Chitsaz Niloofar, Dehghani Leila, Safi Amir, Esmalian-Afyouni Nazgol, Shaygannejad Vahid, Rezvani Majid, Sohrabi Karim, Moridi Kaykhosro, Moayednia Milad
Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran.
Department of Tissue Engineering and Regenerative Medicine, School of Advanced Technologies in Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Iran J Neurol. 2019 Oct 7;18(4):150-153.
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. 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. 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. G6PD deficiency is observed in patients with MS and NMO. Also, supplementary vitamin D may induce favorable results on the G6PD level.
多发性硬化症（MS）和视神经脊髓炎（NMO）均为脱髓鞘疾病，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）通过磷酸戊糖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，还参与抗氧化应激防御。将补充维生素D作为MS治疗计划的一部分进行处方可以增加G6PD基因表达。本研究的目的是确定MS和NMO患者的血清G6PD水平及其与维生素D的关系，因为这方面尚未得到充分探索。在这项病例对照研究中，受试者被分为三个实验组和对照组。实验组包括50例有维生素D服用史的复发缓解型MS（RRMS）患者、50例新诊断的MS患者和50例NMO患者。对照组包括65名健康个体。测量并比较这些组之间的血清G6PD水平。MS和NMO患者的G6PD水平之间未观察到显著差异，但应注意的是，该水平显著低于健康组。与未服用补充维生素D的MS患者相比，之前服用过补充维生素D的MS患者的G6PD血清水平显著更高。MS和NMO患者中观察到G6PD缺乏。此外，补充维生素D可能对G6PD水平产生有利结果。
