Rheumatoid Arthritis (RA) is a chronic inflammatory arthritis that affects multiple synovial lined joints. The natural history of the condition is one of progressive articular damage leading to joint deformation and disabilities.
Rheumatoid Arthritis is associated with a number of co-morbidities particularly in the cardiovascular system. The prevalence of RA seems to be relatively uniform around the world. The risk of developing RA does however vary between ethnic populations in the same global region, demonstrating a genetic component to this disease. The prevalence of Rheumatoid Arthritis in the general population is less than 1% but rises to between 2 – 4% in siblings of RA patients.
Gender and genes largely determine a person's risk of developing rheumatoid arthritis. While the specific cause of rheumatoid arthritis is unknown, it is believed that individuals with the HLA-DR1 or HLA-DR4 alleles have an increased risk for developing the disorder. However, genetics alone are not enough to diagnose rheumatoid arthritis; various lab tests, and x-rays, as well as characteristic signs and symptoms, are generally used to diagnose rheumatoid arthritis. Genetic testing can contribute to a better understanding of the origin of the disease for improved diagnosis and treatment.
Kashi Clinical Laboratories utilizes a combination of PCR-SSO (polymerase chain reaction sequence specific oligonucleotide typing) and SBT (sequence based typing) for testing.
Kashi's in-house laboratory and experienced health professionals ensure that customer service is personal, timely, and tailored to every patient's needs.
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- Cope AP et al. T cell responses to a human cartilage autoantigen in the context of rheumatoid arthritis-associated and nonassociated HLA-DR4 alleles. Arthritis Rheum. 1999; 42:1497.
- du Montcel ST et al. New classification of HLA-DRB1 alleles supports the shared epitope hypothesis of rheumatoid arthritis susceptibility. Arthritis Rheum. 2005; 52:1063.
- Hill JA et al. Cutting edge: the conversion of arginine to citrulline allows for a high-affinity peptide interaction with the rheumatoid arthritis-associated HLA-DRB1*0401 MHC class II molecule. J Immunol. 2003; 171:538.
- Huizinga TW et al. Refining the complex rheumatoid arthritis phenotype based on specificity of the HLA-DRB1 shared epitope for antibodies to citrullinated proteins. Arthritis Rheum. 2005; 52:3433.
- Klareskog L et al. A new model for an etiology of rheumatoid arthritis: smoking may trigger HLA-DR (shared epitope)-restricted immune reactions to autoantigens modified by citrullination. Arthritis Rheum. 2006; 54:38.
- Maksymowych WP et al. HLA and cytokine gene polymorphisms in relation to occurrence of palindromic rheumatism and its progression to rheumatoid arthritis. J Rheumatol. 2002; 29:2319.