Argyrophilic nucleolar organizer regions in Helicobacter pylori-associatedgastric lesions

Citation
V. Misra et al., Argyrophilic nucleolar organizer regions in Helicobacter pylori-associatedgastric lesions, APMIS, 108(6), 2000, pp. 448-452
Citations number
24
Categorie Soggetti
Medical Research General Topics
Journal title
APMIS
ISSN journal
09034641 → ACNP
Volume
108
Issue
6
Year of publication
2000
Pages
448 - 452
Database
ISI
SICI code
0903-4641(200006)108:6<448:ANORIH>2.0.ZU;2-I
Abstract
Three hundred and fifty biopsies from patients undergoing upper gastrointes tinal endoscopy were studied for histopathological changes, H. pylori infec tion and argyrophilic nucleolar organizer region (AgNOR) counts. Histopatho logical examination revealed normal gastric mucosa in 10 (2.85%), gastritis in 254 (72.56%), intestinal metaplasia in 12 (4.0%), dysplasia in 13 (3.7% ) and adenocarcinoma in 61 (17.4%). The mean (SD) AgNOR count was 1.66 (0.2 0) in normal, 2.43 (0.64) in gastritis, 3.09 (0.52) in intestinal metaplasi a, 4.17 (0.31) in dysplasia, and 6.57 (0.98) in carcinoma. A statistically significant difference was observed between the AgNOR count of normal gastr ic mucosa and gastritis (p < 0.001), gastritis and dysplasia (p < 0.001), a nd dysplasia and adenocarcinoma (p < 0.001). A statistically significant in crease in mean AgNOR count was found with increase in H. pylori density in gastric biopsies (p < 0.001) with gastritis. No significant difference was observed between mean AgNOR count of intestinal and diffuse type carcinomas . The AgNOR count in gastric biopsies with adenocarcinoma and H. pylori inf ection was 7.03 (0.85) as compared to 6.89 (0.73) in gastric biopsies with evidence of adenocarcinoma but without H. pylori infection. The difference was not statistically significant. The findings support the role of H. pylo ri as a promoting agent in gastric carcinogenesis by stimulating gastric ep ithelial cell proliferation at the stage of chronic inflammation, thereby m aking the cells more susceptible to endogenous or exogenous carcinogenic ag ents.