|Vitamin D in multiple sclerosis; clinical and immunological implications|| |
|J Hejgaard Laursen1, H Bach Søndergaard1, P Soelberg Sørensen1, F Sellebjerg1, A Oturai1|
|1Copenhagen University Hospital Rigshospitalet, Danish Multiple Sclerosis Center, Copenhagen, Denmark|
|Background: Vitamin D insufficiency is common among multiple sclerosis (MS) patients, and hypovitaminosis D has been associated with MS risk and disease activity. This finding has been supported by in vitro studies, which have demonstrated anti-inflammatory effects of vitamin D. Moreover synergistic effects of vitamin D and interferon-beta (IFN-β) have been suggested. However, the overall evidence for a beneficial effect of vitamin D in MS is inconclusive.|
Objectives: To investigate how screening for vitamin D insufficiency and recommendation on vitamin D3 supplies affect 25(OH)D levels in MS patients and to examine the clinical and immunological implications of this action.
Methods: A cohort of 210 natalizumab-treated relapsing-remitting MS (RRMS) patients was enrolled in the study. In winter 2009/2010 (period 1) patients had a blood sample collected and the procedure was repeated the following winter (period 2). Patients with serum 25(OH)D < 50nmol/l in period 1 were recommended treatment with vitamin D3 (50 to 100µg per day). Information on disease duration, annualized relapse-rate (ARR) and status for neutralizing antibodies (NAbs) to IFN-β was obtained retrospectively from the Danish MS Treatment Register. To asses how changes in 25(OH)D affect the immune system, quantitative real-time PCR analysis of MX1, USP18, PD-1, PD-L1, IFIT1, IFIT2, IL10, IL10RA, FOXP3 and IDO1 was performed on whole blood samples from period 1 and 2 in patients with the highest change in vitamin D level between period 1 and 2, n=30.
Results: Mean 25(OH)D increased significantly from 63 nmol/l (95% CI 58.8-67.7) to 76 nmol/l
(95% CI 71.8-80.7) from period 1 to period 2 (p=5.1x10-8). At the same time mean ARR decreased from 0.61 to 0.54. We found a trend between increasing levels of 25(OH)D and decreasing ARR (p=0.07). None of the ten genes examined were associated with changes in serum 25(OH)D levels.
Conclusions: Recommendation of vitamin D supplies to MS patients with 25(OH)D < 50nmol/l resulted in a significant increase in mean 25(OH)D but was not associated with a statistically significant decrease in ARR. Whether this relates to an insufficient increase in 25(OH)D or lack of efficacy of 25(OH)D supplementation remains to be established. Changes in 25(OH)D levels did not affect gene expression of genes previously associated with either endogenous IFN-response, vitamin D or both, which underlines the complexity of vitamin D research in MS.
MD, PhD student Julie Hejgaard Laursen , Copenhagen University Hospital Rigshospitalet , Copenhagen , DK
Assigned in sessions:
11.09.2014, 15:30-17:00, Poster viewing, poster sessions, P1, Poster Session 1 (P001-P490) and Coffee Break, Hall C