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  • Title: Invasive and non-invasive diagnosis of Helicobacter pylori-associated atrophic gastritis: a comparative study.
    Author: Pasechnikov VD, Chukov SZ, Kotelevets SM, Mostovov AN, Mernova VP, Polyakova MB.
    Journal: Scand J Gastroenterol; 2005 Mar; 40(3):297-301. PubMed ID: 15932170.
    Abstract:
    OBJECTIVE: Helicobacter pylori-associated atrophic gastritis is known to be a significant risk factor for gastric cancer. Among the well-known parameters of atrophic gastritis are the levels of serum gastrin-17 (G-17) and pepsinogen I (PG1), which are biomarkers of gastric antral and corpus mucosal activity, respectively. The aim of study was to compare the production of G-17 and PG1 in patients with or without stomach mucosal atrophy and to investigate the utility of serum PG1 and/or G-17 concentrations for the objective evaluation of atrophic gastritis. MATERIAL AND METHODS: A total of 178 dyspeptic Helicobacter pylori-positive patients underwent diagnostic upper gastrointestinal endoscopy with biopsy. The degree of histologic gastric mucosal atrophy was compared with the fasting levels of PG1, and to the postprandial levels of G-17 detected by enzyme immunoassay. RESULTS: A decrease in serum G-17 levels along with worsening of the antral atrophy was observed; the serum levels of PG1 were reduced during progression of the corpus atrophy. In the multifocal atrophic gastritis, values for PG1 and G-17 serum concentrations were significantly lower than the respective cut-off values. Statistical analysis revealed statistically significant differences between the serum levels of PG1 and G-17 measured at different stages of stomach mucosal atrophy. CONCLUSIONS: A strong reverse correlation was found between histologic/ endoscopic antral atrophy and serum G-17 levels, and between corpus atrophy and serum PG1 levels.
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