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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

1
Department of Medical Biochemistry, Innlandet Hospital Trust, Lillehammer, Norway. Electronic address: Gia.Deyab@sykehuset-innlandet.no.
2
Lillehammer Hospital for Rheumatic Diseases, Norway.
3
Inland Norway University of Applied Sciences, Elverum, Norway; Department of Research, Innlandet Hospital Trust, Brumunddal, Norway.
4
Department of Public Health, Faculty of Nursing sciences, Oslo and Akershus University College, Oslo, Norway.
5
Department of Medical Biochemistry, Innlandet Hospital Trust, Lillehammer, Norway; Department of Research, Innlandet Hospital Trust, Brumunddal, Norway.
6
University Hospital, Ullevål, Norway; Institute of Clinical Sciences, University of Oslo, Norway.
7
Department of Medical Biochemistry, Oslo University Hospital, Ullevål, Norway.
8
Lab1 AS, Sandvika, Norway.
9
Department of Medicine, Innlandet Hospital Trust, Lillehammer, Norway.
10
Department of Biology, Faculty of Sciences-l, Lebanese University, Beirut, Lebanon.
11
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.

Abstract

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 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.

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 were examined 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 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.

CONCLUSION:

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.

KEYWORDS:

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

PMID:
29895378
DOI:
10.1016/j.jtemb.2018.05.001
[Indexed for MEDLINE]

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