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Helicobacter pylori and Esophageal Cancer Risk: A Meta-analysis

Authors' Affiliations: ¹ Digestive Disease Research Center, Medical Sciences/University of Tehran, Tehran, Iran; ² Lifestyle, Environment and Cancer Group, IARC, Lyon, France; ³ King's College London, Thames Cancer Registry, London, United Kingdom; and ⁴ Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Bethesda, Maryland

Requests for reprints: Farin Kamangar, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Room 3034, 6120 Executive Boulevard, Bethesda, MD 20892-7232. Phone: 301-594-2936; Fax: 301-496-6829; E-mail: kamangaf{at}mail.nih.gov.

We conducted this meta-analysis to examine the association between Helicobacter pylori and esophageal adenocarcinoma (EAC) and esophageal squamous cell carcinoma. We searched the PubMed database, the ISI database, and the references of the selected articles. Case-control or nested case-control studies were selected if they used serology or endoscopic methods to detect H. pylori in the stomach and if control subjects were not restricted to upper gastrointestinal tract cancer or peptic ulcer disease patients. A total of 19 studies were used for this analysis. Summary odds ratios (OR) and 95% confidence intervals (95% CI) were calculated using the DerSimonian-Laird method. Q statistics and I² statistics were calculated to examine heterogeneity. Subgroup analyses were conducted by CagA status. For EAC, the summary OR (95% CI) was 0.56 (0.46-0.68). There was little heterogeneity among studies (I² = 15%). Further analysis showed that colonization with CagA-positive strains was inversely associated with EAC risk (OR, 0.41; 95% CI, 0.28-0.62) but colonization with CagA-negative strains was not (OR, 1.08; 95% CI, 0.76-1.53). For esophageal squamous cell carcinoma, the summary OR (95% CI) was 1.10 (0.78-1.55). However, there was substantial heterogeneity among studies (I² = 73%), with statistically significant associations in both directions. Our results suggest an inverse association between CagA-positive H. pylori colonization and risk of EAC. The prominent decline of H. pylori colonization in the past few decades may be partly responsible for the recent increase in EAC incidence in Western countries.

Key Words: Helicobacter pylori • CagA • esophageal cancer • adenocarcinoma • squamous cell carcinoma • colonization

Commentary

Disappearing Microbiota: Helicobacter pylori Protection against Esophageal Adenocarcinoma

Martin J. Blaser
Cancer Prevention Research 2008 1: 308-311. [Full Text] [PDF]

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