gms | German Medical Science

Kongress Medizin und Gesellschaft 2007

17. bis 21.09.2007, Augsburg

Association of Helicobacter pylori infection with chronic atrophic gastritis. A systematic review

Meeting Abstract

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  • Melanie Weck - DKFZ, Heidelberg
  • Hermann Brenner - DKFZ, Heidelberg

Kongress Medizin und Gesellschaft 2007. Augsburg, 17.-21.09.2007. Düsseldorf: German Medical Science GMS Publishing House; 2007. Doc07gmds444

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Veröffentlicht: 6. September 2007

© 2007 Weck et al.
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Introduction / Background: Helicobacter pylori is thought to be a major risk factor for chronic atrophic gastritis (CAG), an important precancerous lesion in the development of stomach cancer. A large variety of definitions of CAG has been used in epidemiologic studies in the past. The aim of this work was to systematically review the association of H. pylori infection with CAG with particular attention to the various definitions of CAG.

Methods: Articles on the association between H. pylori infection and CAG published until March 2007 were identified by searching the MEDLINE database for co-occurence of the following terms in the abstract: helicobacter pylori & association & (i) atrophic gastritis / (ii) pepsinogen. Furthermore, references of all included articles and from reviews on related topics were screened for additional pertinent studies.

Results: Information on the association of H. pylori infection and CAG was retrieved from 43 articles with 13 different definitions of CAG. Associations were very weak when only the serum pepsinogen (PG) I concentration was used for CAG definition (ORs: 0.7 to 1.5). Much stronger associations were seen when a combination of PG I and the ratio of PG I / PG II (ORs: 1.9 to 34.9), the PG-ratio alone (ORs: 1.9 to 21.5) or gastroscopy with biopsy (ORs: 1.9 to 114.6) were applied.

Discussion / Conclusions: Diagnostic method and applied cutoff-value have a major impact on the observed association of H. pylori infection with CAG. The association of H. pylori infection with CAG may have been strongly underestimated in studies relying on pepsinogen I only.