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Serological assessment of gastric mucosal atrophy in gastric cancer

BACKGROUND: Non-invasive tools for gastric cancer screening and diagnosis are lacking. Serological testing with the detection of pepsinogen 1 (PG1), pepsinogen 2 (PG2) and gastrin 17 (G17) offers the possibility to detect preneoplastic gastric mucosal conditions. Aim of this study was to assess the...

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Autores principales: Bornschein, Jan, Selgrad, Michael, Wex, Thomas, Kuester, Doerthe, Malfertheiner, Peter
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3280182/
https://www.ncbi.nlm.nih.gov/pubmed/22289789
http://dx.doi.org/10.1186/1471-230X-12-10
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author Bornschein, Jan
Selgrad, Michael
Wex, Thomas
Kuester, Doerthe
Malfertheiner, Peter
author_facet Bornschein, Jan
Selgrad, Michael
Wex, Thomas
Kuester, Doerthe
Malfertheiner, Peter
author_sort Bornschein, Jan
collection PubMed
description BACKGROUND: Non-invasive tools for gastric cancer screening and diagnosis are lacking. Serological testing with the detection of pepsinogen 1 (PG1), pepsinogen 2 (PG2) and gastrin 17 (G17) offers the possibility to detect preneoplastic gastric mucosal conditions. Aim of this study was to assess the performance of these serological tests in the presence of gastric neoplasia. METHODS: Histological and serological samples of 118 patients with gastric cancer have been assessed for tumor specific characteristics (Laurén type, localisation), degree of mucosal abnormalities (intestinal metaplasia, atrophy) and serological parameters (PG1, PG2, PG1/2-ratio, G17, H. pylori IgG, CagA status). Association of the general factors to the different serological values have been statistically analyzed. RESULTS: Patients with intestinal type gastric cancer had lower PG1 levels and a lower PG1/2-ratio compared to those with diffuse type cancer (p = 0.003). The serum levels of PG2 itself and G17 were not significantly altered. H. pylori infection in general had no influence on the levels of PG1, PG2 and G17 in the serum of gastric cancer patients. There was a trend towards lower PG1 levels in case of positive CagA-status (p = 0.058). The degree of both intestinal metaplasia and atrophy correlated inversely with serum levels for PG1 and the PG1/2-ratio (p < 0.01). Laurén-specific analysis revealed that this is only true for intestinal type tumors. Univariate ANOVA revealed atrophy and CagA-status as the only independent factors for low PG1 and a low PG1/2-ratio. CONCLUSIONS: Glandular atrophy and a positive CagA status are determinant factors for decreased pepsinogen 1 levels in the serum of patients with gastric cancer. The serological assessment of gastric atrophy by analysis of serum pepsinogen is only adequate for patients with intestinal type cancer.
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spelling pubmed-32801822012-02-16 Serological assessment of gastric mucosal atrophy in gastric cancer Bornschein, Jan Selgrad, Michael Wex, Thomas Kuester, Doerthe Malfertheiner, Peter BMC Gastroenterol Research Article BACKGROUND: Non-invasive tools for gastric cancer screening and diagnosis are lacking. Serological testing with the detection of pepsinogen 1 (PG1), pepsinogen 2 (PG2) and gastrin 17 (G17) offers the possibility to detect preneoplastic gastric mucosal conditions. Aim of this study was to assess the performance of these serological tests in the presence of gastric neoplasia. METHODS: Histological and serological samples of 118 patients with gastric cancer have been assessed for tumor specific characteristics (Laurén type, localisation), degree of mucosal abnormalities (intestinal metaplasia, atrophy) and serological parameters (PG1, PG2, PG1/2-ratio, G17, H. pylori IgG, CagA status). Association of the general factors to the different serological values have been statistically analyzed. RESULTS: Patients with intestinal type gastric cancer had lower PG1 levels and a lower PG1/2-ratio compared to those with diffuse type cancer (p = 0.003). The serum levels of PG2 itself and G17 were not significantly altered. H. pylori infection in general had no influence on the levels of PG1, PG2 and G17 in the serum of gastric cancer patients. There was a trend towards lower PG1 levels in case of positive CagA-status (p = 0.058). The degree of both intestinal metaplasia and atrophy correlated inversely with serum levels for PG1 and the PG1/2-ratio (p < 0.01). Laurén-specific analysis revealed that this is only true for intestinal type tumors. Univariate ANOVA revealed atrophy and CagA-status as the only independent factors for low PG1 and a low PG1/2-ratio. CONCLUSIONS: Glandular atrophy and a positive CagA status are determinant factors for decreased pepsinogen 1 levels in the serum of patients with gastric cancer. The serological assessment of gastric atrophy by analysis of serum pepsinogen is only adequate for patients with intestinal type cancer. BioMed Central 2012-01-31 /pmc/articles/PMC3280182/ /pubmed/22289789 http://dx.doi.org/10.1186/1471-230X-12-10 Text en Copyright ©2012 Bornschein et al; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Bornschein, Jan
Selgrad, Michael
Wex, Thomas
Kuester, Doerthe
Malfertheiner, Peter
Serological assessment of gastric mucosal atrophy in gastric cancer
title Serological assessment of gastric mucosal atrophy in gastric cancer
title_full Serological assessment of gastric mucosal atrophy in gastric cancer
title_fullStr Serological assessment of gastric mucosal atrophy in gastric cancer
title_full_unstemmed Serological assessment of gastric mucosal atrophy in gastric cancer
title_short Serological assessment of gastric mucosal atrophy in gastric cancer
title_sort serological assessment of gastric mucosal atrophy in gastric cancer
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3280182/
https://www.ncbi.nlm.nih.gov/pubmed/22289789
http://dx.doi.org/10.1186/1471-230X-12-10
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