Title : The -383A>C TNFRI polymorphism is associated with soluble levels and clinical activity in rheumatoid arthritis. |
Abstract : Tumor necrosis factor-alpha (TNF-alpha) plays a central role in inflammation, and it has been directly implicated in the pathogenesis of rheumatoid arthritis (RA). TNF-alpha activity is mediated through TNFRI and TNFRII cell surface receptors, which act as physiological attenuators of TNF-alpha activity. We recruited 190 RA patients and 190 healthy subjects (HS) in order to associate the -383A>C TNFRI polymorphism with sTNFRI levels and DAS28 score in RA. In results, sTNFRI levels were higher in RA patients than HS (P = 0.04). The -383A>C TNFRI polymorphism did not show significant differences in both studied groups. However, in the RA group the sTNFRI levels were significantly elevated (P = 0.004) in A/A genotype carriers. In addition, the A/A genotype carriers had the higher DAS28 score than A/C genotype (P = 0.02). These data suggest that -383A>C TNFRI polymorphism is not a susceptibility marker in RA, whereas the increased levels of sTNFRI could reflect the clinical activity in RA patients. |
Author : Valle Y,Padilla-Gutierrez JR,Torres-Carrillo NM,Ledezma-Lozano IY,Corona-Sanchez EG,Vazquez-Del Mercado M,Rangel-Villalobos H,Gamez-Nava JI,Gonzalez-Lopez L,Munoz-Valle JF, |
Source : Rheumatol Int. 2010 Mar;30(5):655-9. doi: 10.1007/s00296-009-1049-6. Epub 2009 Jul 7. |