Mehrpour Masoud, Akhoundi Fahimeh H, Delgosha Maryam, Keyvani Hosein, Motamed Mohammad R, Sheibani Behnam, Meysamie Alipasha
*Department of Neurology, Firoozgar Hospital †Firoozgar Clinical Research Development Center ‡Department of Virology, Faculty of Medicine, Iran University of Medical Sciences §Department of Community Medicine, Faculty of Medicine, Tehran University of Medical Sciences, Tehran Iran.
Neurologist. 2015 Oct;20(4):57-60. doi: 10.1097/NRL.0000000000000053.
To investigate the potential role of disease-modifying therapies (DMTs) used to treat multiple sclerosis on inducing brain-derived neurotrophic factor (BDNF) production.
A total of 82 patients entered the study. Sixty (73%) patients were on DMTs (15 on Avonex, 13 on Rebif, 27 on Betaferon, 3 on Mitoxantrone, and 2 on IVIg), whereas 22 received no DMTs. The degree of neurological impairment was recorded using the expanded disability status scale (EDSS). Serum BDNF levels were assessed using the Sandwich ELISA method. We compared mean serum BDNF levels among patient groups based on whether or not they were on DMTs, and the specific agent used. Then, the relationship between BDNF levels and EDSS scores was assessed. The receiver operating characteristic (ROC) curve was used to calculate a cutoff value by which serum BDNF could predict the degree of disability.
The study sample had a mean age of 34.6 years, mean EDSS score of 3.8, and mean BDNF level of 198.9 pg/mL. Patients on interferon-β 1b therapy had significantly higher levels of BDNF compared with patients on Mitoxantrone or patients not on DMTs (237.6, 68.6, and 155.9, respectively; P=0.003). The degree of neurological impairment correlated negatively with BDNF levels (P<0.001). A cutoff value of 190 pg/mL was calculated for BDNF (ROC analysis, area under the curve: 0.729, P=0.002). At BDNF levels >190, the sensitivity for a milder degree of neurological impairment (EDSS<3) was 80%.
This study showed a significant effect of interferon-β 1b therapy on increasing BDNF production in multiple sclerosis.
探讨用于治疗多发性硬化症的疾病修正疗法（DMTs）在诱导脑源性神经营养因子（BDNF）产生方面的潜在作用。
共有82例患者进入该研究。60例（73%）患者接受DMTs治疗（15例使用阿沃那新，13例使用利比，27例使用β-干扰素，3例使用米托蒽醌，2例使用静脉注射免疫球蛋白），而22例未接受DMTs治疗。使用扩展残疾状态量表（EDSS）记录神经功能损害程度。采用夹心酶联免疫吸附测定法评估血清BDNF水平。我们根据患者是否接受DMTs治疗以及所使用的具体药物，比较了各患者组的平均血清BDNF水平。然后，评估BDNF水平与EDSS评分之间的关系。使用受试者工作特征（ROC）曲线计算血清BDNF可预测残疾程度的临界值。
研究样本的平均年龄为34.6岁，平均EDSS评分为3.8，平均BDNF水平为198.9 pg/mL。与使用米托蒽醌的患者或未接受DMTs治疗的患者相比，接受β-干扰素1b治疗的患者BDNF水平显著更高（分别为237.6、68.6和155.9；P = 0.003）。神经功能损害程度与BDNF水平呈负相关（P < 0.001）。计算出BDNF的临界值为190 pg/mL（ROC分析，曲线下面积：0.729，P = 0.002）。当BDNF水平>190时，对较轻程度神经功能损害（EDSS < 3）的敏感性为80%。
本研究表明β-干扰素1b治疗在增加多发性硬化症患者BDNF产生方面具有显著效果。
