Background Emerging evidence suggests that vitamin D plays an important role in immune regulation.
Objectives The objective of this work was to determine if patients with rheumatoid arthritis (RA) are at risk for vitamin D deficiency and whether vitamin D levels correlate with disease activity or immune disorders.
Methods This study was a retrospective research. RA patients who had vitamin D levels and immune function indexes of each other were included. Patients receiving or have received vitamin D, corticosteroids, disease-modifying anti-rheumatic drugs or a tumor necrosis factor antagonist and those who had hepatic or renal insufficiency were excluded. Multivariate analysis was performed to examine correlations and control for confounding factors.
Results As suggested threshold (≤25 ng/ml), the overall prevalence of vitamin D insufficiency was 265 of 280 (94.8%). Mean serum vitamin D insufficiency levels of 11.15±4.74 ng/ml for RA patients were significantly lower compared to controls (31.62±6.46) (p=0.001). Among all the subjects, 208 (72.7%) were females. Vitamin D levels in high disease activity group were lower compared to vitamin D level in patients with low and moderate disease activity (DAS-28 score >5.1, 3.2–5.1, <3.2, respectively, p<0.001) and vitamin D levels had an inverse correlation with DAS28 score (β-coefficient-0.164, p=0.018, per 1 ng/ml). In patients with RA, the levels of vitamin D were moderately and inversely associated with Th 17 (β-coefficient-0.158, p=0.019, per 1 ng/ml). However, no significant relationship was found between vitamin D and these variables (T cell, B cell, NK cell, Treg, Th1, Th2, Th17/Treg) in patients.
Conclusions Lower levels of vitamin D are associated with worse DAS28 and higher levels of Th17 with RA, especially in female patients. The levels of 1,25-dihydroxycholecalciferol (1,25(OH)2D3) could be a marker to monitor the disease activity in RA patients and vitamin D may be an alternative supplementary treatment for RA.
Acknowledgements This work was supported by research grants from the National Natural Science Foundation of China (no. 81301532/H0603) and the Shanxi Science and Technology research projects of China (no. 201603D321074).
Disclosure of Interest None declared