Service de Neurologie 1, Hôpital de la Salpêtrière, Assistance Publique-Hôpitaux de Paris, Université Pierre et Marie Curie (Paris VI), Paris, France.
Ther Adv Neurol Disord. 2012 Jul;5(4):187-98. doi: 10.1177/1756285612447090.
Vitamin D could play a protective role in multiple sclerosis.
In an observational, uncontrolled study, vitamin D3 supplementation (3010 IU/day on average) was given to 156 consecutive patients with relapsing-remitting multiple sclerosis, under first-line immunomodulatory therapy and with initial 25-OH-D serum level lower than 100 nmol/l (40 ng/ml). Relapses were determined for 29.1 ± 8.4 months during vitamin D and 29.8 ± 10.1 months before supplementation. The 25-OH-D level was measured before supplementation and several times during supplementation. The incidence rate of relapses before and during supplementation was estimated using negative binomial regression models with follow-up durations as offset terms. The incidence rate and incidence rate ratio of relapses at various 25-OH-D levels were also calculated using negative binomial regression models.
In 76 patients, immunomodulatory therapy preceded vitamin D supplementation (by 4.2 ± 2.7 years) and in 80 patients both treatments were started simultaneously. Under supplementation, the 25-OH-D level increased from 49 ± 22 nmol/l to 110 ± 26 nmol/l on average. Pooling data collected before and during supplementation, we found a significant strong inverse relationship between the relapse incidence rate and the 25-OH-D level (p < 0.0001), suggesting that vitamin D did indeed influence the relapse rate. Results of univariate, bivariate and multivariate analyses were analogous: in the multivariate model adjusted for age, disease duration and previous use of immunomodulatory therapy, every 10 nmol increase in 25-OH-D level was associated with a reduction in the relapse incidence rate of 13.7%. Dividing iteratively the population made up of pooled periods into two subgroups according to the 25-OH-D levels, the relapse incidence rate ratio decreased as the 25-OH-D level increased up to 110 nmol/l, but a plateau effect was observed beyond this limit.
Further studies are warranted for accurate quantification of the vitamin D effect.
维生素 D 可能在多发性硬化症中发挥保护作用。
在一项观察性、非对照研究中，对 156 例处于缓解-复发期多发性硬化症的患者进行了维生素 D3 补充（平均每天 3010IU），这些患者正在接受一线免疫调节治疗，且初始 25-羟维生素 D 血清水平低于 100nmol/l（40ng/ml）。在补充维生素 D 期间和补充前的 29.1±8.4 个月内确定复发情况。在补充前和补充期间多次测量 25-羟维生素 D 水平。使用负二项回归模型，以随访时间作为偏移项，估计补充前后的复发发生率。还使用负二项回归模型计算了不同 25-羟维生素 D 水平下的复发发生率和复发发生率比。
在 76 例患者中，免疫调节治疗先于维生素 D 补充（提前 4.2±2.7 年），而在 80 例患者中，两种治疗同时开始。在补充期间，25-羟维生素 D 水平从 49±22nmol/l 平均增加到 110±26nmol/l。合并补充前后的数据，我们发现复发发生率与 25-羟维生素 D 水平之间存在显著的强负相关关系（p<0.0001），表明维生素 D 确实影响了复发率。单变量、双变量和多变量分析的结果类似：在调整年龄、疾病持续时间和免疫调节治疗既往使用的多变量模型中，25-羟维生素 D 水平每增加 10nmol，复发发生率降低 13.7%。根据 25-羟维生素 D 水平将合并期组成的人群迭代分为两个亚组，随着 25-羟维生素 D 水平的升高，复发发生率比逐渐降低，但超过 110nmol/l 时观察到平台效应。
需要进一步研究以准确量化维生素 D 的作用。
