Association of Helicobacter pylori Infection with Esophageal Malignancies: Is There a Difference Between Western and Eastern Populations?

Abstract

Purpose: To date, a possible role of Helicobacter pylori (H. pylori) infection in esophageal malignancies is not clear. We aimed to explore the relationship between H. pylori infection and esophageal cancer, different types of esophageal cancer, and different populations by meta-analysis. Methods: By computer and manually, observational studies comparing the prevalence of H. pylori infection in patients with esophageal cancer and controls conducted in adult populations and published in all languages were identified through MEDLINE, EMBASE and Cochrane database searches published until to June Week 1, 2011 (MEDLINE), Week 26, 2011 (EMBASE), and June Week 1, 2011 (Pubmed). H. pylori infection must be confirmed by histology and/or serology and/or RUT and/or culture. Summary effect size was calculated as odds ratios (OR) and 95% confidence intervals (CI) by the randomeffects model with Review Manager 4.2.8. Tests for homogeneity were done. Results: Of 328 citations identified, 21 studies met inclusion criteria. 2947 patients with esophageal cancer and 7243 controls were identified. Overall prevalence of H. pylori infection in esophageal cancer compared with controls was 41.7% (1228/2947) vs 47.8% (3463/7243) (OR = 0.72, 95% CI 0.59-0.87, P = 0.0009) with big heterogeneity (I2 = 69.7%, P<0.00001). The prevalence of H. pylori infection was significantly lower in esophageal adenocarcinoma than that in controls [31.9% (366/1146) vs 41.1% (1779/4327), OR = 0.56, 95% CI 0.46-0.68, P<0.00001] with homogeneity (I2 = 24.1%, P = 0.19) in the 14 studies. However, there was no difference in the H. pylori prevalence between esophageal squamous cell carcinoma and controls [47.8% (775/1622) vs 45.8% (2190/4780), OR = 0.93, 95% CI 0.67-1.29, P = 0.66], with significant heterogeneity (I2 = 82.5%, P<0.00001) in the 11 studies. Interestingly, the prevalence of H. pylori infection was significantly lower in esophageal cancer than that in controls [33.6% (552/1645) vs 41.3% (1780/4307), OR = 0.65, 95% CI 0.54-0.78, P<0.00001] with homogeneity (I2 = 35.9%, P = 0.10) in the 13 studies from the Western populations, but there was no difference in the H. pylori prevalence between esophageal carcinoma and controls [51.9% (676/1302) vs 57.3% (1683/2936), OR = 0.89, 95% CI 0.59-1.32, P = 0.56], with significant heterogeneity (I2 = 84.4%, P<0.00001) in the 8 studies from the Asian populations. Conclusion:H. pylori infection is inversely related to esophageal adenocarcinoma strongly suggesting that H. pylori infection has no aetiological role in esophageal adenocarcinoma. There is no clear relationship between H. pylori infection and esophageal squamous cell carcinoma. There may be a different association of H. pylori infection with esophageal malignancies between Western and Eastern populations.