Glucocorticoid receptor gene polymorphisms and susceptibility to rheumatoid arthritis.

Clin Endocrinol (Oxf) 2007 Sep 28;67(3):342-5. Epub 2007 May 28.

Arthritis Research Campaign Epidemiology Unit (ARC/EU) and Centre for Molecular Medicine (CMM), University of Manchester, Manchester, UK.

Background: A defect in hypothalamic-pituitary-adrenal (HPA) axis function has been suggested to contribute to susceptibility to rheumatoid arthritis (RA).

Objective: To investigate polymorphisms of the glucocorticoid receptor (GR) gene and determine any associations with RA.

Methods: Three GR polymorphisms that tag 95% of all haplotypes across the GR gene were genotyped. These are an intron B Bcl1 polymorphism, a ttg insertion/deletion within intron F (rs2307674) and the single nucleotide polymorphism (SNP) lying in the 3' untranslated region of exon 9b (rs6198). The dye terminator-based SNaPshot method or size resolution by capillary electrophoresis was performed. The study population comprised 198 UK Caucasian RA cases and 393 ethnically matched controls.

Results: No significant single point or haplotypic associations were found for GR polymorphisms with RA susceptibility. Furthermore, no evidence for GR polymorphisms with aspects of RA severity was seen.

Conclusion: In this study of the most comprehensive coverage of GR polymorphisms with RA, no significant contributing role for GR polymorphisms with RA was found.

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http://dx.doi.org/10.1111/j.1365-2265.2007.02887.xDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2040228PMC
September 2007
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