Abstract：
BACKGROUND: Multiple sclerosis (MS) is a chronic demyelinating neurodegenerative disorder. Elevated levels of pro-inflammatory mediators and some oxidative stress parameters can accelerate the demyelination process. We aimed to investigate the efficacy and safety of metformin as an adjuvant therapy to interferon beta 1a (IFNβ-1a) in relapsing-remitting multiple sclerosis (RRMS) patients.
METHODS: Eighty RRMS patients were equally divided into 2 groups: the intervention group receiving IFNβ-1a plus 2 gm of metformin once daily and the control group receiving IFNβ-1a alone. Interleukin 17 (IL17), interleukin 22 (IL22), malondialdehyde (MDA), T2 lesions in magnetic resonance imaging (MRI) and expanded disability status scale (EDSS) were assessed at the baseline and then after 6 months.
RESULTS: At baseline, there were no statistically significant differences between the two groups (p > 0.05). After 6 months, the change in the median (interquartile range) of the results for both the intervention and control group were; IL17 (- 1.39 (4.19) vs - 0.93 (5.48), p = 0.48), IL22 (- 0.14 (0.48) vs - 0.09 (0.6), p = 0.53), and EDSS (0 vs 0, p = 1), respectively. The mean (standard deviation) change in MDA for the intervention and control group was - 0.93 (2.2) vs - 0.5 (2.53), p = 0.038, respectively. For MRI results, 21 patients had stationary and regressive course and 1 patient had a progressive course in the intervention arm vs 12 patients had stationary and regressive course and 4 had a progressive course in the control arm, p = 0.14.
CONCLUSIONS: Adding metformin to IFNβ-1a demonstrated a potential effect on an oxidative stress marker (MDA). However, there is no statistically significant effect on immunological, MRI and clinical outcomes. We recommend larger scale studies to confirm or negate these findings.
BACKGROUND: ClinicalTrials.gov number: NCT05298670, 28/3/2022.
METHODS: Eighty RRMS patients were equally divided into 2 groups: the intervention group receiving IFNβ-1a plus 2 gm of metformin once daily and the control group receiving IFNβ-1a alone. Interleukin 17 (IL17), interleukin 22 (IL22), malondialdehyde (MDA), T2 lesions in magnetic resonance imaging (MRI) and expanded disability status scale (EDSS) were assessed at the baseline and then after 6 months.
RESULTS: At baseline, there were no statistically significant differences between the two groups (p > 0.05). After 6 months, the change in the median (interquartile range) of the results for both the intervention and control group were; IL17 (- 1.39 (4.19) vs - 0.93 (5.48), p = 0.48), IL22 (- 0.14 (0.48) vs - 0.09 (0.6), p = 0.53), and EDSS (0 vs 0, p = 1), respectively. The mean (standard deviation) change in MDA for the intervention and control group was - 0.93 (2.2) vs - 0.5 (2.53), p = 0.038, respectively. For MRI results, 21 patients had stationary and regressive course and 1 patient had a progressive course in the intervention arm vs 12 patients had stationary and regressive course and 4 had a progressive course in the control arm, p = 0.14.
CONCLUSIONS: Adding metformin to IFNβ-1a demonstrated a potential effect on an oxidative stress marker (MDA). However, there is no statistically significant effect on immunological, MRI and clinical outcomes. We recommend larger scale studies to confirm or negate these findings.
BACKGROUND: ClinicalTrials.gov number: NCT05298670, 28/3/2022.
摘要：
背景：多发性硬化（MS）是一种慢性脱髓鞘性神经退行性疾病。促炎介质和一些氧化应激参数的升高水平可以加速脱髓鞘过程。我们旨在研究二甲双胍作为干扰素β1a（IFNβ-1a）辅助治疗复发缓解型多发性硬化（RRMS）患者的疗效和安全性。
方法：80例RRMS患者均分为2组：干预组接受IFNβ-1a加2gm二甲双胍每日一次，对照组仅接受IFNβ-1a。白细胞介素17(IL17),白细胞介素22（IL22），丙二醛（MDA），在基线和6个月后评估磁共振成像（MRI）和扩展残疾状态量表（EDSS）中的T2病变。
结果：在基线时，两组比较差异无统计学意义(p>0.05)。六个月后,干预组和对照组的结果中位数（四分位距）的变化为；IL17（-1.39（4.19）vs-0.93（5.48），p=0.48),IL22（-0.14（0.48）对-0.09（0.6），p=0.53)，和EDSS(0vs0，p=1)，分别。干预组和对照组MDA的平均值（标准差）变化为-0.93（2.2）vs-0.5（2.53），分别为p=0.038。对于MRI结果，21例患者在干预组中有静止和回归过程，1例患者在干预组中有进行性过程，而12例患者在控制组中有静止和回归过程，4例患者在控制组中有进行性过程。p=0.14。
结论：在IFNβ-1a中添加二甲双胍对氧化应激标志物（MDA）具有潜在作用。然而,对免疫学没有统计学上的显著影响，MRI和临床结果。我们建议进行更大规模的研究来证实或否定这些发现。
背景：ClinicalTrials.gov编号：NCT05298670，28/3/2022。
方法：80例RRMS患者均分为2组：干预组接受IFNβ-1a加2gm二甲双胍每日一次，对照组仅接受IFNβ-1a。白细胞介素17(IL17),白细胞介素22（IL22），丙二醛（MDA），在基线和6个月后评估磁共振成像（MRI）和扩展残疾状态量表（EDSS）中的T2病变。
结果：在基线时，两组比较差异无统计学意义(p>0.05)。六个月后,干预组和对照组的结果中位数（四分位距）的变化为；IL17（-1.39（4.19）vs-0.93（5.48），p=0.48),IL22（-0.14（0.48）对-0.09（0.6），p=0.53)，和EDSS(0vs0，p=1)，分别。干预组和对照组MDA的平均值（标准差）变化为-0.93（2.2）vs-0.5（2.53），分别为p=0.038。对于MRI结果，21例患者在干预组中有静止和回归过程，1例患者在干预组中有进行性过程，而12例患者在控制组中有静止和回归过程，4例患者在控制组中有进行性过程。p=0.14。
结论：在IFNβ-1a中添加二甲双胍对氧化应激标志物（MDA）具有潜在作用。然而,对免疫学没有统计学上的显著影响，MRI和临床结果。我们建议进行更大规模的研究来证实或否定这些发现。
背景：ClinicalTrials.gov编号：NCT05298670，28/3/2022。
