Haug Sara J, Hien Doan Luong, Uludag Gunay, Ngoc Than Trong Tuong, Lajevardi Sherin, Halim M Sohail, Sepah Yasir J, Do Diana V, Khanani Arshad M
Southwest Eye Consultants, Durango, CO, USA.
Spencer Center for Vision Research, Byers Eye Institute, Stanford University, Palo Alto, CA, USA.
Am J Ophthalmol Case Rep. 2020 Mar 31;18:100680. doi: 10.1016/j.ajoc.2020.100680. eCollection 2020 Jun.
To describe retinal arterial occlusion and vasculitis following intravitreal brolucizumab administration in a patient with neovascular age-related macular degeneration (nAMD).
An 88-year-old Caucasian woman with neovascular age-related macular degeneration (nAMD) complained of painless loss of vision with light sensitivity in both eyes (OU) four weeks after bilateral intravitreal brolucizumab. Upon examination, her visual acuity decreased to 20/40 in the right eye (OD) and 20/50 in the left eye (OS). Examination revealed 0.5+ and 1+ anterior chamber cells in OD and OS, respectively. The patient was treated with 1% prednisolone acetate eyedrops in both eyes, and after several weeks, the anterior chamber cells resolved. However, the patient still reported a decline in visual acuity (VA). Fluorescein angiography (FA) revealed retinal arterial occlusion, vasculitis, and optic nerve inflammation in the left eye. Retinal intra-arterial grayish materials were also detected. Laboratory evaluations were performed for common infectious and inflammatory causes and were normal or negative. A delayed inflammatory reaction to brolucizumab was suspected as the cause of the ocular inflammation and retinal vasculitis. An intravitreal dexamethasone implant was inserted into the left eye to treat the inflammation. One week after the dexamethasone implant, VA improved to 20/40 in OU; FA showed improvement, but residual peri-vascular leakage remained.
Medication-associated uveitis is a rare adverse effect that can lead to vision loss. The index report illustrates a case of intraocular inflammation, retinal arterial vaso-occlusion and vasculitis associated with intravitreal brolucizumab. The delay in developing uveitis suggests that the inflammation is due to a delayed hypersensitivity reaction which can occur several days or weeks after administration of the inciting agent. Recently, several cases of uveitis and vasculitis associated with brolucizumab have been presented and those cases have similar features compared to the index case (1). Therapy with steroids (either intraocular or systemic), after infectious etiologies have been excluded, may be beneficial in halting inflammation and preventing further vision loss.
描述在一名患有新生血管性年龄相关性黄斑变性(nAMD)的患者中,玻璃体内注射布罗珠单抗后出现的视网膜动脉阻塞和血管炎。
一名88岁患有新生血管性年龄相关性黄斑变性(nAMD)的白人女性,在双眼玻璃体内注射布罗珠单抗四周后,主诉双眼无痛性视力丧失并伴有光敏感。检查时,她的右眼(OD)视力降至20/40,左眼(OS)视力降至20/50。检查发现右眼和左眼的前房细胞分别为0.5+和1+。该患者双眼均使用1%醋酸泼尼松龙滴眼液治疗,几周后,前房细胞消退。然而,患者仍报告视力(VA)下降。荧光素血管造影(FA)显示左眼存在视网膜动脉阻塞、血管炎和视神经炎症。还检测到视网膜动脉内有灰白色物质。对常见的感染性和炎症性病因进行了实验室评估,结果均正常或为阴性。怀疑对布罗珠单抗的延迟炎症反应是眼部炎症和视网膜血管炎的原因。左眼植入了玻璃体内地塞米松植入物以治疗炎症。地塞米松植入物植入一周后,双眼视力提高到20/40;FA显示有所改善,但仍有残留的血管周围渗漏。
药物相关性葡萄膜炎是一种罕见的不良反应,可导致视力丧失。本报告病例说明了一例与玻璃体内注射布罗珠单抗相关的眼内炎症、视网膜动脉血管阻塞和血管炎。葡萄膜炎发生延迟表明炎症是由迟发型超敏反应引起的,这种反应可在激发剂给药后数天或数周出现。最近,已经报告了几例与布罗珠单抗相关的葡萄膜炎和血管炎病例,这些病例与本病例具有相似特征(1)。在排除感染性病因后,使用类固醇(眼内或全身)治疗可能有助于控制炎症并防止进一步的视力丧失。