目的：探讨蛋白A免疫吸附联合糖皮质激素治疗对MOG抗体相关视神经炎（MOG antibody-associated optic neuritis， MOG-ON）患者的临床疗效及安全性。方法：回顾性分析2022年6月—2024年12月在广东三九脑科医院神经内科确诊并接受蛋白A免疫吸附联合糖皮质激素治疗的7例MOG-ON患者。所有患者均接受蛋白A免疫吸附治疗（隔天1次，共5次为1个疗程）并同期联合糖皮质激素治疗。评估治疗前及治疗后3个月、6个月的视力变化、扩展伤残状态量表（expanded disability status scale，EDSS）评分变化及MOG抗体滴度变化，并记录不良反应。结果：治疗后6个月，6/7患者视力较治疗前改善，其中4/7视力改善显著。左眼LogMAR视力值从治疗前的0.20(0.14，0.70)改善至0.10(0.10，0.42)，右眼LogMAR视力值从0.30(0.19，0.47)改善至0.18(0.10，0.21)，EDSS视力评分从2.86±1.68降至1.43±1.51（P < 0.05）。治疗前血清MOG抗体滴度几何平均数为1:52.0（几何标准差GSD = 3.7），治疗后3个月降至1:8.8（GSD = 1.9）（P = 0.027），治疗后6个月降至1:13.0（GSD = 4.1）（P = 0.027）。7例患者共接受35次免疫吸附治疗，未观察到严重不良反应，仅有轻微可控的不良事件。结论：蛋白A免疫吸附联合糖皮质激素治疗能够有效降低血液中MOG抗体水平，改善MOG-ON患者的视力。
Objective: To investigate the clinical efficacy and safety of protein A immunoadsorption combined with glucocorticoid therapy in patients with myelin oligodendrocyte glycoprotein antibody-associated optic neuritis（MOG-ON）. Methods: A retrospective analysis was conducted on 7 patients with MOG-ON who were diagnosed and treated with protein A immunoadsorption combined with glucocorticoid therapy at the Department of Neurology，Guangdong Sanjiu Brain Hospital from June 2022 to December 2024. All patients underwent protein A immunoadsorption therapy （once every other day, with 5 sessions constituting one course） in conjunction with concurrent steroid therapy. Visual acuity changes, EDSS score changes, and MOG antibody titer changes were assessed before treatment, as well as at 3 and 6 months after treatment. Additionally, adverse events were meticulously recorded. Results: At the 6 months post-treatment mark, 6 patients （85.7%） demonstrated an improvement in visual acuity compared to their baseline levels, with 4 patients （57.1%） achieving a significant improvement. The median LogMAR visual acuity values in the left eye improved from 0.20(0.14,0.70) to 0.10(0.10,0.42), and in the right eye, they improved from 0.30(0.19,0.47) to 0.18(0.10,0.21). MeanWhile, the EDSS visual score decreased from 2.86±1.68 to 1.43±1.51（P < 0.05）. The geometric mean serum MOG antibody titer declined from 1:52.0（GSD = 3.7） before treatment to 1:8.8（GSD = 1.9） at 3 months after treatment（P = 0.027）, and further decreased to 1:13.0（GSD = 4.1） at 6 months after treatment（P = 0.027）. A total of 35 immunoadsorption sessions were administered to the 7 patients, and no serious adverse reactions were observed; only minor and manageable adverse events occurred. Conclusion: Protein A immunoadsorption combined with glucocorticoid therapy can effectively lower serum MOG antibody levels and enhance visual outcomes in patients with MOG-ON.
“锌”在青光眼研究舞台上正扮演着越来越重要的角色。糖皮质激素，作为人体内重要的激素之一，其对锌的调控已在诸多系统中被证实。研究发现，在糖皮质激素的影响下，小梁网中的锌离子转运受阻，导致细胞外基质降解失衡，从而干扰小梁网正常流出道功能，加重青光眼的病情。而视神经损伤后，锌离子在神经突触间的异常传递、不平衡分布与胞内异常累积影响视网膜神经节细胞存活和轴突的再生能力，进而损害视功能，可能成为青光眼视神经损伤发病及进展的关键因素。这些研究进展为视神经保护策略提供了新的视角，“锌”作为治疗靶点的潜力正在被逐步挖掘，通过调节锌水平来干预青光眼病理进程成为可能治疗手段。
本期封面中将汉字“锌”设计为飞天舞者，其超越时空的永恒美感，呼应了“锌”在青光眼研究中突破传统、开辟新程的角色。轻盈与自由的飞天舞者，象征着“锌”在细胞内外穿梭，精妙调控生理功能，维系细胞的和谐与平衡，为青光眼患者带来新的治疗希望。
“锌”在青光眼研究舞台上正扮演着越来越重要的角色。糖皮质激素，作为人体内重要的激素之一，其对锌的调控已在诸多系统中被证实。研究发现，在糖皮质激素的影响下，小梁网中的锌离子转运受阻，导致细胞外基质降解失衡，从而干扰小梁网正常流出道功能，加重青光眼的病情。而视神经损伤后，锌离子在神经突触间的异常传递、不平衡分布与胞内异常累积影响视网膜神经节细胞存活和轴突的再生能力，进而损害视功能，可能成为青光眼视神经损伤发病及进展的关键因素。这些研究进展为视神经保护策略提供了新的视角，“锌”作为治疗靶点的潜力正在被逐步挖掘，通过调节锌水平来干预青光眼病理进程成为可能治疗手段。本期封面中将汉字“锌”设计为飞天舞者，其超越时空的永恒美感，呼应了“锌”在青光眼研究中突破传统、开辟新程的角色。轻盈与自由的飞天舞者，象征着“锌”在细胞内外穿梭，精妙调控生理功能，维系细胞的和谐与平衡，为青光眼患者带来新的治疗希望。
糖皮质激素(glucocorticoid, GC)由于其抗炎特性被广泛用于治疗眼部炎症，而G C诱导性青光眼(glucocorticoid-induced glaucoma, GIG) 作为一种常见并发症，其发病机制长期受到关注。文章综述了锌在GIG中的关键作用及其调控机制，揭示了锌在青光眼发病机制中的重要角色。锌作为人体中含量第二丰富的过渡金属，对蛋白质结构、酶催化和细胞信号调节至关重要。GC对锌分布的调控作用在不同组织和细胞类型中表现出复杂性，影响锌的摄取和释放，进而参与青光眼的病理过程。锌通过影响小梁网细胞外基质(extracellular matrix, ECM)的降解和重塑，以及视网膜神经节细胞的存活和轴突再生，在GIG的发病机制中发挥着复杂的作用。文章同时介绍了体内锌调控的现有途径，包括补充锌和减少锌的策略，提供了潜在的治疗途径。未来的研究应深入探索锌在青光眼中的作用机制以及与GC的相互作用，评估锌补充或螯合在青光眼治疗中的安全性和有效性，以及开发新型锌递送和螯合系统，有助于全面揭示锌在青光眼中的作用及治疗潜力，以实现更加精准的防治方案，改善患者预后。
Glucocorticoid (GC) is widely used in the treatment of ocular inflammation for its anti-inflammatory propery. However, glucocorticoid-induced glaucoma (GIG) is a common complication, and its pathogenesis has been extensively studied. This review summarizes the crucial role of zinc in GIG and its regulatory mechanisms, highlighting zinc's significant involvement in the pathogenesis of glaucoma. Zinc, the second most abundant transition metal in the human body, is essential for protein structure, enzyme catalysis, and cell signaling regulation. The effects of GC on zinc distribution vary across different tissues and cell types, affecting zinc uptake and release, which may contribute to the pathological processes of glaucoma. Zinc influences the degradation and remodeling of the trabecular meshwork extracellular matrix and the survival and axonal regeneration of retinal ganglion cells, playing complex roles in the pathogenesis of GIG. We discuss available strategies for regulating zinc in vivo, including zinc supplementation and reduction strategies, providing potential therapeutic approaches. Future research should explore the mechanisms of zinc's role in glaucoma and its interaction with glucocorticoids, evaluate the safety and efficacy of zinc supplementation or chelation in glaucoma treatment, and develop novel zinc delivery and chelation systems. These efforts will help fully elucidate the role of zinc in glaucoma and its therapeutic potential, enabling more precise prevention and treatment strategies to improve patient outcomes.
