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Serum levels of amidated gastrin-17 and pepsinogen I in atrophic gastritis: an observational case-control study.
Scand J Gastroenterol. 2002 Jul; 37(7):785-91.SJ

Abstract

BACKGROUND

Helicobacter pylori infection is often diagnosed with non-endoscopic methods, such as serology or breath or antigen stool tests. These tests provide information on the presence or absence of the H. pylori gastritis only. We investigated whether atrophic gastritis can be diagnosed and typed non-endoscopically if the serum levels of pepsinogen I (S-PGI) and gastrin-17 (S-G-17) are assayed in connection with H. pylori testing.

METHODS

The present investigation is an observational case-control study comprising 100 selected dyspeptic outpatients with (cases) or without (controls) advanced (moderate or severe) atrophic gastritis. Before the blood tests, all patients underwent a diagnostic gastroscopy with multiple biopsies. The series of cases includes 56 patients. Eight had an advanced antrum limited atrophic gastritis, 13 had resected antrum (in two of whom the corpus mucosa in the stump was atrophic), and 30 had corpus-limited atrophic gastritis. Four patients had an advanced atrophic gastritis in both the antrum and corpus (multifocal atrophic gastritis), and the whole stomach was removed in one patient. Twenty of the 44 controls had a non-atrophic H. pylori gastritis. Both the antrum and corpus were normal and healthy in 24 patients. The S-PGI and S-G-17 were determined with EIA methods using monoclonal antibodies to PGI and amidated G-17. Postprandial S-G-17 (S-G-17prand) was measured 20 min after a protein-rich drink. The H. pylori antibodies were assayed with a polyclonal EIA method.

RESULTS

A low S-PGI (<25 microg/l; an empirical cut-off with best discrimination) was found in 31 of 37 patients (84%) with and in 3 of 63 patients (5%) without corpus atrophy in the biopsy specimens. A low S-G-17prand (<5 pmol/l) was found in all 8 patients with H. pylori-associated antral atrophy and in 11 of 14 patients (79%) with resected antrum but in 3 of 20 control patients (15%) with H. pylori-related non-atrophic gastritis. Median and mean values of both S-G-17prand and S-PGI decreased with increasing grade of antral and corpus atrophy, respectively. Among all patients with atrophic gastritis (multifocal atrophic gastritis, or atrophic gastritis limited to antrum or corpus) or resected stomach, 50 of 56 patients (89%; Cl 95%: 81%-97%) had a low S-PGI and/or a low S-G-17prand with positive H. pylori serology. Such low values werc found in 3 of the 44 control patients (7%; CI 95%: 0%-14%).

CONCLUSIONS

Low serum levels of G-17prand and PGI are conceivable biomarkers of atrophic antral and corpus gastritis, respectively. A low S-G-17prand is a sign of the multifocal or antrum-limited atrophic gastritis in patients infected with H. pylori.

Authors+Show Affiliations

Dept of Pathology, Helsinki District University Central Hospital, Espoo, Finland. pentti.sipponen@hus.fiNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article

Language

eng

PubMed ID

12190091

Citation

Sipponen, P, et al. "Serum Levels of Amidated Gastrin-17 and Pepsinogen I in Atrophic Gastritis: an Observational Case-control Study." Scandinavian Journal of Gastroenterology, vol. 37, no. 7, 2002, pp. 785-91.
Sipponen P, Ranta P, Helske T, et al. Serum levels of amidated gastrin-17 and pepsinogen I in atrophic gastritis: an observational case-control study. Scand J Gastroenterol. 2002;37(7):785-91.
Sipponen, P., Ranta, P., Helske, T., Kääriäinen, I., Mäki, T., Linnala, A., Suovaniemi, O., Alanko, A., & Härkönen, M. (2002). Serum levels of amidated gastrin-17 and pepsinogen I in atrophic gastritis: an observational case-control study. Scandinavian Journal of Gastroenterology, 37(7), 785-91.
Sipponen P, et al. Serum Levels of Amidated Gastrin-17 and Pepsinogen I in Atrophic Gastritis: an Observational Case-control Study. Scand J Gastroenterol. 2002;37(7):785-91. PubMed PMID: 12190091.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Serum levels of amidated gastrin-17 and pepsinogen I in atrophic gastritis: an observational case-control study. AU - Sipponen,P, AU - Ranta,P, AU - Helske,T, AU - Kääriäinen,I, AU - Mäki,T, AU - Linnala,A, AU - Suovaniemi,O, AU - Alanko,A, AU - Härkönen,M, PY - 2002/8/23/pubmed PY - 2003/1/17/medline PY - 2002/8/23/entrez SP - 785 EP - 91 JF - Scandinavian journal of gastroenterology JO - Scand. J. Gastroenterol. VL - 37 IS - 7 N2 - BACKGROUND: Helicobacter pylori infection is often diagnosed with non-endoscopic methods, such as serology or breath or antigen stool tests. These tests provide information on the presence or absence of the H. pylori gastritis only. We investigated whether atrophic gastritis can be diagnosed and typed non-endoscopically if the serum levels of pepsinogen I (S-PGI) and gastrin-17 (S-G-17) are assayed in connection with H. pylori testing. METHODS: The present investigation is an observational case-control study comprising 100 selected dyspeptic outpatients with (cases) or without (controls) advanced (moderate or severe) atrophic gastritis. Before the blood tests, all patients underwent a diagnostic gastroscopy with multiple biopsies. The series of cases includes 56 patients. Eight had an advanced antrum limited atrophic gastritis, 13 had resected antrum (in two of whom the corpus mucosa in the stump was atrophic), and 30 had corpus-limited atrophic gastritis. Four patients had an advanced atrophic gastritis in both the antrum and corpus (multifocal atrophic gastritis), and the whole stomach was removed in one patient. Twenty of the 44 controls had a non-atrophic H. pylori gastritis. Both the antrum and corpus were normal and healthy in 24 patients. The S-PGI and S-G-17 were determined with EIA methods using monoclonal antibodies to PGI and amidated G-17. Postprandial S-G-17 (S-G-17prand) was measured 20 min after a protein-rich drink. The H. pylori antibodies were assayed with a polyclonal EIA method. RESULTS: A low S-PGI (<25 microg/l; an empirical cut-off with best discrimination) was found in 31 of 37 patients (84%) with and in 3 of 63 patients (5%) without corpus atrophy in the biopsy specimens. A low S-G-17prand (<5 pmol/l) was found in all 8 patients with H. pylori-associated antral atrophy and in 11 of 14 patients (79%) with resected antrum but in 3 of 20 control patients (15%) with H. pylori-related non-atrophic gastritis. Median and mean values of both S-G-17prand and S-PGI decreased with increasing grade of antral and corpus atrophy, respectively. Among all patients with atrophic gastritis (multifocal atrophic gastritis, or atrophic gastritis limited to antrum or corpus) or resected stomach, 50 of 56 patients (89%; Cl 95%: 81%-97%) had a low S-PGI and/or a low S-G-17prand with positive H. pylori serology. Such low values werc found in 3 of the 44 control patients (7%; CI 95%: 0%-14%). CONCLUSIONS: Low serum levels of G-17prand and PGI are conceivable biomarkers of atrophic antral and corpus gastritis, respectively. A low S-G-17prand is a sign of the multifocal or antrum-limited atrophic gastritis in patients infected with H. pylori. SN - 0036-5521 UR - https://www.unboundmedicine.com/medline/citation/12190091/Serum_levels_of_amidated_gastrin_17_and_pepsinogen_I_in_atrophic_gastritis:_an_observational_case_control_study_ L2 - https://medlineplus.gov/helicobacterpyloriinfections.html DB - PRIME DP - Unbound Medicine ER -