Many have been waiting for this – the results of the SOLAR study, a phase II study that investigated the effect of high-dose vitamin D as an add-on to immunomodulatory therapy with interferon-beta 1a s.c. A total of 229 relapsing MS patients who were already stable on interferon-beta 1a 3 x 44 µg/week and whose vitamin D3 levels were < 150 µmol/l were included in the study. These patients were randomized 1:1 either into the Interferon + Vitamin D group or Interferon + Placebo group. The two groups were homogeneous in terms of most basic parameters, however, the patients in the Interferon + Placebo group were on average a little longer ill (14.8 months vs. 10.4 months) than those in the Interferon + Vitamin D3 group.The treatment group received 6670 IU daily for 4 weeks, followed by 14.007 IU daily for the rest of the study period. The study was originally planned for two years, but was limited to 48 weeks due to recruitment problems. NEDA was chosen as the primary endpoint (NEDA = no evidence of disease activity, which means “no evidence of disease activity” in terms of relapses, disability increase and new MRI lesions). Secondary endpoints were the annual relapse rate, disease progression as measured by the EDSS, and various MRI parameters.
To cut a long story short – the primary study endpoint, which determines whether a study is negatively or positively rated, was not reached. In terms of NEDA, there was no difference between interferon patients with or without intake of high-dose vitamin D. No evidence of disease activity was achieved by 37.2% of the treatment group and 35.3% of the placebo group. An important secondary endpoint was also missed. There was no evidence of a delay in disability progression with the intake of vitamin D. The annual relapse rate was reduced by the intake of vitamin D (0.28 in the treatment group vs. 0.41 in the placebo group), but this result was not statistically significant – only a trend was evident here. A significant difference, however, was observed in terms of MRI activity, which was reduced under the intake of vitamin D.
So the study is actually “neither fish nor fowl”. On the one hand, the primary endpoint was missed – making the study negative; there is therefore no evidence for the use of vitamin D as an intervention in MS. On the other hand, some of the secondary endpoints either show a good result (MRI) or at least a trend in favor of a desired reduction in inflammatory activity. Given that the study was very short and the design had to be changed due to poor recruitment, from my point of view we are not much wiser than before.
Sure, there may now be no reason to treat MS patients with high-dose vitamin D therapy – but there are also not enough reasons to abandon the pragmatic vitamin D substitution, as it is currently being carried out in many MS patients (Dekristol 20,000 IU 1x per week etc.). So, ultimately everything remains the same.
