TY - JOUR T1 - Lack of Association Between TRAF1/C5 Gene Polymorphisms and Biopsy-proven Giant Cell Arteritis JF - The Journal of Rheumatology JO - J Rheumatol SP - 131 LP - 135 DO - 10.3899/jrheum.090646 VL - 37 IS - 1 AU - ORLANDO TORRES AU - ROGELIO PALOMINO-MORALES AU - TOMAS R. VAZQUEZ-RODRIGUEZ AU - SANTOS CASTAÑEDA AU - INMACULADA C. MORADO AU - JOSE A. MIRANDA-FILLOY AU - NORBERTO ORTEGO-CENTENO AU - ISIDORO GONZALEZ-ALVARO AU - BENJAMIN FERNANDEZ-GUTIERREZ AU - JAVIER MARTIN AU - MIGUEL A. GONZALEZ-GAY Y1 - 2010/01/01 UR - http://www.jrheum.org/content/37/1/131.abstract N2 - Objective. A novel association with a 100-kb region on chromosome 9 that contains the tumor necrosis factor receptor-associated factor 1 (TRAF1) and C5 genes has been observed in some autoimmune rheumatic diseases, in particular in rheumatoid arthritis. We analyzed the influence of 2 single-nucleotide polymorphisms (SNP) from the TRAF1/C5 region in susceptibility to giant cell arteritis (GCA). Methods. We assessed 220 patients with biopsy-proven GCA and 410 matched controls. DNA from patients and controls was obtained from peripheral blood. Samples were genotyped for the rs10818488 and rs2900180 TRAF1/C5 gene polymorphisms by polymerase chain reaction, using a predesigned TaqMan allele discrimination assay. Results. A genotyping rate of 95% was achieved in this series of GCA. No significant differences in the genotype distribution between GCA patients and controls were found for the 2 SNP. GCA patients exhibited a reduced frequency of TRAF1/C5 AA homozygosity (7.6%) compared to controls (12.7%) but the difference was only marginally significant (OR 0.58, 95% CI 0.30–1.11, p = 0.07). The frequency of minor allele T of TRAF1/C5 rs2900180 was also slightly reduced in patients (24.3%) compared to controls (27.8%) (p = 0.19). No significant differences were observed when patients were stratified according to the presence of specific clinical disease features. Conclusion. Our results showed no influence of rs10818488 and rs2900180 TRAF1/C5 gene polymorphisms in susceptibility to and clinical expression of GCA. ER -