Vitamin D as an early predictor of multiple sclerosis activity and progression

Xavier Montalbán, Alberto Ascherio*, Kassandra L. Munger, Karl Köchert, Rick White, Kelly Claire Simon, Chris H. Polman, Mark S. Freedman, Hans Peter Hartung, David H. Miller, Gilles Edan, Frederik Barkhof, Dirk Pleimes, Ernst Wilhelm Radü, Rupert Sandbrink, Ludwig Kappos, Christoph Pohl

*Autor corresponent d’aquest treball

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417 Cites (Scopus)

Resum

IMPORTANCE: 

It remains unclear whether vitamin D insufficiency, which is common in individuals with multiple sclerosis (MS), has an adverse effect on MS outcomes.

OBJECTIVES: 

To determine whether serum concentrations of 25-hydroxyvitamin D (25[OH]D), a marker of vitamin D status, predict disease activity and prognosis in patients with a first event suggestive of MS (clinically isolated syndrome). 

DESIGN, SETTING, AND PARTICIPANTS: 

The Betaferon/Betaseron in Newly Emerging multiple sclerosis For Initial Treatment study was a randomized trial originally designed to evaluate the impact of early vs delayed interferon beta-1b treatment in patients with clinically isolated syndrome. Serum 25(OH)D concentrations were measured at baseline and 6, 12, and 24 months. A total of 465 of the 468 patients randomized hadat least 125(OH)D measurement, and 334 patients had them at both the 6- and 12-month (seasonally asynchronous) measurements. Patients were followed up for 5 years clinically and by magnetic resonance imaging. 

MAIN OUTCOMESAND MEASURES: 

New active lesions, increased T2 lesion volume, and brain volume on magnetic resonance imaging, as well as MS relapses and disability (Expanded Disability Status Scale score). 

RESULTS: 

Higher 25(OH)D levels predicted reduced MS activity and a slower rate of progression. A 50-nmol/L (20-ng/mL) increment in average serum 25(OH)D levels within the first 12 months predicted a 57% lower rate of new active lesions (P < .001), 57% lower relapse rate (P = .03), 25% lower yearly increase in T2 lesion volume (P < .001), and 0.41% lower yearly loss in brain volume (P = .07) from months 12 to 60. Similar associations were found between 25(OH)D measured up to 12 months and MSactivity or progression from months 24 to 60. In analyses using dichotomous 25(OH)D levels, values greater than or equal to 50 nmol/L (20 ng/mL) at up to 12 months predicted lower disability (Expanded Disability Status Scale score, -0.17; P = .004) during the subsequent 4 years. 

CONCLUSIONS AND RELEVANCE: 

Among patients with MS mainly treated with interferon beta-1b, low 25(OH)D levels early in the disease course are a strong risk factor for long-term MS activity and progression.

Multiple sclerosis (MS) is a common cause ofneurological disability in young adults.1 Mostpatients experience bouts of inflammatory demyelination (relapsing-remittingMS) followed years later by treatment-resistant disease progression and brainatrophy.2 Ahigher MS risk in individuals with low vitamin D intake3 orlow circulating 25-hydroxyvitamin D (25[OH]D),4-7 aswell as an inverse correlation between vitamin D status and MS activity, havebeen reported8-11 andsuggest that vitamin D is related to the disease process that leads to andperpetuates MS. However, previous clinical studies were conducted amongpatients with variable disease duration and could not determine whether low vitaminD is a consequence of MS activity12 orwhether vitamin D levels early in the disease course contribute to predictlong-term progression and disability. Because the prevalence of vitamin Dinsufficiency (25[OH]D<50 nmol/L [20 ng/mL]) is high,13 supplementationcould potentially benefit a large proportion of patients with MS.

Therefore, we aimed to determine whether vitamin Dstatus early in the disease process influenced long-term disease course amongparticipants in the Betaferon/Betaseron in Newly Emerging multiple sclerosis ForInitial Treatment (BENEFIT) trial.


Idioma originalAnglès
Pàgines (de-a)306-314
Nombre de pàgines9
RevistaJAMA Neurology
Volum71
Número3
DOIs
Estat de la publicacióPublicada - de març 2014

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