBE and LSBE [36.7% (18/49) and 37.8% (14/37) respectively, OR = 0.51, 95% CI 0.08–3.04, P= 0.46], with homogeneity (P= 0.14). Conclusion: The prevalence of H. pylori infection in LSBE is significantly lower than in SSBE, which suggests that H. pylori infection plays a different role, if any, in these two subtypes of BE and does not “protect” in patients with SSBE. Current evidence does not confirm a role for cagA+ in subtypes of BE although the sample size was small. Large prospective studies are needed to confirm these results in the future.