Evidence of subclinical quantitative retinal layer abnormalities in AQP4-IgG seropositive NMOSD.

Evidence of subclinical quantitative retinal layer abnormalities in AQP4-IgG seropositive NMOSD.
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AQP4-IgG 血清阳性 NMOSD 亚临床定量视网膜层异常的证据。

DOI:
10.1177/1352458520977771
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发表时间:
2021-10
期刊:
Multiple sclerosis (Houndmills, Basingstoke, England)
影响因子:
--
通讯作者:
Sotirchos ES
Sotirchos ES
中科院分区:
其他
文献类型:
--
作者:
Filippatou AG;Vasileiou ES;He Y;Fitzgerald KC;Kalaitzidis G;Lambe J;Mealy MA;Levy M;Liu Y;Prince JL;Mowry EM;Saidha S;Calabresi PA;Sotirchos ES

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先前的研究表明,亚临床视网膜异常可能存在于水通道蛋白-4(AQP 4)-IgG血清阳性视神经肌炎谱系障碍(NMOSD)中,而无视神经炎(ON)的临床病史。比较无ON病史的AQP 4-IgG+ NMOSD眼(AQP 4-nonON)和健康对照眼(HC)的中央凹和周围黄斑的视网膜层厚度。在这项单中心横断面研究中,采用频域光学相干断层扫描(OCT)研究了83只AQP 4非ON和154只HC眼。总中心凹厚度在AQP 4-nonON和HC眼之间没有差异。与HC相比,AQP 4-nonON眼睛在中央凹(ONL:−4.01±2.03μm,p=0.049; IS:−0.32±0.14μm,p=0.029)和周围黄斑(ONL:−1.98±0.95μm,p=0.037; IS:−0.16±0.07μm,p=0.023)处表现出较低的外核层(ONL)和内感光细胞段(IS)厚度。与HC眼相比,AQP 4-nonON眼的黄斑视网膜神经纤维层(RNFL:−1.34±0.51μm,p=0.009)和神经节细胞+内网状层(GCIPL:−2.44±0.93μm,p=0.009)厚度也较低。敏感性分析的结果相似,仅限于任何一只眼睛从未经历过ON的AQP 4-IgG+患者。AQP 4-nonON眼表现出亚临床视网膜神经节细胞神经元和轴突损失的证据,以及感光层参与的结构证据。这些发现支持AQP 4-IgG+ NMOSD可能发生亚临床前部视觉通路受累。
Prior studies have suggested that subclinical retinal abnormalities may be present in aquaporin-4 (AQP4)-IgG seropositive neuromyelitis optica spectrum disorder (NMOSD), in the absence of a clinical history of optic neuritis (ON). To compare retinal layer thicknesses at the fovea and surrounding macula between AQP4-IgG+ NMOSD eyes without a history of ON (AQP4-nonON) and healthy controls (HC). In this single-center cross-sectional study, 83 AQP4-nonON and 154 HC eyes were studied with spectral-domain optical coherence tomography (OCT). Total foveal thickness did not differ between AQP4-nonON and HC eyes. AQP4-nonON eyes exhibited lower outer nuclear layer (ONL) and inner photoreceptor segment (IS) thickness at the fovea (ONL:−4.01±2.03μm, p=0.049; IS:−0.32±0.14μm, p=0.029) and surrounding macula (ONL:−1.98±0.95μm, p=0.037; IS:−0.16±0.07μm, p=0.023), compared to HC. Macular retinal nerve fiber layer (RNFL:−1.34±0.51μm, p=0.009) and ganglion cell + inner plexiform layer (GCIPL:−2.44±0.93μm, p=0.009) thicknesses were also lower in AQP4-nonON compared to HC eyes. Results were similar in sensitivity analyses restricted to AQP4-IgG+ patients who had never experienced ON in either eye. AQP4-nonON eyes exhibit evidence of subclinical retinal ganglion cell neuronal and axonal loss, as well as structural evidence of photoreceptor layer involvement. These findings support that subclinical anterior visual pathway involvement may occur in AQP4-IgG+ NMOSD.
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