Skip Navigation



Rheumatology Advance Access published online on June 29, 2004

Rheumatology, doi:10.1093/rheumatology/keh283
Rheumatology © British Society for Rheumatology 2004; all rights reserved
This Article
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
43/9/1182    most recent
keh283v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Gonzalez-Gay, M. A.
Right arrow Articles by Martin, J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Gonzalez-Gay, M. A.
Right arrow Articles by Martin, J.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Received January 11, 2004
Accepted May 28, 2004

Original Papers

Inducible but not endothelial nitric oxide synthase polymorphism is associated with susceptibility to rheumatoid arthritis in northwest Spain

M. A. Gonzalez-Gay 1*, J. Llorca 2, E. Sanchez 3, M. A. Lopez-Nevot 4, M. M. Amoli 5, C. Garcia-Porrua 1, W. E. R. Ollier 5, J. Martin 3

1 Division of Rheumatology, Hospital Xeral-Calde, Lugo, Spain
2 Division of Preventive Medicine and Public Health, School of Medicine, University of Cantabria, Santander, Spain
3 Instituto de Parasitologia y Biomedicina Lopez-Neyra, CSIC, Granada, Spain
4 Division of Immunology, Hospital Virgen de las Nieves, Granada, Spain
5 Centre for Integrated Genomic Medical Research, School of Epidemiology and Health Sciences, University of Manchester, Manchester, UK

* To whom correspondence should be addressed. E-mail: miguelaggay{at}hotmail.com.


   Abstract

Objective. To assess the influence of inducible and endothelial nitric oxide synthase (iNOS and eNOS) polymorphisms in susceptibility to rheumatoid arthritis (RA).

Methods. Two hundred RA patients fulfilling the 1987 American College of Rheumatology classification criteria followed at the out-patient rheumatology clinic of the Hospital Xeral-Calde (Lugo, Spain) and 251 ethnically matched controls were studied. Patients and controls were genotyped by PCR-based techniques for a multiallelic (CCTTT)n repeat in the promoter region of the iNOS gene and for a T/C polymorphism at position -786 in the promoter region and a polymorphism in exon 7 (298Glu/Asp or 5557G/T) of the eNOS gene.

Results. No significant difference in allele or genotype frequencies for either polymorphism in the eNOS gene was observed between RA patients and controls. The overall iNOS CCTTTn allelic or genotypic distribution did not show statistical significant differences between RA patients and controls. Interestingly, when we stratified the iNOS alleles into short (8-11) and long (12-16) repeats, significant differences were observed between RA patients and controls (P = 0.021; odds ratio = 1.37, 95% confidence interval 1.04-1.81). Of note, individuals carrying two alleles with a repeat number less than 12 (fewer than 196 base pairs) exhibited a double risk of developing RA (P = 0.005, odds ratio 2.26, 95% confidence interval 1.25-4.08).

Conclusions. Significant differences in the iNOS promoter polymorphism genotype frequency between northwest Spanish RA patients and controls suggest a potential role for this polymorphism in susceptibility to RA.

Keywords: Rheumatoid arthritis; Disease susceptibility; Rheumatoid factor; Genetics; Nitric oxide synthases; Polymorphism.
Drs Gonzalez-Gay and Martin share senior authorship in this study.
Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?




Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.