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In patients with rheumatoid arthritis (RA), chronic inflammation on a background of established cardiovascular disease (CVD) risk factors is thought to contribute to atherosclerosis, resulting in the observed increased mortality from CVD.1
Recent studies suggest a role for interleukin-6 receptor (IL6R) in both CVD2 ,3 and RA.4 A functional, non-synonymous genetic variant found within the IL6R gene (rs2228145) conferring an amino acid change (Asp358Ala) influential in determining levels of soluble IL6R5 has been convincingly associated with both CVD occurrence2 ,3 and RA.4 This amino acid change within the IL6R gene has a similar effect to the RA therapy, tocilizumab, which targets the IL6R pathway, leading to an increase in IL6R and soluble IL6 levels, as well as a decrease in C-reactive protein (CRP) levels. Although unlikely to be causal in disease,6 CRP levels …
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