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生物标志物时代的视神经炎。

Optic neuritis in the era of biomarkers.

机构信息

Department of Ophthalmology, Mayo Clinic College of Medicine, Rochester, Minnesota, USA; Department of Neurology, Mayo Clinic College of Medicine, Rochester, Minnesota, USA.

Department of Neurology, Mayo Clinic College of Medicine, Rochester, Minnesota, USA; Department of Laboratory Medicine and Pathology, Mayo Clinic College of Medicine, Rochester, Minnesota, USA; Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic College of Medicine, Rochester, Minnesota, USA.

出版信息

Surv Ophthalmol. 2020 Jan-Feb;65(1):12-17. doi: 10.1016/j.survophthal.2019.08.001. Epub 2019 Aug 16.

DOI:10.1016/j.survophthal.2019.08.001
PMID:31425702
Abstract

The Optic Neuritis Treatment Trial, a landmark study completed in 1991, stratified the risk of multiple sclerosis in patients with optic neuritis. Since that time, unique biomarkers for optic neuritis have been found. The antibody against aquaporin-4 (AQP4)-immunoglobulin G (IgG) discovered in 2004 was found to be both the pathologic cause and a reliable biomarker for neuromyelitis optica spectrum disorders. This finding enabled an expanded definition of the phenotype of neuromyelitis optica spectrum disorder and improved treatment of the disease. Subsequently, myelin oligodendrocyte glycoprotein (MOG) IgG was recognized to be a marker for MOG-IgG-associated disorder, a central demyelinating disease characterized by recurrent optic neuritis, prominent disk edema, and perineural optic nerve enhancement on magnetic resonance imaging. Most multiple sclerosis disease-modifying agents are ineffective for AQP4-IgG-positive neuromyelitis optica spectrum disorder and MOG-IgG-associated disorder. Because there are crucial differences in treatment and prognosis between multiple sclerosis, AQP4-IgG-positive neuromyelitis optica spectrum disorder, and MOG-IgG-associated disorder, ophthalmologists should be aware of these new biomarkers of optic neuritis and incorporate their testing in all patients with atypical optic neuritis.

摘要

视神经炎治疗试验是 1991 年完成的一项具有里程碑意义的研究,对视神经炎患者的多发性硬化风险进行了分层。自那时以来,已经发现了独特的视神经炎生物标志物。2004 年发现的水通道蛋白-4(AQP4)-免疫球蛋白 G(IgG)抗体既是视神经脊髓炎谱系疾病的病理原因,也是可靠的生物标志物。这一发现使视神经脊髓炎谱系疾病的表型得到了扩展,并改善了疾病的治疗。随后,髓鞘少突胶质细胞糖蛋白(MOG)IgG 被认为是 MOG-IgG 相关疾病的标志物,这是一种以复发性视神经炎、明显的盘状水肿和磁共振成像上的神经周围视神经增强为特征的中枢脱髓鞘疾病。大多数多发性硬化症的疾病修正治疗药物对 AQP4-IgG 阳性视神经脊髓炎谱系疾病和 MOG-IgG 相关疾病无效。由于多发性硬化症、AQP4-IgG 阳性视神经脊髓炎谱系疾病和 MOG-IgG 相关疾病在治疗和预后方面存在关键差异,因此眼科医生应该了解这些新的视神经炎生物标志物,并在所有患有非典型视神经炎的患者中进行检测。

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