Du Kui Fang, Shi Xue Hui, Zhang Chang Ping, Dong Hong Wei, Kong Wen Jun, Jonas Jost B, Wei Wen Bin, Wang Ya Xing
Department of Ophthalmology, Beijing Youan Hospital, Capital Medical University, Beijing, China.
Beijing Ophthalmology and Visual Science Key Lab, Beijing Key Laboratory of Intraocular Tumor Diagnosis and Treatment, Beijing Tongren Eye Center, Beijing Tongren Hospital, Capital Medical University, Beijing, China.
J Ophthalmic Inflamm Infect. 2025 Sep 26;15(1):71. doi: 10.1186/s12348-025-00532-3.
The retinal toxicity of intravitreal ganciclovir (GCV) is contentious. Our study aims to describe new clinical findings following intravitreal GCV and propose a mechanism for the pathogenesis of those post-injection retinal changes.
A retrospective case series included 114 patients with cytomegalovirus retinitis (CMVR) receiving intravitreal GCV (2.5 mg/0.05 mL) combined with systemic therapy. Patients with presumed retinal toxicity following intravitreal GCV injection were enrolled. Clinical data, laboratory tests, ocular examination, and multimodal images of the retina were collected. Serial optical coherence tomography (OCT) was performed to monitor pre- and post-retinal changes.
Five patients (7 eyes) (4.4%±2.6%) with macular spared from CMVR lesions experienced acute vision loss and transient macular edema after the GCV injection; 1 patient (0.9%±2.6%) with bilateral CMVR developed chronic and progressive retinal pigment epithelium (RPE) atrophy in the CMVR-spared areas of the eye receiving repeated GCV injections, contrasting with untreated contralateral eyes. Three of them were additionally diagnosed as cytomegalovirus-immune recovery retinitis. With OCT, all eyes showed intact Bruch’s membrane and normal thickness of inner retinal layers. Seven eyes with acute vision loss showed outer retinal changes within 24 h post-injection, including macular SRF (7 eyes), macular vertical hyperreflective foci (5 eyes), and ONL edema (4 eyes), and resolving spontaneously weeks later.
Intravitreal GCV treatment may trigger acute macular edema and chronic RPE degeneration in CMVR patients. We hypothesize that RPE dysfunction is the pivotal pathogenic mechanism, potentially induced by multifactorial interplay, including chemical irritation, cumulative exposure, systemic comorbidities, and ocular inflammatory cascades.
The online version contains supplementary material available at 10.1186/s12348-025-00532-3.
玻璃体内注射更昔洛韦（GCV）的视网膜毒性存在争议。我们的研究旨在描述玻璃体内注射GCV后的新临床发现，并提出这些注射后视网膜变化的发病机制。
一项回顾性病例系列研究纳入了114例接受玻璃体内注射GCV（2.5mg/0.05mL）联合全身治疗的巨细胞病毒性视网膜炎（CMVR）患者。纳入玻璃体内注射GCV后疑似视网膜毒性的患者。收集临床数据、实验室检查、眼部检查及视网膜多模态图像。进行连续光学相干断层扫描（OCT）以监测视网膜前后变化。
5例（7只眼）（4.4%±2.6%）黄斑未受CMVR病变累及的患者在注射GCV后出现急性视力丧失和短暂性黄斑水肿；1例（0.9%±2.6%）双侧CMVR患者在接受重复GCV注射的眼的CMVR未累及区域出现慢性进行性视网膜色素上皮（RPE）萎缩，与未治疗的对侧眼形成对比。其中3例还被诊断为巨细胞病毒免疫恢复性视网膜炎。通过OCT检查，所有眼的布鲁赫膜均完整，视网膜内层厚度正常。7只出现急性视力丧失的眼在注射后24小时内出现视网膜外层变化，包括黄斑下视网膜积液（7只眼）、黄斑垂直高反射灶（5只眼）和外层神经视网膜层水肿（4只眼），数周后自发消退。
玻璃体内注射GCV治疗可能引发CMVR患者急性黄斑水肿和慢性RPE变性。我们推测RPE功能障碍是关键的致病机制，可能由多因素相互作用诱发，包括化学刺激、累积暴露、全身合并症和眼部炎症级联反应。
在线版本包含可在10.1186/s12348-025-00532-3获取的补充材料。
