Vitamin D supplementation and monitoring in multiple sclerosis: who, when and wherefore.
Acta Neurol Scand Suppl
; (195): 63-9, 2012.
Article
in En
| MEDLINE
| ID: mdl-23278659
ABSTRACT
OBJECTIVES:
Observational studies suggest that increasing the serum concentration of 25-hydroxyvitamin D with 50 nm could halve the relapse risk in relapsing-remitting multiple sclerosis (MS). Assuming that the association between disease activity and vitamin D status is entirely causal may however exaggerate the potential benefit. The aim of this paper is to address whether and how vitamin D should be monitored in patients with MS.METHODS:
Possible benefits of vitamin D supplementation were assessed from observational, experimental and clinical studies. Based on repeated measurements of 25-hydroxyvitamin D in Norwegian patients with MS , we estimate the effect of different supplementation regimes.RESULTS:
Serum levels of 25-hydroxyvitamin in the upper physiological range are associated with lower risk of relapses and magnetic resonance imaging disease activity, but the causality is uncertain. Osteoporosis develops early in patients with MS , and 25-hydroxyvitamin vitamin should therefore at least be 50 nm throughout the year. Levels between 75 and 125 nmol may offer some additional benefit for bone health, are not toxic and are associated with low disease activity. Adding 400 IU (10 µg) vitamin D daily would only bring 56% of the patients >50 nm and 11% >75 nm throughout the year, whereas 800 IU (20 µg) would maintain 97% >50 nm and 67% >75 nm.CONCLUSION:
We recommend that MS patients are supplemented with 800 IU of vitamin D at least from autumn to spring. Alternatively, 25-hydroxyvitamin D should be measured and the nadir level estimated and supplementation given to a target level between approximately 75 and 125 nm.
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Main subject:
Vitamin D
/
Dietary Supplements
/
Multiple Sclerosis
Type of study:
Etiology_studies
/
Observational_studies
Limits:
Humans
Language:
En
Journal:
Acta Neurol Scand Suppl
Year:
2012
Document type:
Article