Department of Medicine (Neurology) (JKC, VD, A-LS, RC, AT), University of British Columbia, Vancouver, Canada; Department of Neurology (EHMdL, SA-A), Center of Neuroimmunology, Hospital Clinic of Barcelona, Institut d'Investigacions Biomèdiques August Pi Sunyer (IDIBAPS), University of Barcelona, Barcelona, Spain; Department of Statistics (CT), University of British Columbia, Vancouver, Canada; Department of Neruology (A-LN), University of Melbourne, Melbourne, Australia; Royal Melbourne Hospital (A-LN), Melbourne, Australia; and Departments of Clinical Neurosciences and Surgery (Ophthalmology) (FC), University of Calgary, Clinician Scientist with the Hotchkiss Brain Institute (HBI), Calgary, Canada.
Department of Neurology and Neurotherapeutics (SCB), University of Texas Southwestern Medical Center, Dallas, Texas.
J Neuroophthalmol. 2020 Mar;40(1):37-43. doi: 10.1097/WNO.0000000000000802.
Patients with multiple sclerosis (MS) experience progressive thinning in optical coherence tomography (OCT) measures of neuroaxonal structure regardless of optic neuritis history. Few prospective studies have investigated the effects of disease-modifying therapies on neuroaxonal degeneration in the retina. Alemtuzumab is a monoclonal antibody shown to be superior to interferon β-1a in treating relapsing-remitting MS (RRMS). The purpose of this study was to assess the effects of alemtuzumab and first-line injectable treatments on OCT measures of neuroaxonal structure including peripapillary retinal nerve fiber layer (RNFL) thickness and combined ganglion cell-inner plexiform (GCIP) layer volume in RRMS patients followed up over 5 years.
In this retrospective pilot study with prospectively collected double cohort data, spectral domain OCT measures of RNFL thickness and GCIP volume were compared between alemtuzumab-treated RRMS patients (N = 24) and RRMS patients treated with either interferon-β or glatiramer acetate (N = 21).
Over a median of 60 months (range 42-60 months), the alemtuzumab cohort demonstrated a change in the mean RNFL thickness (thinning from baseline) of -0.88 μm (95% confidence interval [CI] -2.63 to 0.86; P = 0.32) and mean GCIP volume of +0.013 mm (95% CI -0.006 to 0.032; P = 0.18). Over the same time period, the first-line therapy-treated cohort demonstrated greater degrees of RNFL thinning (mean change in RNFL thickness was -3.65 μm [95% CI -5.40 to -1.89; P = 0.0001]). There was also more prominent GCIP volume loss relative to baseline in the first-line therapy group (-0.052 mm [95% CI -0.070 to -0.034; P < 0.0001]).
Alemtuzumab-treated patients with RRMS demonstrated relative stability of OCT-measured neuroaxonal structure compared with RRMS patients treated with either interferon-β or glatiramer acetate over a 5-year period. These findings, along with previous demonstration of improved brain atrophy rates, suggest that alemtuzumab may offer long-term preservation of neuroaxonal structure in patients with RRMS.
多发性硬化症（MS）患者的神经轴突结构的光学相干断层扫描（OCT）测量值会逐渐变薄，无论是否有视神经炎病史。很少有前瞻性研究调查疾病修正疗法对视网膜神经轴突变性的影响。阿仑单抗是一种单克隆抗体，已被证明在治疗复发缓解型多发性硬化症（RRMS）方面优于干扰素β-1a。本研究的目的是评估阿仑单抗和一线注射治疗对 RRMS 患者的 OCT 神经轴突结构测量值的影响，包括 5 年以上随访的视盘周围视网膜神经纤维层（RNFL）厚度和联合节细胞内丛状层（GCIP）体积。
在这项具有前瞻性收集双队列数据的回顾性试点研究中，比较了阿仑单抗治疗的 RRMS 患者（N=24）和接受干扰素-β或那他珠单抗治疗的 RRMS 患者（N=21）的 OCT 测量的 RNFL 厚度和 GCIP 体积。
在中位数为 60 个月（范围 42-60 个月）的时间内，阿仑单抗组的平均 RNFL 厚度（从基线开始变薄）变化为-0.88μm（95%置信区间[CI] -2.63 至 0.86；P=0.32），平均 GCIP 体积变化为+0.013mm（95%CI 0.006 至 0.032；P=0.18）。在同一时期，一线治疗组表现出更大程度的 RNFL 变薄（平均 RNFL 厚度变化为-3.65μm[95%CI -5.40 至 -1.89；P=0.0001]）。与基线相比，一线治疗组的 GCIP 体积也明显减少（-0.052mm[95%CI -0.070 至 -0.034；P<0.0001]）。
与接受干扰素-β或那他珠单抗治疗的 RRMS 患者相比，在 5 年期间，接受阿仑单抗治疗的 RRMS 患者的 OCT 测量的神经轴突结构表现出相对稳定。这些发现，以及之前显示的脑萎缩率的改善，表明阿仑单抗可能为 RRMS 患者提供神经轴突结构的长期保护。
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