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. 2013 Mar;6(2):81-116. doi: 10.1177/1756285612473513.
The contribution of vitamin D insufficiency to the pathogenesis of multiple sclerosis (MS) is reviewed. Among the multiple recently discovered actions of vitamin D, an immunomodulatory role has been documented in experimental autoimmune encephalomyelitis and in humans. This action in the peripheral immune system is currently the main known mechanism through which vitamin D might influence MS, but other types of actions could be involved within the central nervous system. Furthermore, vitamin D insufficiency is widespread in temperate countries and in patients with MS at the earliest stages of the disease, suggesting that the deleterious effects related to vitamin D insufficiency may be exerted in these patients. In fact, many genetic and environmental risk factors appear to interact and contribute to MS. In genetics, several human leukocyte antigen (HLA) alleles (more particularly HLA-DRB1*1501) could favour the disease whereas some others could be protective. Some of the genes involved in vitamin D metabolism (e.g. CYP27B1) also play a significant role. Furthermore, three environmental risk factors have been identified: past Epstein-Barr virus infection, vitamin D insufficiency and cigarette smoking. Interactions between genetic and environmental risk or protective factors may occur during the mother's pregnancy and could continue during childhood and adolescence and until the disease is triggered in adulthood, therefore possibly modulating the MS risk throughout the first decades of life. Furthermore, some clinical findings already strongly suggest that vitamin D status influences the relapse rate and radiological lesions in patients with MS, although the results of adequately powered randomized clinical trials using vitamin D supplementation have not yet been reported. While awaiting these incontrovertible results, which might be long in coming, patients with MS who are currently in vitamin D insufficiency should be supplemented, at least for their general health status, using moderate doses of the vitamin.
维生素 D 不足在多发性硬化症 (MS) 的发病机制中的作用。在最近发现的维生素 D 的多种作用中,其在实验性自身免疫性脑脊髓炎和人类中的免疫调节作用已得到证实。这种在外周免疫系统中的作用是目前已知的维生素 D 影响 MS 的主要机制,但其他类型的作用也可能发生在中枢神经系统内。此外,维生素 D 不足在温带国家和疾病早期的 MS 患者中很普遍,这表明与维生素 D 不足相关的有害影响可能在这些患者中发挥作用。事实上,许多遗传和环境风险因素似乎相互作用并促成 MS。在遗传学方面,几种人类白细胞抗原 (HLA) 等位基因(特别是 HLA-DRB1*1501)可能有利于疾病,而其他一些等位基因可能具有保护作用。一些涉及维生素 D 代谢的基因(例如 CYP27B1)也起着重要作用。此外,已经确定了三个环境风险因素:过去的 Epstein-Barr 病毒感染、维生素 D 不足和吸烟。遗传和环境风险或保护因素之间的相互作用可能发生在母亲怀孕期间,并可能在儿童和青少年时期持续存在,直到成年后疾病发作,因此可能会在生命的头几十年中调节 MS 风险。此外,一些临床发现已经强烈表明维生素 D 状态会影响 MS 患者的复发率和放射学病变,尽管使用维生素 D 补充剂进行的充分有力的随机临床试验的结果尚未报告。在等待这些无可争议的结果(可能需要很长时间)的同时,目前处于维生素 D 不足的 MS 患者应补充维生素,至少应补充适量的维生素,以改善其整体健康状况。