Effect of anti-rheumatic treatment on selenium levels in inflammatory arthritis
Gia Deyab1, Ingrid Hokstad2, Jan Aaseth3
1Department of Medical Biochemistry, Innlandet Hospital Trust, Lillehammer, Norway.
Insights
Inflammatory arthritis patients have low serum selenium, increasing cardiovascular disease risk. Anti-rheumatic treatments rapidly improve selenium levels, correlating with reduced inflammation.
Area of Science:
- Rheumatology and Immunology
- Cardiovascular Disease Research
- Nutritional Biochemistry
Background:
- Increased cardiovascular disease (CVD) risk is a concern in inflammatory arthritis (IA).
- Selenium deficiency is implicated in CVD, with optimal cardioprotective levels potentially higher than current reference ranges.
- Serum selenium (s-selenium) status in rheumatoid arthritis (RA), psoriatic arthritis (PsA), and ankylosing spondylitis (AS) requires investigation.
Purpose of the Study:
- To measure s-selenium levels in patients with RA, PsA, and AS.
- To evaluate the impact of anti-rheumatic treatments (methotrexate or anti-TNF therapy) on s-selenium levels.
- To assess the relationship between s-selenium levels and disease activity markers and CVD risk factors.
Main Methods:
- Sixty-four RA, 40 PsA, and 26 AS patients with active disease were enrolled.
- Patients initiated methotrexate monotherapy or anti-TNF therapy (with or without methotrexate).
- S-selenium, inflammatory biomarkers (CRP, ESR), endothelial function, and other variables were measured at baseline, 6 weeks, and 6 months.
Main Results:
- S-selenium levels increased significantly within 6 weeks of anti-rheumatic treatment and remained stable for 6 months.
- No significant differences in s-selenium changes were observed between diagnostic groups or treatment regimens.
- Increases in s-selenium were negatively correlated with reductions in C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR), but not with other CVD risk parameters.
Conclusions:
- IA patients exhibit s-selenium levels within the reference range but potentially below optimal for CVD protection.
- Anti-rheumatic treatments effectively and sustainably increase s-selenium levels, linked to reduced inflammation.
- While direct links to CVD risk parameters were not found, suboptimal selenium levels in IA warrant further investigation regarding premature CVD pathogenesis.
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.
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