Non-endoscopic diagnosis of multifocal atrophic gastritis; efficacy of serum gastrin-17, pepsinogens and Helicobacter pylori antibodies.
OBJECTIVE
Infection with H. pylori is an important risk factor for the development of gastric cancer and glandular atrophy is an intermediate stage in gastric carcinogenesis. While screening the patients with atrophic gastritis by endoscopy is unrealistic, a concept of "serological gastric biopsy" based on measurement of gastric secretory proteins and peptides should be further validated. We sought to determine if the laboratory panel composed of serum PGI and protein stimulated gastrin-17 might select patients with MAG, and what is diagnostic significance of H. pylori serology in population of high prevalence of H. pylori infection.


METHODS
55 consecutive patients of both sexes (M/F 25/30; range of age 55 -81 years) were referred for gastroscopy with antrum and corpus mucosal biopsies. Patients with histological signs of glandular atrophy at any site of the stomach were considered to have multifocal atrophic gastritis. A first blood sample was collected for measurement of basal gastrin-17, pepsinogens and H. pylori IgG-antibodies, and second was taken 20 minutes after use of protein-rich drink to measure stimulated gastrin-17.


RESULTS
Signs of mucosal atrophy were found in 19 patients, while 29 patients showed non-atrophic gastritis and seven H. pylori-negative patients had no histological pathology. Low serum level of stimulated gastrin-17 (< 5 pmol/l) and/or pepsinogen I (< 50 microg/l), were found in 16 of 19 patients (84.2%) with and in 7 of 36 patients (19.4%) without atrophy in the histological study. Combining of H. pylori serology with serum levels of secretory peptides had no significant effect on diagnostic sensitivity of the test panel.


CONCLUSIONS
The test panel composed of pepsinogen I and protein stimulated gastrin-17 may be used as the "serological gastric biopsy" detecting multifocal atrophic gastritis. The diagnostic sensitivity of this test panel is not increased by knowledge of H. pylori status.
Hartleb
M
M
Department of Gastroenterology, Silesian University of Medicine, Katowice, Poland. lakmus@poczta.wprost.pl
Wandzel
P
P
Waluga
M
M
Matyszczyk
B
B
Bołdys
H
H
Romañczyk
T
T
D000368:Aged; D000369:Aged, 80 and over; D000907:Antibodies, Bacterial / Q000097:blood / Q000276:immunology; D015415:Biomarkers / Q000097:blood; D005260:Female; D005755:Gastrins / Q000097:blood; D005757:Gastritis, Atrophic / Q000097:blood / Q000175:diagnosis* / Q000201:enzymology / Q000382:microbiology; D005773:Gastroscopy; D016481:Helicobacter Infections / Q000097:blood / Q000175:diagnosis; D016480:Helicobacter pylori / Q000276:immunology / Q000378:metabolism; D006801:Humans; D008297:Male; D008875:Middle Aged; D020116:Pepsinogen A / Q000097:blood; D011446:Prospective Studies; D012680:Sensitivity and Specificity; D012698:Serologic Tests
D000907:Antibodies, Bacterial; D015415:Biomarkers; D005755:Gastrins; C013550:gastrin 17; D020116:Pepsinogen A