Basal vitamin D levels and disease activity in multiple sclerosis patients treated with fingolimod
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Several studies have shown an association between 25-hydroxyvitamin D (25[OH]D) levels and multiple sclerosis (MS) susceptibility and/or level of disease activity in patients treated with first line drugs.
To investigate whether baseline 25[OH]D values could influence disease activity also during treatment with the second-line drug fingolimod (FTY).
Patients and methods
We enrolled 176 MS patients who started FTY at the San Raffaele Hospital (OSR) MS center with available 25[OH]D measurement at the time of treatment start. We then prospectively followed them for 2 years with periodic clinical examinations and MRI scans.
We found no linear correlation between baseline 25[OH]D levels and annualized relapse rate (ARR) or time to first relapse. However, we observed that patients with serum 25[OH]D ≥ 100 nmol/l showed a lower number of Gd+ and combined unique activity (CUA) lesions at baseline compared to patients with the lowest 25[OH]D levels (less than 50 nmol/l, p value < 0.05). Moreover, they showed fewer CUA lesions at 2-year follow-up also when accounting for baseline level of disease activity (p value < 0.05).
In patients treated with FTY, those with the highest baseline 25(OH)D levels had a significantly lower number of active lesions at baseline; the same effect, even if weaker, was observed also at 2-year follow-up when adjusting for baseline disease activity. Given Vitamin D supplementation safety profile, also if a causal effect has not yet been shown, most of MS patients could probably benefit from 25[OH]D levels above those currently considered to be sufficient.
KeywordsMultiple sclerosis 25-hydroxyvitamin D Fingolimod Disease activity MRI
The study was funded by a grant from Fondazione Italiana Sclerosi Multipla (grant number FISM2013/R/13).
Compliance with ethical standards
Conflict of interest
The author(s) declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article:
L. Ferre’ reports no disclosures.
F. Clarelli reports no disclosures.
G. Sferruzza reports no disclosures.
M.A. Rocca received speaker’s honoraria from Biogen Idec, Novartis, Genzyme, Sanofi-Aventis, Teva, and Merk Serono and receives research support from the Italian Ministry of Health and Fondazione Italiana Sclerosi Multipla.
E. Mascia reports no disclosures.
M. Radaelli reports no disclosures.
F. Sangalli reports no disclosures.
G. Dalla Costa reports no disclosures.
L. Moiola received honoraria for speaking at meetings or for attending to advisory board from Sanofi-Genzyme, Biogen-Idec, Novartis, and TEVA.
M. Aboulwafa reports no disclosures.
F. Martinelli Boneschi has received compensation for activities with Teva Neuroscience, Biogen Idec, and Merck Serono as speaker and/or advisor.
G. Comi has received compensation for consulting services with the following companies: Novartis, Teva, Sanofi, Genzyme, Merck, Biogen, Excemed, Roche, Almirall, Chugai, Receptos, Forward Pharma and compensation for speaking activities from Novartis, Teva, Sanofi, Genzyme, Merk, Biogen, Excemed, and Roche.
M. Filippi is Editor-in-Chief of the Journal of Neurology; serves on a scientific advisory board for Teva Pharmaceutical Industries; has received compensation for consulting services and/or speaking activities from Biogen Idec, ExceMED, Novartis, and Teva Pharmaceutical Industries; and receives research support from Biogen Idec, Teva Pharmaceutical Industries, Novartis, Italian Ministry of Health, Fondazione Italiana Sclerosi Multipla, Cure PSP, Alzheimer’s Drug Discovery Foundation (ADDF), the Jacques and Gloria Gossweiler Foundation (Switzerland), and ARiSLA (Fondazione Italiana di Ricerca per la SLA).
V. Martinelli has received honoraria for consulting and speaking activities from Biogen-Idec, Merck, Bayer, TEVA, Novartis, and Genzyme.
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