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布罗利尤单抗治疗后多层色素上皮脱离薄片的新消退——病例报告

Novel Resolution of Multilayered Pigment Epithelial Detachment Lamellae Following Brolucizumab Treatment-A Case Report.

作者信息

Nair Unnikrishnan, Nair Indu J, Sheth Jay U, Soman Manoj

机构信息

Department of Vitreoretinal Services, Chaithanya Eye Hospital and Research Institute, Trivandrum, India.

Department of Research, Chaithanya Innovation in Technology and Eye Care (Research), Trivandrum, India.

出版信息

Case Rep Ophthalmol Med. 2025 Mar 6;2025:9953015. doi: 10.1155/crop/9953015. eCollection 2025.

DOI:10.1155/crop/9953015
PMID:40224928
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11991755/
Abstract

The aim of this study is to report a unique case where brolucizumab administration resolved multilayered pigment epithelial detachment (MLPED) lamellae. An 80-year-old gentleman with polypoidal choroidal vasculopathy developed MLPED from long-term ranibizumab treatment. Switching to brolucizumab led to visual acuity improvement after three doses and complete resolution of fluid, reduced choroidal thickness, and MLPED collapse. Notably, the patient experienced a recurrence of MLPED, which again resolved after the fourth dose of brolucizumab. This case underscores the effectiveness of brolucizumab in resolving MLPED lamellae, a previously unreported phenomenon. Furthermore, it highlights the potential for visual acuity improvement despite MLPED resolution. Brolucizumab's mechanism of action, including its potent antivascular endothelial growth factor properties and enhanced tissue penetration, may contribute to the collapse of MLPED by modulating subretinal pigment epithelial fluid dynamics. Further research into molecular pathways, cellular interactions, and safety profiles is warranted to optimize the therapeutic role of brolucizumab.

摘要

本研究的目的是报告一例独特病例,其中使用布罗卢izumab治疗使多层色素上皮脱离(MLPED)薄片消退。一名患有息肉样脉络膜血管病变的80岁男性因长期使用雷珠单抗治疗而出现MLPED。改用布罗卢izumab后,三剂后视力改善,液体完全消退,脉络膜厚度降低,MLPED塌陷。值得注意的是,患者出现了MLPED复发,在第四剂布罗卢izumab后再次消退。该病例强调了布罗卢izumab在消退MLPED薄片方面的有效性,这是一种以前未报道的现象。此外,它突出了尽管MLPED消退但仍有视力改善的潜力。布罗卢izumab的作用机制,包括其强大的抗血管内皮生长因子特性和增强的组织穿透力,可能通过调节视网膜下色素上皮液动力学导致MLPED塌陷。有必要对分子途径、细胞相互作用和安全性进行进一步研究,以优化布罗卢izumab的治疗作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e7f/11991755/d2eac09c41ec/CRIOPM2025-9953015.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e7f/11991755/a4831d21bb3e/CRIOPM2025-9953015.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e7f/11991755/b26738bf7df5/CRIOPM2025-9953015.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e7f/11991755/d2eac09c41ec/CRIOPM2025-9953015.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e7f/11991755/a4831d21bb3e/CRIOPM2025-9953015.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e7f/11991755/b26738bf7df5/CRIOPM2025-9953015.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e7f/11991755/d2eac09c41ec/CRIOPM2025-9953015.003.jpg

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