多发性硬化症和视神经脊髓炎患者血清葡萄糖-6-磷酸脱氢酶水平的评价。

Iranian Journal of Neurology Pub Date : 2019-10-07
Niloofar Chitsaz, Leila Dehghani, Amir Safi, Nazgol Esmalian-Afyouni, Vahid Shaygannejad, Majid Rezvani, Karim Sohrabi, Kaykhosro Moridi, Milad Moayednia
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引用次数: 0

摘要

背景:多发性硬化症(MS)和视神经脊髓炎(NMO)都是脱髓鞘疾病,氧化应激被认为在其发病机制中起作用。葡萄糖-6-磷酸脱氢酶(G6PD)通过戊糖磷酸途径产生烟酰胺腺嘌呤二核苷酸磷酸(NADPH)。NADPH不仅参与髓鞘形成所需脂肪酸的合成,还参与氧化应激的防御。作为MS治疗计划的一部分,处方补充维生素D可以增加G6PD基因表达。本研究的目的是确定MS和NMO患者血清G6PD水平及其与维生素D的关系,因为它还没有被深入探讨。方法:采用病例对照研究,将受试者分为实验组和对照组。实验组包括50名有维生素D摄入史的复发缓解型多发性硬化症(RRMS)患者,50名新诊断的多发性硬化症患者和50名NMO患者。对照组包括65名健康个体。测定各组血清G6PD水平并进行比较。结果:MS患者与NMO患者G6PD水平无显著差异,但值得注意的是,G6PD水平明显低于健康组。与未补充维生素D的患者相比,先前服用维生素D的MS患者血清G6PD水平明显更高。结论:MS合并NMO患者存在G6PD缺乏。此外,补充维生素D可能会对G6PD水平产生有利的影响。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Evaluation of glucose-6-phosphate dehydrogenase serum level in patients with multiple sclerosis and neuromyelitis optica.

Evaluation of glucose-6-phosphate dehydrogenase serum level in patients with multiple sclerosis and neuromyelitis optica.

Background: Multiple sclerosis (MS) and neuromyelitis optica (NMO) are both demyelinating disorders and oxidative stress is suggested to have a role in their pathogenesis. Glucose-6-phosphate dehydrogenase (G6PD) produces nicotinamide adenine dinucleotide phosphate (NADPH) via the pentose phosphate pathway. NADPH is not only involved in the synthesis of fatty acids necessary for myelination, but also it is involved in the defense against oxidative stress. Prescribing supplementary vitamin D as a part of the MS treatment plan can increase G6PD gene expression. The aim of this study was to determine the serum level of G6PD in patients with MS and NMO and its relationship with vitamin D, since it is yet to be explored thoroughly. Methods: In this case-control study, subjects were divided into three experimental and control groups. The experimental groups comprised 50 patients with relapsing-remitting MS (RRMS) who had a history of vitamin D consumption, 50 newly-diagnosed MS patients, and 50 patients with NMO. Control group included 65 healthy individuals. Serum level of G6PD was measured and compared among these groups. Results: No significant difference was seen between the G6PD level in patients with MS and NMO, but it should be noted that this level was significantly lower than the healthy group. G6PD serum level was significantly higher in patients with MS who had previously consumed supplementary vitamin D compared to those who had not. Conclusion: G6PD deficiency is observed in patients with MS and NMO. Also, supplementary vitamin D may induce favorable results on the G6PD level.

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Iranian Journal of Neurology
Iranian Journal of Neurology CLINICAL NEUROLOGY-
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