Annals of the Rheumatic Diseases 2008;67:1759-1764
BASIC AND TRANSLATIONAL RESEARCH
Association between β2 adrenergic receptor polymorphisms and rheumatoid arthritis in conjunction with human leukocyte antigen (HLA)-DRB1 shared epitope
Medical Clinic IV, University Hospital, Liebigstraße 22, Leipzig, 04103 Germany
O Malysheva, Medical clinic IV, University Hospital, Liebigstraße 22, 04103 Leipzig Germany; Olga.Malysheva{at}medizin.uni-leipzig.de
Objective: In the present work, the frequency of inherited polymorphisms of the β2 adrenergic receptor (β2AR) gene and their association with rheumatoid arthritis (RA) as well as human leukocyte antigen (HLA)-DRB1 alleles was examined.
Methods: An allele-specific polymerase chain reaction was used to determine the common variants of the β2AR at positions 16, 27 and 164 in patients with RA (n = 310) and ethnically matched healthy controls (n = 305) from Germany. HLA-DRB1 genotyping was performed by oligonucleotide hybridisation of enzymatically amplified DNA allowing low-resolution HLA-DRB1 genotyping comprising specificities DRB1*01 to DRB1*17.
Results: Arginine (Arg) at codon 16 was present in 278 patients with RA (89.7%) compared to 202 controls (66.2%; odds ratio (OR) 4.43, 95% CI 2.81 to 7.02, p<0.001). Homozygosity for Arg16 was found in 107 patients with RA (34.5%) compared to 14 controls (4.6%; OR 10.9, CI 5.9 to 20.5, p<0.001). Stratifying patients for their HLA-DR status revealed that homozygosity for Arg16 exhibited the greatest risk for RA in combination with HLA-DRB1*04 (OR 17.1, 95% CI 1.71 to 414.4, p = 0.004). Interestingly, patients with the Arg16 allele have a younger mean (SD) age at disease onset compared to patients without Arg16 (46.1 (2.0) vs 53.1 (2.7) respectively, p<0.05). Furthermore, 93.3% patients with homozygosity for Arg16 were positive for anti-cyclic citrullinated peptide (CCP) antibodies vs 75% patients with homozygosity for Gly16 (p<0.05).
Conclusion: There was a highly significant distortion between patients with RA and controls in the distribution of β2AR polymorphisms at codon 16, contributing (together with the HLA-DR alleles) to the genetic background of RA.
CiteULike 
Complore 
Connotea 
Del.icio.us 
Digg 
Reddit 
Technorati What's this?
- Full Text
- Full Text (PDF)
-
All Versions of this Article:
ard.2007.083782v1
67/12/1759 most recent - Submit a response
- Alert me when this article is cited
- Alert me when eLetters are posted
- Alert me if a correction is posted
- Citation Map
Services
- Email this link to a friend
- Similar articles in this journal
- Similar articles in PubMed
- Add article to my folders
- Download to citation manager
- Request Permissions
Citing Articles
Google Scholar
PubMed
Topic Collections
-
Genetics
-
Immunology (including allergy)
-
Connective tissue disease
-
Degenerative joint disease
-
Musculoskeletal syndromes
Bookmark with
Register for free content
The full back archive is now available for all BMJ Journals. Institutional subscribers may access the entire archive as part of their subscription. Personal subscribers will also have access to all content when logged in. Non-subscribers who register have free access to all articles published before 2006 right back to volume 1 issue 1. Register here to access the free archive of all BMJ Journals.
Don't forget to sign up for content alerts so you keep up to date with all the articles as they are published.
