L Ferre'1,2, F Clarelli2, G Sferruzza1,2, M A Rocca1,3, E Mascia2, M Radaelli1, F Sangalli1, G Dalla Costa1, L Moiola1, M Aboulwafa3, F Martinelli Boneschi1,2, G Comi1,2, M Filippi1,3, V Martinelli1, F Esposito4,5. 1. Department of Neurology, San Raffaele Scientific Institute, Via Olgettina, 48, 20132, Milan, Italy. 2. Laboratory of Human Genetics of Neurological Disorders, CNS Inflammatory Unit & INSPE, San Raffaele Scientific Institute, Milan, Italy. 3. Neuroimaging Research Unit, INSPE, Division of Neuroscience, San Raffaele Scientific Institute, Vita-Salute San Raffaele University, Milan, Italy. 4. Department of Neurology, San Raffaele Scientific Institute, Via Olgettina, 48, 20132, Milan, Italy. esposito.federica@hsr.it. 5. Laboratory of Human Genetics of Neurological Disorders, CNS Inflammatory Unit & INSPE, San Raffaele Scientific Institute, Milan, Italy. esposito.federica@hsr.it.
Abstract
BACKGROUND: 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. AIMS: 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. RESULTS: 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). CONCLUSIONS: 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.
BACKGROUND: 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. AIMS: 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 MSpatients 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. RESULTS: 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). CONCLUSIONS: 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 MSpatients could probably benefit from 25[OH]D levels above those currently considered to be sufficient.
Authors: Alberto Ascherio; Kassandra L Munger; Rick White; Karl Köchert; Kelly Claire Simon; Chris H Polman; Mark S Freedman; Hans-Peter Hartung; David H Miller; Xavier Montalbán; Gilles Edan; Frederik Barkhof; Dirk Pleimes; Ernst-Wilhelm Radü; Rupert Sandbrink; Ludwig Kappos; Christoph Pohl Journal: JAMA Neurol Date: 2014-03 Impact factor: 18.302
Authors: Kathryn C Fitzgerald; Kassandra L Munger; Karl Köchert; Barry G W Arnason; Giancarlo Comi; Stuart Cook; Douglas S Goodin; Massimo Filippi; Hans-Peter Hartung; Douglas R Jeffery; Paul O'Connor; Gustavo Suarez; Rupert Sandbrink; Ludwig Kappos; Christoph Pohl; Alberto Ascherio Journal: JAMA Neurol Date: 2015-12 Impact factor: 18.302
Authors: Chris H Polman; Stephen C Reingold; Brenda Banwell; Michel Clanet; Jeffrey A Cohen; Massimo Filippi; Kazuo Fujihara; Eva Havrdova; Michael Hutchinson; Ludwig Kappos; Fred D Lublin; Xavier Montalban; Paul O'Connor; Magnhild Sandberg-Wollheim; Alan J Thompson; Emmanuelle Waubant; Brian Weinshenker; Jerry S Wolinsky Journal: Ann Neurol Date: 2011-02 Impact factor: 10.422
Authors: Dalia L Rotstein; Brian C Healy; Muhammad T Malik; Robert L Carruthers; Alexander J Musallam; Pia Kivisakk; Howard L Weiner; Bonnie Glanz; Tanuja Chitnis Journal: Neurol Neuroimmunol Neuroinflamm Date: 2015-10-29