Original article—alimentary tract
Relationship Between Helicobacter pylori Infection and Esophageal Neoplasia: A Meta-analysis

A preliminary report of some of the results in this study has been presented at the XIX International Workshop on Helicobacter and Related Bacteria in Chronic Digestive Inflammation, Wroclaw, Poland, September 7-9, 2006.
https://doi.org/10.1016/j.cgh.2007.08.010Get rights and content

Background & Aims:Helicobacter pylori is an important causative factor in gastric carcinogenesis. However, its role in extragastric gastrointestinal malignancies, such as esophageal cancer, is controversial. The aim of this study was to explore the relationship of H pylori infection and H pylori cagA–positive strain with this malignancy by performing meta-analysis of all relevant studies. Methods: Extensive MEDLINE English language medical literature searches for human studies were performed through February 2007 with suitable keywords. Pooled estimates were obtained by using fixed or random-effects model as appropriate. Heterogeneity between studies was evaluated with the Cochran Q test, whereas the likelihood of publication bias was assessed by constructing funnel plots. Their symmetry was estimated by the Begg and Mazumdar adjusted rank correlation test. Results: In adenocarcinoma patients there were inverse significant relationships with both the H pylori prevalence (pooled odds ratio [OR], 0.52; 95% confidence interval [CI], 0.37–0.73; P < .001) and the prevalence of H pylori cagA–positive strain (pooled OR, 0.51; 95% CI, 0.31–0.82; P = .006). Similarly in patients with Barrett’s esophagus there were inverse significant relationships (pooled OR, 0.64; 95% CI, 0.43–0.94; P = .025 and pooled OR, 0.39; 95% CI, 0.21–0.76; P = .005, respectively). In patients with squamous cell carcinoma there were no significant relationships with both H pylori prevalence (pooled OR, 0.85; 95% CI, 0.55–1.33; P = .48) and the prevalence of H pylori cagA–positive strains (pooled OR, 1.22; 95% CI, 0.7–2.13; P = .48). Conclusions: The results showed an inverse statistically significant relationship of H pylori infection with both esophageal adenocarcinoma and Barrett’s esophagus, which might suggest a protective role of the infection in these entities. On the contrary, no statistically significant relationship with squamous cell carcinoma was found.

Section snippets

Data Identification and Extraction

We searched the PubMed, MEDLINE, and Embase databases through February 2007 to identify all relevant English language medical literature for human studies under the search text terms helicobacter pylori AND (esophageal cancer OR esophageal neoplasms OR Barrett’s esophagus OR adenocarcinoma OR squamous cell carcinoma). We also performed a full manual search of all review articles, recently published editorials, and retrieved original studies. Data were extracted independently from each study by

Descriptive Assessment and Study Characteristics

A flow chart describing the process of study selection is shown in Figure 1. Of 238 titles initially generated by the literature searches, 18 studies, of which 9 were case-control and 9 cohort studies, remained eligible for meta-analysis.19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31, 32, 33, 34, 35, 36 Initial agreement between the reviewers for the selection of relevant articles was high (κ = 0.94, 95% CI, 0.86–1).

In the 18 meta-analysis studies there were 22 sets of data comparing H

Discussion

In this study we pooled the data of published studies in an effort to examine the relationships between H pylori infection and esophageal neoplasia by meta-analysis of all relevant cohort and case-control studies.

The results showed an inverse relationship of H pylori as well as the H pylori cagA–positive strain prevalence with both BE and AC, suggesting that H pylori infection might play a protective role in this type of esophageal malignancy. The results are in accordance with those of a

Supplementary Data

Note: To access the supplementary material accompanying this article, visit the online version of Clinical Gastroenterology and Hepatology at www.cghjournal.org.

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