利妥昔单抗治疗多发性硬化相关视网膜萎缩的疗效观察。
Modulation of Retinal Atrophy With Rituximab in Multiple Sclerosis.
机构信息
From the Department of Neurology (J.L., H.R., A.G.F., O.C.M., E.S.S., H.E., E.O., N.P., B.T., N.J.L., S.D., N.F., O.K., P.A.C., K.C.F., S.S.), Johns Hopkins University School of Medicine; and Department of Electrical and Computer Engineering (J.L.P.), Johns Hopkins University, Baltimore, MD.
出版信息
Neurology. 2021 May 18;96(20):e2525-e2533. doi: 10.1212/WNL.0000000000011933. Epub 2021 Apr 7.
OBJECTIVE
To investigate the effects of rituximab on retinal atrophy in patients with relapsing-remitting multiple sclerosis (RRMS), we performed serial optical coherence tomography (OCT) scans among a cohort of patients with RRMS on rituximab and compared rates of ganglion cell + inner plexiform layer (GCIPL) atrophy to those observed among age- and sex-matched glatiramer acetate (GA)-and natalizumab-treated patients with RRMS and healthy controls (HCs).
METHODS
In this observational study, patients with RRMS treated with a single disease-modifying therapy and HCs were followed with serial OCT for a median duration of 2.8 years. Participants with uncontrolled hypertension, diabetes mellitus, or glaucoma, and eyes with optic neuritis ≤6 months prior to baseline OCT, or during follow-up, were excluded. Statistical analyses were performed using linear mixed-effects regression.
RESULTS
During the overall follow-up period, rates of GCIPL atrophy were -0.28 ± 0.11 µm/y among rituximab-treated patients with RRMS (n = 35). This was similar to GA-treated (n = 49; -0.33 ± 0.05 µm/y; = 0.69) and natalizumab-treated patients (n = 88; -0.17 ± 0.10 µm/y; = 0.13) and faster than HCs (n = 78; -0.15 ± 0.03 µm/y; = 0.006). Rituximab-treated patients exhibited 0.55 ± 0.23 µm/y faster rates of GCIPL atrophy during the first 12 months of treatment, relative to afterwards (n = 25; = 0.02), during which period GCIPL atrophy rates were -0.14 ± 0.13 µm/y.
CONCLUSIONS
Retinal atrophy in RRMS is modulated by rituximab. Greater attenuation of retinal atrophy may occur after 12 months of rituximab treatment, following which time GCIPL atrophy rates are similar to those observed among natalizumab-treated patients with RRMS and HCs. Our findings raise the possibility that the neuroprotective therapeutic response with rituximab in RRMS may take up to 12 months, which should be confirmed by larger studies.
CLASSIFICATION OF EVIDENCE
This study provides Class IV evidence on the difference in rate of change of the GCIPL thickness in patients with RRMS comparing rituximab to other disease-modifying therapies.
目的
通过对接受利妥昔单抗治疗的复发性缓解型多发性硬化症（RRMS）患者进行系列光学相干断层扫描（OCT）检查，探讨利妥昔单抗对视网膜萎缩的影响。我们将 RRMS 患者的神经节细胞+内丛状层（GCIPL）萎缩率与年龄和性别匹配的接受那他珠单抗和干扰素β-1a 治疗的 RRMS 患者以及健康对照者（HCs）的萎缩率进行比较。
方法
在这项观察性研究中，对接受单药疾病修正治疗的 RRMS 患者进行了中位 2.8 年的系列 OCT 随访。排除了患有未控制的高血压、糖尿病或青光眼的患者，以及在基线 OCT 前 6 个月内或随访期间有视神经炎的患者。采用线性混合效应回归进行统计学分析。
结果
在整个随访期间，RRMS 患者的 GCIPL 萎缩率为 -0.28 ± 0.11 µm/y（n = 35）。这与接受干扰素β-1a 治疗的患者（n = 49；-0.33 ± 0.05 µm/y； = 0.69）和接受那他珠单抗治疗的患者（n = 88；-0.17 ± 0.10 µm/y； = 0.13）相似，且快于 HCs（n = 78；-0.15 ± 0.03 µm/y； = 0.006）。利妥昔单抗治疗的患者在治疗的前 12 个月内，GCIPL 萎缩率比之后（n = 25； = 0.02）快 0.55 ± 0.23 µm/y，在此期间，GCIPL 萎缩率为 -0.14 ± 0.13 µm/y。
结论
RRMS 中的视网膜萎缩受利妥昔单抗的调节。在利妥昔单抗治疗 12 个月后，可能会出现更大程度的视网膜萎缩抑制，此后 GCIPL 萎缩率与接受那他珠单抗治疗的 RRMS 患者和 HCs 相似。我们的研究结果提示，RRMS 中利妥昔单抗的神经保护治疗反应可能需要长达 12 个月的时间，这需要更大规模的研究来证实。
证据分类
本研究提供了 IV 级证据，表明 RRMS 患者中比较利妥昔单抗与其他疾病修正治疗的 GCIPL 厚度变化率的差异。
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