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Cancer Epidemiology Biomarkers & Prevention 16, 322-326, February 1, 2007. doi: 10.1158/1055-9965.EPI-06-0885
© 2007 American Association for Cancer Research

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Smoking, Helicobacter pylori Virulence, and Type of Intestinal Metaplasia in Portuguese Males

Bárbara Peleteiro1, Nuno Lunet1, Céu Figueiredo2,3, Fátima Carneiro2,3,4, Leonor David2,3 and Henrique Barros1

Departments of 1 Hygiene and Epidemiology and 2 Pathology, Medical Faculty of the University of Porto; 3 Institute of Molecular Pathology and Immunology, University of Porto (IPATIMUP); and 4 Department of Pathology, Hospital S. João, Porto, Portugal

Requests for reprints: Bárbara Peleteiro, Serviço de Higiene e Epidemiologia, Faculdade de Medicina da Universidade do Porto, Al. Prof. Hernâni Monteiro, 4200-319 Porto, Portugal. Phone: +351-22-551-3652; Fax: +351-22-551-3653. E-mail: barbarap{at}med.up.pt

High-virulence Helicobacter pylori strains and smoking increase the risk of gastric precancerous lesions. However, its association with specific types of intestinal metaplasia has been poorly studied. We aimed to quantify the association between different types of intestinal metaplasia (complete, incomplete, and mixed) and these two risk factors. Male volunteers (n = 227) underwent an upper digestive endoscopy and completed symptoms and lifestyle questionnaires. A histologic diagnosis was assigned based on the lesions found in any of the biopsy specimens (antrum, body, or incisura). H. pylori vacA and cagA were directly genotyped by multiplex PCR and reverse hybridization. Each participant's smoking status at the time of endoscopy was assessed. Logistic and multinomial logistic regression models were fitted (including H. pylori virulence, smoking, age, and education as independent variables) using normal/chronic nonatrophic gastritis as the reference category. Compared with never smokers infected with low-virulence strains, the risk of intestinal metaplasia was increased in subjects infected with high-virulence strains [odds ratio (OR), 5.74; 95% confidence interval (95% CI), 1.68-19.63] and in ever smokers (OR, 3.54; 95% CI, 1.30-9.61). In ever smokers infected with high-virulence H. pylori strains, the risk of intestinal metaplasia was further increased (OR, 8.61; 95% CI, 3.07-24.17). Infection with high-virulence strains significantly increased the risk of incomplete (OR, 9.81; 95% CI, 2.39-40.31) and mixed (OR, 3.28; 95% CI, 1.51-7.14) intestinal metaplasia. Complete (OR, 2.82; 95% CI, 1.01-7.88) and mixed (OR, 2.97; 95% CI, 1.12-7.84) intestinal metaplasia were more frequent among ever smokers. High-virulence H. pylori strains and smoking are differentially associated with the complete and incomplete types of intestinal metaplasia, suggesting divergent pathways in gastric carcinogenesis. (Cancer Epidemiol Biomarkers Prev 2007;16(2):322–6)







HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cancer Prevention Research
Cancer Prevention Journals Portal Cancer Reviews Online
Annual Meeting Education Book Meeting Abstracts Online
Copyright © 2007 by the American Association for Cancer Research.