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J Trace Elem Med Biol. 2018 Sep;49:91-97. doi: 10.1016/j.jtemb.2018.05.001. Epub 2018 May 3.

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

Author information

Department of Medical Biochemistry, Innlandet Hospital Trust, Lillehammer, Norway. Electronic address:
Lillehammer Hospital for Rheumatic Diseases, Norway.
Inland Norway University of Applied Sciences, Elverum, Norway; Department of Research, Innlandet Hospital Trust, Brumunddal, Norway.
Department of Public Health, Faculty of Nursing sciences, Oslo and Akershus University College, Oslo, Norway.
Department of Medical Biochemistry, Innlandet Hospital Trust, Lillehammer, Norway; Department of Research, Innlandet Hospital Trust, Brumunddal, Norway.
University Hospital, Ullevål, Norway; Institute of Clinical Sciences, University of Oslo, Norway.
Department of Medical Biochemistry, Oslo University Hospital, Ullevål, Norway.
Lab1 AS, Sandvika, Norway.
Department of Medicine, Innlandet Hospital Trust, Lillehammer, Norway.
Department of Biology, Faculty of Sciences-l, Lebanese University, Beirut, Lebanon.
Lillehammer Hospital for Rheumatic Diseases, Norway; Department of Research, Innlandet Hospital Trust, Brumunddal, Norway; Harvard Medical School, Boston, USA; Brigham and Women's Hospital, Boston, USA.



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 general population. Although the reference range of serum selenium (s-selenium) is 50-120 μg/L, there are indications that levels up to 85 μg/L might not be sufficient for optimal cardioprotection. Our aim was to examine s-selenium levels in rheumatoid arthritis (RA), psoriatic arthritis (PsA) and ankylosing spondylitis (AS), to evaluate the effect of anti-rheumatic treatment on s-selenium levels, and to assess relationships between s-selenium levels and clinical and laboratory parameters including markers of disease activity and CVD risk.


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 were examined at baseline and after 6 weeks and 6 months of treatment.


In the total IA group, s-selenium increased within 6 weeks of anti-rheumatic treatment, and thereafter the levels remained stable until the end of the 6 months follow-up period. There were no significant differences in s-selenium changes between the three diagnostic groups and between the two treatment regimens. Changes in s-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 including EF.


IA patients had s-selenium within the reference range, but below the level that might be necessary for 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 we have not revealed any significant relationships between s-selenium and CVD risk parameters, the role of suboptimal s-selenium levels in pathogenesis of premature CVD in IA cannot be ruled out.


Anti-tumor necrosis factor; Inflammatory arthritis; Methotrexate; Selenium

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