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多发性硬化症患者血浆25(OH)D水平降低。与由扩展残疾状态量表(EDSS)、多发性硬化症综合评分量表(MSSS)、进展指数和赫伯特量表严重程度分级所表示的疾病严重程度的相关性。

Decreased plasma levels of 25(OH)D in multiple sclerosis patients. Correlation with disease severity expressed by EDSS, MSSS, progression index and Herbert´s scale severity grade.

作者信息

Bucova M, Durmanova V, Cudrakova D, Blazickova S, Gmitterova K, Klimova E, Lisa I, Kluckova K, Majernikova B

出版信息

Bratisl Lek Listy. 2019;120(10):723-729. doi: 10.4149/BLL_2019_120.

DOI:10.4149/BLL_2019_120
PMID:31663345
Abstract

OBJECTIVES

Multiple sclerosis is a chronic inflammatory and autoimmune demyelinating disease of the brain and spinal cord. Vitamin D has anti-inflammatory and anti-Th1, Th17 activities, activates the function of regulatory T cells, shifts the immune response towards Th2, so it might be favorable for downregulation of the disease pathogenesis, and if inflammation and Th1 and Th17 immunity are hyperactivated. The aim of our study was to highlight the role of vitamin D in multiple sclerosis pathogenesis.

METHODS

We investigated 178 patients with multiple sclerosis. Plasma levels of 25(OH)D and HMGB1 were investigated.

RESULTS

Despite a regular use of VD by patients, the plasma levels of 25(0H)D were significantly decreased in 57% of them, 14.1% had VD deficiency (level of 25(OH)D < 20 ng/mL) and more than 6 % of patients had VD severe deficiency with the plasma level of 25(OH)D < 12 ng/mL. The level of 25(OH)D negatively correlated with the severity of the disease (EDSS, index of progression, duration of the disease) and negative association was found also with Herbert´s six severity grades. HMGB1 levels were higher in patients (p < 0.0001).

CONCLUSION

Our result showed that vitamin D deficiency plays a role in multiple sclerosis pathogenesis. We believe that administration of vitamin D to patients at a sufficient dose providing a physiological level of vitamin D could have a positive effect on the course of the disease. However, regular monitoring of vitamin D levels is required, which should be at least within 30-75 ng/mL, and even more, but below the toxicity limit (Tab. 6, Ref. 66).

摘要

目的

多发性硬化症是一种脑和脊髓的慢性炎症性自身免疫性脱髓鞘疾病。维生素D具有抗炎、抗Th1、Th17活性,可激活调节性T细胞功能,使免疫反应向Th2偏移,因此如果炎症以及Th1和Th17免疫反应过度激活,维生素D可能有利于下调疾病发病机制。我们研究的目的是突出维生素D在多发性硬化症发病机制中的作用。

方法

我们调查了178例多发性硬化症患者。检测了血浆25(OH)D和HMGB1水平。

结果

尽管患者常规使用维生素D,但其中57%的患者血浆25(0H)D水平显著降低,14.1%的患者存在维生素D缺乏(25(OH)D水平<20 ng/mL),超过6%的患者存在严重维生素D缺乏,血浆25(OH)D水平<12 ng/mL。25(OH)D水平与疾病严重程度(扩展残疾状态量表、进展指数、疾病持续时间)呈负相关,与赫伯特六级严重程度分级也呈负相关。患者的HMGB1水平较高(p<0.0001)。

结论

我们的结果表明维生素D缺乏在多发性硬化症发病机制中起作用。我们认为,给予患者足够剂量的维生素D以提供生理水平的维生素D可能对疾病进程产生积极影响。然而,需要定期监测维生素D水平,其应至少在30 - 75 ng/mL之间,甚至更高,但要低于毒性极限(表6,参考文献66)。

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