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Variation in Serum Pepsinogens With Severity and Topography of Helicobacter pylori ‐Associated Chronic Gastritis in Dyspeptic Patients Referred for Endoscopy
Author(s) -
Bodger Keith,
Wyatt Judy I.,
Heatley Richard V.
Publication year - 2001
Publication title -
helicobacter
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.206
H-Index - 79
eISSN - 1523-5378
pISSN - 1083-4389
DOI - 10.1046/j.1523-5378.2001.00031.x
Subject(s) - gastritis , gastroenterology , helicobacter pylori , medicine , chronic gastritis , antrum , pepsin , biopsy , endoscopy , gastric mucosa , stomach , biology , biochemistry , enzyme
ABSTRACT Background. It has long been recognised that specific patterns of gastritis are linked with different gastroduodenal diseases and that serum pepsinogens vary with the histological state of the gastric mucosa. With the discovery of the role of Helicobacter pylori in chronic gastritis and the availability of noninvasive tests for H. pylori infection, individuals with H. pylori gastritis can now be identified without endoscopic biopsy. However, without a knowledge of the pattern and severity of gastritis it is impossible to predict the likelihood of significant associated gastroduodenal pathology. Aims. The aim of this study was to evaluate the diagnostic potential of serum pepsinogens I and II in predicting the topography and severity of gastritis in H. pylori ‐infected dyspeptic patients attending for endoscopy. Methods. Fasting serum was obtained from consecutive dyspeptic patients attending for endoscopy, and pairs of gastric biopsies obtained from the mid‐body and antrum. Gastritis was graded according to the Sydney System, and serum pepsinogen levels determined by radio‐immunoassay. Results. Sixty‐nine dyspeptic patients were studied (mean age: 49.6 years) of whom 34 had H. pylori ‐associated chronic gastritis (Hp‐gastritis) – antral predominant gastritis (APG) in 41.2%, pangastritis (PAN) in 52.9%, and corpus predominant (CPG) in 5.9%. Serum pepsinogen II levels were significantly higher, and the serum pepsinogen I : II ratio significantly lower, in the H. pylori positive group than in other groups. Within the Hp‐gastritis group, there was a step‐wise decrease in serum pepsinogen I levels with progression from APG through PAN to CPG pattern (a cut‐off value of ≥ 100 ng/ml would have identified APG with a positive predictive value of 77%, though with low sensitivity). Within the Hp‐gastritis group, serum pepsinogen I and II levels were correlated with antral chronic inflammation score and serum pepsinogen II levels also with antral activity score. Serum pepsinogen I and the pepsinogen I : II ratio were lowest in severe gastric corpus atrophy. Conclusion. In dyspeptic patients known to be infected with H. pylori , serum pepsinogen values provide an assessment of the overall topography of gastritis, the severity of antral inflammation and the presence of severe corpus atrophy.