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Gastric epithelial cell proliferation and cagA status in Helicobacter pylori gastritis at different gastric sites.
Scand J Gastroenterol. 2007 May; 42(5):545-54.SJ

Abstract

OBJECTIVE

Helicobacter pylori infection causes hyperproliferation which is believed to predispose to the development of gastric carcinoma. The aim of this study was to analyze epithelial cell proliferation topographically in H. pylori gastritis in relationship to cagA status.

MATERIAL AND METHODS

The proliferative index (PI: Ki-67-labeled nuclei/total number of foveolar nuclei) was determined in gastric mucosa biopsies taken at the antrum (lesser and greater curvatures), incisura, and corpus (greater curvature) from 78 patients with H. pylori gastritis and 20 H. pylori-negative patients. H. pylori and cagA status were determined by polymerase chain reaction (PCR) and serology.

RESULTS

PIs were significantly higher in H. pylori- and cagA-positive patients, in comparison with H. pylori- and cagA-negative patients, at all sites (p<or=0.002 and p<or=0.009) and in the antrum in comparison to the corpus, in both H. pylori-negative (p=0.04) and positive patients (p<10(-3)). At the antral lesser curvature, PIs were higher than in all the other sites, both in H. pylori- (p<or=0.002) and cagA-positive groups (p<or=0.02). The PI correlated directly and significantly with inflammation in infected patients (r=0.45, p<10(-3)) and in cagA-positive patients (r=0.41, p=0.005). The PI was significantly higher in the antrum of infected patients with atrophy (p=0.03) and intestinal metaplasia (p=0.05) than in those without atrophy and intestinal metaplasia, respectively.

CONCLUSIONS

We demonstrated that H. pylori infection and cagA-positive strains promote epithelial proliferation that was correlated with host inflammatory reaction and mostly at the antral lesser curvature, which is recognized as the area where most carcinomas arise.

Authors+Show Affiliations

Faculty of Medicine, Department of Pathology, Laboratory of Research in Bacteriology, University Hospital Federal University of Minas Gerais, Brazil.No 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
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

17454874

Citation

Cabral, Mônica M D A., et al. "Gastric Epithelial Cell Proliferation and cagA Status in Helicobacter Pylori Gastritis at Different Gastric Sites." Scandinavian Journal of Gastroenterology, vol. 42, no. 5, 2007, pp. 545-54.
Cabral MM, Oliveira CA, Mendes CM, et al. Gastric epithelial cell proliferation and cagA status in Helicobacter pylori gastritis at different gastric sites. Scand J Gastroenterol. 2007;42(5):545-54.
Cabral, M. M., Oliveira, C. A., Mendes, C. M., Guerra, J., Queiroz, D. M., Rocha, G. A., Rocha, A. M., & Nogueira, A. M. (2007). Gastric epithelial cell proliferation and cagA status in Helicobacter pylori gastritis at different gastric sites. Scandinavian Journal of Gastroenterology, 42(5), 545-54.
Cabral MM, et al. Gastric Epithelial Cell Proliferation and cagA Status in Helicobacter Pylori Gastritis at Different Gastric Sites. Scand J Gastroenterol. 2007;42(5):545-54. PubMed PMID: 17454874.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Gastric epithelial cell proliferation and cagA status in Helicobacter pylori gastritis at different gastric sites. AU - Cabral,Mônica M D A, AU - Oliveira,Celso A, AU - Mendes,Cláudia M C, AU - Guerra,Juliana, AU - Queiroz,Dulciene M M, AU - Rocha,Gifone A, AU - Rocha,Andreia M C, AU - Nogueira,Ana M M F, PY - 2007/4/25/pubmed PY - 2008/4/18/medline PY - 2007/4/25/entrez SP - 545 EP - 54 JF - Scandinavian journal of gastroenterology JO - Scand J Gastroenterol VL - 42 IS - 5 N2 - OBJECTIVE: Helicobacter pylori infection causes hyperproliferation which is believed to predispose to the development of gastric carcinoma. The aim of this study was to analyze epithelial cell proliferation topographically in H. pylori gastritis in relationship to cagA status. MATERIAL AND METHODS: The proliferative index (PI: Ki-67-labeled nuclei/total number of foveolar nuclei) was determined in gastric mucosa biopsies taken at the antrum (lesser and greater curvatures), incisura, and corpus (greater curvature) from 78 patients with H. pylori gastritis and 20 H. pylori-negative patients. H. pylori and cagA status were determined by polymerase chain reaction (PCR) and serology. RESULTS: PIs were significantly higher in H. pylori- and cagA-positive patients, in comparison with H. pylori- and cagA-negative patients, at all sites (p<or=0.002 and p<or=0.009) and in the antrum in comparison to the corpus, in both H. pylori-negative (p=0.04) and positive patients (p<10(-3)). At the antral lesser curvature, PIs were higher than in all the other sites, both in H. pylori- (p<or=0.002) and cagA-positive groups (p<or=0.02). The PI correlated directly and significantly with inflammation in infected patients (r=0.45, p<10(-3)) and in cagA-positive patients (r=0.41, p=0.005). The PI was significantly higher in the antrum of infected patients with atrophy (p=0.03) and intestinal metaplasia (p=0.05) than in those without atrophy and intestinal metaplasia, respectively. CONCLUSIONS: We demonstrated that H. pylori infection and cagA-positive strains promote epithelial proliferation that was correlated with host inflammatory reaction and mostly at the antral lesser curvature, which is recognized as the area where most carcinomas arise. SN - 0036-5521 UR - https://www.unboundmedicine.com/medline/citation/17454874/Gastric_epithelial_cell_proliferation_and_cagA_status_in_Helicobacter_pylori_gastritis_at_different_gastric_sites_ L2 - https://www.tandfonline.com/doi/full/10.1080/00365520601014034 DB - PRIME DP - Unbound Medicine ER -