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Helicobacter pylori and esophageal cancer risk: a meta-analysis.
Cancer Prev Res (Phila). 2008 Oct; 1(5):329-38.CP

Abstract

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 I(2) 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 (I(2) = 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 (I(2) = 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.

Authors+Show Affiliations

Digestive Disease Research Center, Medical Sciences/University of Tehran, Tehran, Iran.No affiliation info available

Pub Type(s)

Journal Article
Meta-Analysis
Research Support, N.I.H., Extramural

Language

eng

PubMed ID

19138977

Citation

Islami, Farhad, and Farin Kamangar. "Helicobacter Pylori and Esophageal Cancer Risk: a Meta-analysis." Cancer Prevention Research (Philadelphia, Pa.), vol. 1, no. 5, 2008, pp. 329-38.
Islami F, Kamangar F. Helicobacter pylori and esophageal cancer risk: a meta-analysis. Cancer Prev Res (Phila). 2008;1(5):329-38.
Islami, F., & Kamangar, F. (2008). Helicobacter pylori and esophageal cancer risk: a meta-analysis. Cancer Prevention Research (Philadelphia, Pa.), 1(5), 329-38. https://doi.org/10.1158/1940-6207.CAPR-08-0109
Islami F, Kamangar F. Helicobacter Pylori and Esophageal Cancer Risk: a Meta-analysis. Cancer Prev Res (Phila). 2008;1(5):329-38. PubMed PMID: 19138977.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Helicobacter pylori and esophageal cancer risk: a meta-analysis. AU - Islami,Farhad, AU - Kamangar,Farin, PY - 2009/1/14/entrez PY - 2009/1/14/pubmed PY - 2009/3/6/medline SP - 329 EP - 38 JF - Cancer prevention research (Philadelphia, Pa.) JO - Cancer Prev Res (Phila) VL - 1 IS - 5 N2 - 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 I(2) 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 (I(2) = 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 (I(2) = 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. SN - 1940-6215 UR - https://www.unboundmedicine.com/medline/citation/19138977/Helicobacter_pylori_and_esophageal_cancer_risk:_a_meta_analysis_ L2 - http://cancerpreventionresearch.aacrjournals.org/cgi/pmidlookup?view=long&pmid=19138977 DB - PRIME DP - Unbound Medicine ER -