Nov 11, 2009 - Research

Three New Genetic Variants Associated With Rheumatoid Arthritis Risk

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The most common type of arthritis, osteoarthritis, occurs due to accumulated wear and tear — welcome to old age! — or from repetitive movements or injury.   Rheumatoid arthritis, on the other hand, is caused by an autoimmune attack on the lining of the joints, resulting in stiffness, muscle aches, and general fatigue. Approximately two million people in the U.S. suffer from rheumatoid arthritis, and although women are affected more often than men, men tend to have more severe symptoms.

Research has identified a number of genetic factors that contribute to one’s risk of developing rheumatoid arthritis, and new studies continue to reveal more genes that seem to be involved in this complex disease. In a report published this week in Nature Genetics, a team led by Soumya Raychaudhuri and Robert Plenge of Brigham and Women’s Hospital in Boston describe three new genetic associations with rheumatoid arthritis risk.

Using a computational algorithm that incorporates information from the scientific literature, Raychaudhuri and his colleagues identified 22 candidate SNPs that have a large number of connections to previously validated genetic risk factors for rheumatoid arthritis. When they tested these SNPs in a set of almost 8,000 Caucasians with rheumatoid arthritis  and 12,000 controls, seven emerged as highly significant associations. After combining this study population with that from a previous study — for a total of more than 11,000 individuals with rheumatoid arthritis and 22,000 without  — three of the variants rose to the top.

All three variants are in genes not previously linked to  rheumatoid arthritis.

These three SNPs are located near genes involved in the immune response, and, in some cases, near genetic variations that have been associated with other autoimmune disorders, such as Crohn’s disease and type 1 diabetes. Although a detailed, cohesive picture of the causes underlying rheumatoid arthritis remains elusive, each new association discovered by researchers contributes to our understanding of the biological players involved in this autoimmune disease.

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