Optic Neuritis-Independent Retinal Atrophy in Neuromyelitis Optica Spectrum Disorder.
Optic Neuritis-Independent Retinal Atrophy in Neuromyelitis Optica Spectrum Disorder.
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DOI：
10.1097/wno.0000000000001282
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发表时间：
2022-03-01
期刊：
影响因子：
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通讯作者：
Sotirchos ES
中科院分区：
文献类型：
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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
背景：少数研究调查了视神经肌萎缩症谱系障碍（NMOSD）中存在独立于临床复发的持续疾病活动，数据相互矛盾。我们的研究的目的是检查是否与水通道蛋白-4（AQP 4）-IgG血清阳性NMOSD患者表现出进行性视网膜神经轴索损失，独立的视神经炎（ON）attacks.Methods：在这个单中心，纵向研究，32 AQP 4-IgG+ NMOSD患者和48名健康对照（HC）进行了系列光谱域光学相干断层扫描和视力（VA）评估。排除基线前ON少于6个月的NMOSD患者，而随访期间ON患者的数据在ON前末次访视时删失。VA恶化定义为高对比度VA单眼字母视力下降≥ 5个字母，低对比度VA单眼字母视力下降≥ 7个字母。分析进行了调整的年龄，性别，和race.Results混合效应线性回归模型：随访时间中位数为4.2年（四分位数范围：1.8-7.5）。相对于HC，NMOSD眼的视乳头周围视网膜神经纤维层（pRNFL）更快（β=− 0.25 µm/年更快，95%置信区间[CI]：− 0.45至− 0.05，P= 0.014），GCIPL变薄（β=− 0.09 µm/年更快，95% CI：− 0.17至0，P= 0.05）。这种差异似乎是由无ON病史的NMOSD眼中pRNFL和GCIPL变薄速度比HC更快所致（GCIPL：β=− 0.15 µm/年更快; P= 0.005; pRNFL：β=− 0.43 µm/年更快，P< 0.001），而NMOSD-ON和HC眼中pRNFL（β：− 0.07 µm/年，P= 0.53）和GCIPL（β=− 0.01 µm/年，P= 0.90）变薄速度没有差异。结论：在这项纵向研究中，我们观察到进行性pRNFL和GCIPL萎缩的AQP 4-IgG+ NMOSD眼睛不受ON。这些结果支持，亚临床参与的前视觉通路可能发生在AQP 4-IgG+ NMOSD。
Background:A limited number of studies have investigated the presence of ongoing disease activity independent of clinical relapses in neuromyelitis optica spectrum disorder (NMOSD), and data are conflicting. The objective of our study was to examine whether patients with aquaporin-4 (AQP4)-IgG seropositive NMOSD exhibit progressive retinal neuroaxonal loss, independently of optic neuritis (ON) attacks.Methods:In this single-center, longitudinal study, 32 AQP4-IgG+ NMOSD patients and 48 healthy controls (HC) were followed with serial spectral-domain optical coherence tomography and visual acuity (VA) assessments. NMOSD patients with ON less than 6 months before baseline were excluded, whereas data from patients with ON during follow-up were censored at the last visit before ON. VA worsening was defined as a decrease in monocular letter acuity≥ 5 letters for high-contrast VA and≥ 7 letters for low-contrast VA. Analyses were performed with mixed-effects linear regression models adjusted for age, sex, and race.Results:The median follow-up duration was 4.2 years (interquartile range: 1.8–7.5). Relative to HC, NMOSD eyes had faster peripapillary retinal nerve fiber layer (pRNFL)(β=− 0.25 µm/year faster, 95% confidence interval [CI]:− 0.45 to− 0.05, P= 0.014) and GCIPL thinning (β=− 0.09 µm/year faster, 95% CI:− 0.17 to 0, P= 0.05). This difference seemed to be driven by faster pRNFL and GCIPL thinning in NMOSD eyes without a history of ON compared with HC (GCIPL: β=− 0.15 µm/year faster; P= 0.005; pRNFL: β=− 0.43 µm/year faster, P< 0.001), whereas rates of pRNFL (β:− 0.07 µm/year, P= 0.53) and GCIPL (β=− 0.01 µm/year, P= 0.90) thinning did not differ between NMOSD-ON and HC eyes. Nine NMOSD eyes had VA worsening during follow-up.Conclusions:In this longitudinal study, we observed progressive pRNFL and GCIPL atrophy in AQP4-IgG+ NMOSD eyes unaffected by ON. These results support that subclinical involvement of the anterior visual pathway may occur in AQP4-IgG+ NMOSD.