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AB0086 IL - 17 Levels with Vitamin D Repletion in Rheuamtoid Arthritis
  1. U. Haque1,
  2. C. Bingham2,
  3. T. Guhr2,
  4. S. Bartlett3,
  5. S. Ghazarian1,
  6. F. Boin2
  1. 1Johns Hopkins University, Baltimore, Maryland, United States
  2. 2Rheumatology, Johns Hopkins University, Baltimore, Maryland, United States
  3. 3McGill, Montreal, Canada

Abstract

Background Increasing scientific evidence implicates a pathogenic role of Th17 cells and associated cytokines in rheumatoid arthritis (RA). Vitamin D may have suppressive effect on Th17 cells. In vitro studies show that vitamin D suppresses IL-17 production in stimulated PMBCs1 in patients with early RA. In a recent study2, serum 25(OH)D levels were inversely associated with IL-17 levels in RA patients. However, the effect of vitamin D repletion on IL-17 levels in RA remains untested. This is of clinical importance as correction of vitamin D deficiency may reduce IL-17 related inflammation in RA.

Objectives Our goal was to compare serum IL-17 levels in vitamin D sufficient vs vitamin D deficient RA patients and to investigate the effect of vitamin D repletion on IL 17 levels in vitamin D deficient RA subjects.

Methods Sera from RA patients (1987 ARA criteria) enrolled in a randomized controlled trial were used. 25(OH)D levels were measured using Diasorin radioimmunoassay. Vitamin D deficiency was classified as 25(OH)D level <30ng/ml. Vitamin D deficient patients were randomly assigned to either vitamin D therapy [50,000 IU ergocalciferol/week for 8 or 16 weeks until repletion [25(OH)D≥30 ng/ml] was achieved OR placebo for 16 weeks. Sera were collected and stored at -70 degrees every study visit. IL-17 was measured in both vitamin D sufficient (n=56) and deficient (n=83) patients at baseline. IL-17 was also measured in patients who completed vitamin D therapy and achieved repletion. We compared pre- and post-treatment IL-17 levels in this group. A commercially available Ruthenium based electro-chemoluminescence platform was used to measure IL-17 (lowest quantification level =0.2 pg/ml). Unpaired and paired students t-test and regression analyses were used.

Results Participants (n=139) were mostly female (80%), white (79.1%) with a mean (SD) age of 53.4 (12.3) yrs, body mass index of 30.5 (6.9) m/kg2 and disease duration of 9.9 (9) yrs. Mean 25(OH)D levels were 28.3 (11.1)ng/mL (range 6.3 – 72.8 ng/ml). 83 participants (60%) patients had 25(OH)D levels <30 ng/ml and entered the RCT. 68 participants completed vitamin D repletion therapy. Mean increase in vitamin D in this group was 17.3 (12.9) ng/ml.

In a cross-sectional analysis, no significant difference was noted in IL-17 levels at baseline between vitamin D sufficient and deficient groups (mean IL 17 0.71±1.27 pg/ml vs 0. 62±0.65 pg/ml respectively, p value=0.62). Using linear regression, baseline vitamin D sufficiency/deficiency was a non-significant predictor of IL -17 levels (beta= -0.04, p=0.622). After vitamin D repletion therapy, no differences were noted in IL-17 levels before and after repletion (IL-17 at baseline vs repletion, 0.61 (0.61) pg/ml vs 0.68 (0.93) pg/ml respectively, p=0.60).

Conclusions These data suggest that IL-17 levels do not differ between vitamin D deficient and sufficient RA patients. Moreover, vitamin D repletion does not impact IL-17 levels. This is the first study to investigate the effect of vitamin D repletion therapy on IL-17 in RA and our results suggest that vitamin D may not have a therapeutic role in modulating IL-17 associated inflammation in RA. Larger studies are needed to confirm these results.

References

  1. Colin EM et al. A & R, 2010.

  2. Ranganathan P et al. J Rheum. 2013 Sep.

Acknowledgements Stabler Foundation

Disclosure of Interest None declared

DOI 10.1136/annrheumdis-2014-eular.2075

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