Vitamin D and disease activity in multiple sclerosis before and during interferon-β treatment.

نویسندگان

  • Kristin I Løken-Amsrud
  • Trygve Holmøy
  • Søren J Bakke
  • Antonie Giaever Beiske
  • Kristian S Bjerve
  • Bård T Bjørnarå
  • Harald Hovdal
  • Finn Lilleås
  • Rune Midgard
  • Tom Pedersen
  • Jurate Saltyte Benth
  • Leiv Sandvik
  • Oivind Torkildsen
  • Stig Wergeland
  • Kjell-Morten Myhr
چکیده

OBJECTIVE Studies based on deseasonalized vitamin D levels suggest that vitamin D may influence the disease activity in multiple sclerosis (MS), and high doses are suggested as add-on treatment to interferon-β (IFN-β). Seasonal fluctuation of vitamin D varies between individuals, thus the relationship to disease activity should preferentially be studied by repeated and simultaneous vitamin D and MRI measurements from each patient. METHODS This was a cohort study comprising 88 patients with relapsing-remitting MS who were followed for 6 months with 7 MRI and 4 25-hydroxyvitamin D measurements before initiation of IFN-β, and for 18 months with 5 MRI and 5 25-hydroxyvitamin D measurements during IFN-β treatment. RESULTS Prior to IFN-β treatment, each 10 nmol/L increase in 25-hydroxyvitamin D was associated with 12.7% (p = 0.037) reduced odds for new T1 gadolinium-enhancing lesions, 11.7% (p = 0.044) for new T2 lesions, and 14.1% (p = 0.024) for combined unique activity. Patients with the most pronounced fluctuation in 25-hydroxyvitamin D displayed larger proportion of MRI scans with new T1 gadolinium-enhancing lesions (51% vs 23%, p = 0.004), combined unique activity (60% vs 32%, p = 0.003), and a trend for new T2 lesions (49% vs 28%, p = 0.052) at the lowest compared to the highest 25-hydroxyvitamin D level. No association between 25-hydroxyvitamin D and disease activity was detected after initiation of IFN-β. HLA-DRB1*15 status did not affect the results. CONCLUSION In untreated patients with MS, increasing levels of 25-hydroxyvitamin D are inversely associated with radiologic disease activity irrespective of their HLA-DRB1*15 status.

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عنوان ژورنال:
  • Neurology

دوره 79 3  شماره 

صفحات  -

تاریخ انتشار 2012