光学相干断层扫描揭示视神经脊髓炎谱系障碍不同治疗下视网膜损伤的纵向变化。
Optical Coherence Tomography Reveals Longitudinal Changes in Retinal Damage Under Different Treatments for Neuromyelitis Optica Spectrum Disorder.
作者信息
Zeng Pei, Du Chen, Zhang Rui, Jia Dongmei, Jiang Feng, Fan Moli, Zhang Chao
机构信息
Department of Neurology, Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, China.
Department of Ophthalmology, Tianjin Medical University General Hospital, Tianjin, China.
出版信息
Front Neurol. 2021 Jul 19;12:669567. doi: 10.3389/fneur.2021.669567. eCollection 2021.
Progressive retinal neuroaxonal damage after acute optic neuritis may occur in neuromyelitis optica spectrum disorder (NMOSD). However, it is unclear if treatments used to prevent attacks influence neurodegeneration. We aimed to investigate retinal damage in patients treated with disease-modifying drugs in a longitudinal study. We retrospectively included 50 patients with aquaporin 4-antibody-seropositive NMOSD. Peripapillary retinal nerve fiber layer (pRNFL) thickness, macular ganglion cell complex (mGCC) thickness, total macular volume (TMV), and optic disc measures were acquired by spectral domain optical coherence tomography in patients treated with tocilizumab, rituximab, and azathioprine. Longitudinally, in eyes with a history of ON (NMOSD), we observed annual thinning of mGCC [tocilizumab: -1.77 (-3.44, -0.09) μm, = 0.041; rituximab: -2.03 (-3.58, -0.48) μm, = 0.017; azathioprine: -1.79 (-2.22, -1.37) μm, < 0.001], and pRNFL [tocilizumab: -2.07 (-0.75, -3.39) μm, = 0.005; rituximab: -2.18 (-0.36, -4.00) μm, = 0.023; azathioprine: -2.37 (-0.98, -3.75) μm, = 0.003], reduced TMV [tocilizumab: -0.12 (-0.22, -0.01) mm, = 0.028; rituximab: -0.15 (-0.21, -0.08) mm, = 0.001; azathioprine: -0.12 (-0.20, -0.04) mm, = 0.006], and increased cup area [tocilizumab: 0.08 (-0.01, 0.16) mm, = 0.010; rituximab: 0.07 (0.01, 0.12) mm, = 0.019; azathioprine: 0.14 (0.02, 0.26) mm, = 0.023]. However, we detected no significant differences in annual changes in mGCC, pRNFL, TMV, and cup area between patients with tocilizumab, rituximab, and azathioprine in NMOSD eyes. NMOSD eyes did not display mGCC or pRNFL thinning in patients treated with tocilizumab and rituximab. Intriguingly, we observed significant thinning of mGCC in patients treated with azathioprine compared with tocilizumab [-0.84 (-1.50, -0.18) μm vs. -0.19 (-0.87, 0.48) μm, = 0.012] and rituximab [-0.84 (-1.50, -0.18) μm vs. -0.07 (-1.25, -2.51) μm, = 0.015] in NMOSD eyes. This study demonstrated that retinal ganglion cell loss is independent of ON attacks in NMOSD. Tocilizumab and rituximab may delay mGCC thinning in NMOSD eyes compared with azathioprine.
急性视神经炎后进行性视网膜神经轴突损伤可能发生在视神经脊髓炎谱系障碍（NMOSD）中。然而，用于预防发作的治疗方法是否会影响神经退行性变尚不清楚。我们旨在通过一项纵向研究调查接受疾病修饰药物治疗的患者的视网膜损伤情况。我们回顾性纳入了50例水通道蛋白4抗体血清阳性的NMOSD患者。通过光谱域光学相干断层扫描测量了接受托珠单抗、利妥昔单抗和硫唑嘌呤治疗的患者的视乳头周围视网膜神经纤维层（pRNFL）厚度、黄斑神经节细胞复合体（mGCC）厚度、黄斑总体积（TMV）和视盘测量值。纵向来看，在有视神经炎（NMOSD）病史的眼睛中，我们观察到mGCC每年变薄[托珠单抗：-1.77（-3.44，-0.09）μm，P = 0.041；利妥昔单抗：-2.03（-3.58，-0.48）μm，P = 0.017；硫唑嘌呤：-1.79（-2.22，-1.37）μm，P < 0.001]，pRNFL也变薄[托珠单抗：-2.07（-0.75，-3.39）μm，P = 0.005；利妥昔单抗：-2.18（-0.36，-4.可编辑）μm，P = 0.023；硫唑嘌呤：-2.37（-0.98，-3.75）μm，P = 0.003]，TMV减小[托珠单抗：-0.12（-0.22，-0.01）mm，P = 0.028；利妥昔单抗：-0.15（-0.21，-0.08）mm，P = 0.001；硫唑嘌呤：-0.12（-0.20，-0.04）mm，P = 0.006]，杯面积增加[托珠单抗：0.08（-0.01，0.16）mm，P = 0.010；利妥昔单抗：0.07（0.01，0.12）mm，P = 0.019；硫唑嘌呤：0.14（0.02，0.26）mm，P = 0.023]。然而，我们未检测到NMOSD眼睛中接受托珠单抗、利妥昔单抗和硫唑嘌呤治疗的患者在mGCC、pRNFL、TMV和杯面积的年度变化上有显著差异。在接受托珠单抗和利妥昔单抗治疗的患者中，NMOSD眼睛未显示mGCC或pRNFL变薄。有趣的是，与托珠单抗[-0.84（-1.50，-0.18）μm对-0.19（-0.87，0.48）μm，P = 0.012]和利妥昔单抗[-0.84（-1.50，-0.18）μm对-0.07（-1.25，-2.51）μm，P = 0.015]相比，我们观察到接受硫唑嘌呤治疗的NMOSD眼睛中的mGCC显著变薄。这项研究表明，视网膜神经节细胞丢失在NMOSD中与视神经炎发作无关。与硫唑嘌呤相比，托珠单抗和利妥昔单抗可能会延缓NMOSD眼睛中mGCC的变薄。
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