Effect of anti-rheumatic treatment on selenium levels in inflammatory arthritis

Objectives: The reason for increased cardiovascular risk in inflammatory arthritis (IA) is unclear. Interestingly,selenium-deficiency is suspected to contribute to the development of cardiovascular disease (CVD) in the generalpopulation. Although the reference range of serum selenium (s-selenium) is 50–120 μg/L, there are indicationsthat levels up to 85 μg/L might not be sufficient for optimal cardioprotection. Our aim was to examine s-seleniumlevels in rheumatoid arthritis (RA), psoriatic arthritis (PsA) and ankylosing spondylitis (AS), to evaluate theeffect of anti-rheumatic treatment on s-selenium levels, and to assess relationships between s-selenium levels andclinical and laboratory parameters including markers of disease activity and CVD risk.Methods: We examined 64 patients with RA, 40 with PsA and 26 with AS starting with methotrexate (MTX)monotherapy or anti-tumor necrosis factor therapy (anti-TNF) with or without methotrexate (anti-TNF ± MTX)due to active disease. S-selenium, inflammatory biomarkers, endothelial function (EF) and other variables wereexamined at baseline and after 6 weeks and 6 months of treatment.Results: In the total IA group, s-selenium increased within 6 weeks of anti-rheumatic treatment, and thereafterthe levels remained stable until the end of the 6 months follow-up period. There were no significant differencesin s-selenium changes between the three diagnostic groups and between the two treatment regimens. Changes ins-selenium were negatively related to changes in C-reactive protein (CRP) and erythrocyte sedimentation rate(ESR), but there were no significant relationships to any other of the examined risk parameters for CVD includingEF.Conclusion: IA patients had s-selenium within the reference range, but below the level that might be necessaryfor optimal CVD protection.Anti-rheumatic treatment had a relatively rapid and sustained effect on s-selenium levels. The increase in s-selenium was related to reduction in inflammatory activity. In theory, anti-rheumatic drugs might improve s-selenium levels through inhibition of pro-inflammatory processes or through other mechanisms. Although wehave not revealed any significant relationships between s-selenium and CVD risk parameters, the role of sub-optimal s-selenium levels in pathogenesis of premature CVD in IA cannot be ruled out