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Contribution of vitamin D insufficiency to the pathogenesis of multiple sclerosis

机译:维生素D缺乏对多发性硬化症发病机制的贡献

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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.
机译:综述了维生素D功能不足对多发性硬化症(MS)发病机理的影响。在最近发现的多种维生素D作用中,免疫调节作用已在实验性自身免疫性脑脊髓炎和人类中得到证明。目前,外周免疫系统中的这种作用是维生素D可能影响MS的主要已知机制,但中枢神经系统也可能涉及其他类型的作用。此外,维生素D功能不全在温带国家和疾病早期的MS患者中普遍存在,这表明与维生素D功能不足有关的有害作用可能在这些患者中发挥作用。实际上,许多遗传和环境风险因素似乎相互作用并有助于MS。在遗传学上,几个人类白细胞抗原(HLA)等位基因(更特别是HLA-DRB1 * 1501)可能有利于该疾病,而另一些可能具有保护性。某些与维生素D代谢有关的基因(例如CYP27B1)也起着重要作用。此外,已经确定了三个环境危险因素:过去的爱泼斯坦-巴尔病毒感染,维生素D功能不足和吸烟。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,并且可能持续到儿童期和青春期,直到该疾病在成年期被触发为止,因此可能在生命的最初几十年中调节了MS的风险。此外,尽管尚未报道使用维生素D补充的充分有力的随机临床试验的结果,但一些临床发现已经强烈表明维生素D的状况会影响MS患者的复发率和放射损伤。在等待这些无可辩驳的结果(可能会很久)的同时,应补充中等剂量的维生素,以补充目前处于维生素D功能不足的MS患者,至少在其一般健康状况方面。

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