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Helicobacter pylori CagA status, mucosal oxidative damage and gastritis phenotype: a potential pathway to cancer?
Helicobacter 2003; 8(3):227-34H

Abstract

BACKGROUND

Oxidative DNA damage is associated with Helicobacter pylori infection, atrophy and intestinal metaplasia. H. pylori-cagA-positive strains are associated with the highest risk of gastric cancer.

AIMS

To ascertain whether cagA-positive H. pylori infection correlates with higher concentrations of 8OHdG and the presence of precancerous changes.

PATIENTS AND METHODS

118 patients were studied (65M/53F, age 61 +/- 14 years). Twelve were H. pylori-negative. Among the H. pylori-positive patients, 34 were cagA-positive and 40 were cagA negative. In 32 patients H. pylori had been eradicated at least 6 months before endoscopic sampling. The phenotype of the gastritis (atrophic compared with nonatrophic, with and without intestinal metaplasia) was scored in biopsy samples obtained from the antrum, corpus, and angularis incisura. In antral biopsy samples, 8-hydroxydeoxyguanosine was assessed by HPLC (electrochemical detector). CagA status was determined by PCR.

RESULTS

The highest scores for both mononuclear inflammation and activity of gastritis were significantly associated with cagA status (p = 0.036 antrum and p = 0.02 corpus). cagA-positive infection significantly correlated with a higher prevalence of atrophic-metaplastic lesions (p = 0.04). cagA-positive patients had higher 8-hydroxydeoxyguanosine levels than both cagA-negative and H. pylori-negative cases (p = 0.01). The 8-hydroxydeoxyguanosine levels were significantly higher in multifocal atrophic gastritis (p = 0.04). The odds ratio for cagA-positive patients having 8OHdG levels above a cut-off calculated on the basis of the ROC curves were 7.12, overall, reaching 11.25 when only patients younger than 50 were considered.

CONCLUSIONS

cagA-positive patients were characterized: first, for higher scores for gastritis, activity and atrophic and metaplastic lesions; and second for greater oxidative DNA damage overall, at younger age and in the presence of multifocal atrophy. This setting may represent a cancer-prone biological context.

Authors+Show Affiliations

Dipartimento di Scienze Chirurgiche e Gastroenterologiche - Sezione di Gastroenterologia, Università degli Studi di Padova, Italy.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

12752735

Citation

Farinati, Fabio, et al. "Helicobacter Pylori CagA Status, Mucosal Oxidative Damage and Gastritis Phenotype: a Potential Pathway to Cancer?" Helicobacter, vol. 8, no. 3, 2003, pp. 227-34.
Farinati F, Cardin R, Russo VM, et al. Helicobacter pylori CagA status, mucosal oxidative damage and gastritis phenotype: a potential pathway to cancer? Helicobacter. 2003;8(3):227-34.
Farinati, F., Cardin, R., Russo, V. M., Busatto, G., Franco, M., & Rugge, M. (2003). Helicobacter pylori CagA status, mucosal oxidative damage and gastritis phenotype: a potential pathway to cancer? Helicobacter, 8(3), pp. 227-34.
Farinati F, et al. Helicobacter Pylori CagA Status, Mucosal Oxidative Damage and Gastritis Phenotype: a Potential Pathway to Cancer. Helicobacter. 2003;8(3):227-34. PubMed PMID: 12752735.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Helicobacter pylori CagA status, mucosal oxidative damage and gastritis phenotype: a potential pathway to cancer? AU - Farinati,Fabio, AU - Cardin,Romilda, AU - Russo,Valentina M, AU - Busatto,Graziella, AU - Franco,Monica, AU - Rugge,Massimo, PY - 2003/5/20/pubmed PY - 2003/8/7/medline PY - 2003/5/20/entrez SP - 227 EP - 34 JF - Helicobacter JO - Helicobacter VL - 8 IS - 3 N2 - BACKGROUND: Oxidative DNA damage is associated with Helicobacter pylori infection, atrophy and intestinal metaplasia. H. pylori-cagA-positive strains are associated with the highest risk of gastric cancer. AIMS: To ascertain whether cagA-positive H. pylori infection correlates with higher concentrations of 8OHdG and the presence of precancerous changes. PATIENTS AND METHODS: 118 patients were studied (65M/53F, age 61 +/- 14 years). Twelve were H. pylori-negative. Among the H. pylori-positive patients, 34 were cagA-positive and 40 were cagA negative. In 32 patients H. pylori had been eradicated at least 6 months before endoscopic sampling. The phenotype of the gastritis (atrophic compared with nonatrophic, with and without intestinal metaplasia) was scored in biopsy samples obtained from the antrum, corpus, and angularis incisura. In antral biopsy samples, 8-hydroxydeoxyguanosine was assessed by HPLC (electrochemical detector). CagA status was determined by PCR. RESULTS: The highest scores for both mononuclear inflammation and activity of gastritis were significantly associated with cagA status (p = 0.036 antrum and p = 0.02 corpus). cagA-positive infection significantly correlated with a higher prevalence of atrophic-metaplastic lesions (p = 0.04). cagA-positive patients had higher 8-hydroxydeoxyguanosine levels than both cagA-negative and H. pylori-negative cases (p = 0.01). The 8-hydroxydeoxyguanosine levels were significantly higher in multifocal atrophic gastritis (p = 0.04). The odds ratio for cagA-positive patients having 8OHdG levels above a cut-off calculated on the basis of the ROC curves were 7.12, overall, reaching 11.25 when only patients younger than 50 were considered. CONCLUSIONS: cagA-positive patients were characterized: first, for higher scores for gastritis, activity and atrophic and metaplastic lesions; and second for greater oxidative DNA damage overall, at younger age and in the presence of multifocal atrophy. This setting may represent a cancer-prone biological context. SN - 1083-4389 UR - https://www.unboundmedicine.com/medline/citation/12752735/Helicobacter_pylori_CagA_status_mucosal_oxidative_damage_and_gastritis_phenotype:_a_potential_pathway_to_cancer L2 - https://onlinelibrary.wiley.com/resolve/openurl?genre=article&sid=nlm:pubmed&issn=1083-4389&date=2003&volume=8&issue=3&spage=227 DB - PRIME DP - Unbound Medicine ER -