## Abstract ## Background. Gastroesophageal reflux, by exposing the pharynx to __Helicobacter pylori__ (__H. pylori__), is a potential risk factor for laryngohypopharyngeal carcinoma. Its possible association has been inconsistent. In this caseโcontrol study, we investigated the relationship betwe
Association between Helicobacter pylori infection and inflammatory bowel disease: A meta-analysis and systematic review of the literature
โ Scribed by Jay Luther; Maneesh Dave; Peter D.R. Higgins; John Y. Kao
- Publisher
- John Wiley and Sons
- Year
- 2010
- Tongue
- English
- Weight
- 451 KB
- Volume
- 16
- Category
- Article
- ISSN
- 1078-0998
No coin nor oath required. For personal study only.
โฆ Synopsis
Background: Epidemiologic data suggest a protective effect of Helicobacter pylori infection against the development of autoimmune disease. Laboratory data illustrate H. pylori's ability to induce immune tolerance and limit inflammatory responses. Numerous observational studies have investigated the association between H. pylori infection and inflammatory bowel disease (IBD). Our aim was to perform a systematic review and meta-analysis of this association.
Methods: Medline, EMBASE, bibliographies, and meeting abstracts were searched by 2 independent reviewers. Of 369 abstracts reviewed, 30 promising articles were reviewed in detail. Twentythree studies met our inclusion criteria (subject N ยผ 5903). Metaanalysis was performed with the metan command in Stata 10.1.
Results: Overall, 27.1% of IBD patients had evidence of infection with H. pylori compared to 40.9% of patients in the control group. The estimated relative risk of H. pylori infection in IBD patients was 0.64 (95% confidence interval [CI]: 0.54-0.75). There was significant heterogeneity in the included studies that could not be accounted for by the method of IBD and H. pylori diagnosis, study location, or study population age.
Conclusions: These results suggest a protective benefit of H. pylori infection against the development of IBD. Heterogeneity among studies and the possibility of publication bias limit the certainty of this finding. Further studies investigating the effect of eradication of H. pylori on the development of IBD are warranted. Because environmental hygiene and intestinal microbiota may be strong confounders, further mechanistic studies in H. pylori mouse models are also necessary to further define the mechanism of this negative association.
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