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Review
. 2022 Apr;27(2):e12872.
doi: 10.1111/hel.12872. Epub 2022 Jan 8.

Pepsinogen II in gastritis and Helicobacter pylori infection

Francesco Di Mario  1 , Pellegrino Crafa  1 , Alberto Barchi  1 , Lorella Franzoni  1 , Marilisa Franceschi  2 , Michele Russo  1 , Ludovica Bricca  3 , Lorenzo Brozzi  2 , Kryssia Rodriguez Castro  2 , Massimo Rugge  3   4
Affiliations
Review

Pepsinogen II in gastritis and Helicobacter pylori infection

Francesco Di Mario et al. Helicobacter. 2022 Apr.

Abstract

Background and aim: In the gastric mucosa, pepsinogen II (PgII) is produced/secreted by glands in the mucus-secreting antral and cardia compartments, but also by the chief cells and the oxyntic glands. Increasing PgII serum levels are associated with the whole spectrum of gastric inflammatory diseases, including gastritis induced by Helicobacter pylori (H. pylori). This review critically addresses the clinical value of PgII serology for assessing gastric mucosal inflammation, and as a marker of H. pylori status, in both H. pylori-positive patients and after eradication therapy.

Results: A search in PubMed/Scopus records yielded 39 out of 1190 published scientific studies meeting the selection criteria for this study. In the studies considered, PgII levels were significantly associated with non-atrophic gastric inflammatory lesions (p-values: 0.025-0.0001). H. pylori-positive patients had significantly higher PgII levels than H. pylori-negative individuals (p-values: 0.o5-0.0001). While a significant drop in serum PgII levels is consistently reported in H. pylori-eradicated patients (p-values: from 0.05 to 0.0001), inconsistencies in the related negative and positive predictive values significantly lower the clinical reliability of PgII testing by comparison with other available non-invasive tests.

Conclusions: PgII serology may provide clinically useful information on gastric inflammatory diseases, particularly if they are non-atrophic. PgII serology is inconsistent, however, for the purposes of distinguishing patients whose H. pylori eradication therapy is successful from those who remain infected.

Keywords: Helicobacter pylori; dyspepsia; gastritis; pepsinogen II.

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References

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