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Vitamin D and MS: Kampman


Department of Neurology,
University Hospital of North Norway, PO Box 33
NO-9038 Tromsø , Norway
Institute of Clinical Medicine,
University of Tromsø,
Tromsø , Norway
T +47 77626000
F +47 77627074

PubMed: Kampman MT

Clinical trial
Can Vitamin D Supplementation Prevent Bone Loss in Persons With Multiple Sclerosis Identifier: NCT00785473
Study Completion Date: Completed

25th Congress of the European Committee for the treatment and Research in Multiple Sclerosis (ECTRIMS)

Thursday, September 10, 2009, 15:30 - 17:00
P 485
Vitamin D status in individuals with multiple sclerosis at baseline and after supplementation with 20,000 IU cholecalciferol a week for 48 weeks
L. Steffensen, M. Brustad, G. Skeie, L. Jørgensen, Y. Figenschau, M. Kampman (Tromsø, NO)

In studies from several countries, vitamin D levels were lower in individuals with MS than in controls. This has been attributed to low UV-exposure. Vitamin D may have therapeutical potential in MS, but necessary levels of 25 (OH) vitamin D (25(OH)D) have not been defined. For the general population, optimal 25(OH)D levels of ≥ 50 or ≥ 75 nmol/L have been proposed. The vitamin D intake required to obtain these levels has not been determined. We assess the contributions of oral vitamin D intake and UV-exposure to 25(OH)D at baseline and evaluate the effect on 25(OH)D values of supplementing 20,000 IU (500 µg) cholecalciferol a week and 500 mg calcium a day for 48 weeks in individuals with MS ( NCT00785473).

At week 48, 49/50 women and 20/22 men remained in the study. Serum for measurement of 25(OH)D was obtained at the end of winter (28.1.-27.3.08 and 16.2.-31.3.09). Multiple linear regression analysis was used to determine associations of UV-exposure and vitamin D intake from diet and supplements with 25(OH)D at baseline. The effect of supplementation with cholecalciferol on 25(OH)D was analysed without knowledge of treatment group.

Participants’ median (range) age was 41 (21-50) years, EDSS 2.5 (0-4.5). At baseline, oral vitamin D intake was at or above the recommended 7.5 µg/d in 37/64 and 36/69 had been on sunshine vacations or used a tanning bed the past year. None were considered 25(OH)D deficient (< 25 nmol/L). A regression model showed associations of baseline 25(OH)D with age (beta=0.020, P<0.001), sunshine vacations or tanning bed use (beta=0.167, P=0.002), and daily vitamin D intake of 7.5 µg or more (beta=0.163, P=0.031), but not BMI or sex. Median (range) 25(OH)D increased from 58 (25 to 123) nmol/L at baseline to 81(35 to 171) nmol/L in week 48. The proportion of both insufficient and marginal (25-49 and 50-74 nmol/L) values decreased by 22% while optimal (≥ 75 nmol/L) values increased from 17% at baseline to 61% at week 48. Blood samples taken every 12 weeks did not reveal disturbances of calcium metabolism.

At baseline, we found a significant contribution of UV-induced vitamin D production in the skin to vitamin D status in the MS patients studied. Supplementing half of the participants in the study with 20,000 IU cholecalciferol a week increased the proportion of individuals with optimal vitamin D status (≥ 75 nmol/L) from 17 to 61% and did not cause adverse effects.

September 17-20, 2008 Montreal, Canada

Bone mineral density, motor function, and vitamin D status in fully ambulatory persons with relapsing-remitting multiple sclerosis - population based cross-sectional data
Svein I. Mellgren(1), Linn H. Steffensen(2), Margitta Kampman(2)
(1) Department of Neurology, University of Tromso, Tromso, Norway;
(2) University Hospital of North Norway, Tromso, Norway


Several studies have shown that bone mineral density (BMD) at the femoral neck decreases with increasing physical handicap (Expanded Disability Status Scale (EDSS)) in multiple sclerosis (MS) patients.

To estimate determinants of BMD in fully ambulatory persons with MS based on screening data from a randomised controlled trial (‘Can supplementation with vitamin D prevent bone loss in persons with relapsing-remitting MS?’).


Examinations at screening (performed in February and March 2008) included EDSS, multiple sclerosis functional composite, 10 ft timed tandem walk, strength of grip, BMD (total hip, femoral neck, lumbar spine, forearm), and blood tests including 25(OH) vitamin D measurements. Results: Sixty-one women and 26 men aged 19–50 years (median 31) were examined. Median duration of disease was 9 years from first symptom, median EDSS 2.5 (range 0–5.0). High dose intravenous methylprednisolone had been used in the treatment of 38% of the participants; none had received a cumulative dose of
more than 1 g oral prednisolone. Abnormal BMD (z-score ≤ -2.0) was found in 12/84 individuals at one (n=10), two (n=1) or three (n=1) of the following sites: total hip and/or femoral neck; ultradistal radius; lumbar spine. Vitamin D status was considered deficient in 35% of participants (serum 25(OH) vitamin D 25–49 nmol/L), and only 15% had optimal values (>75 nmol/L). Preliminary analyses show statistically significant correlations between motor function and BMD in both lower and upper extremities. Linear regression analysis will be applied to estimate the effects of motor function, serum 25(OH) vitamin D, disease duration, cumulative corticosteroid treatment, use of disease modifying treatment, smoking, age, and sex on BMD.


Low BMD is likely to develop into osteoporosis with increasing age and duration of MS. Prevention of osteoporosis is a high priority, because treatment of the established disease remains sub-optimal. Results from the 2-year trial will show whether fully ambulatory persons with MS benefit from supplementation with 20,000 IU cholecalciferol weekly, a dose expected to increase 25(OH) to optimal levels (>75 nmol/L).

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Page last edited: October 26, 2014
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