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厄达替尼诱发的继发性黄斑病变。

Erdafitinib-Induced Secondary Maculopathy.

作者信息

Becker Brian, El Hamichi Sophia, Gold Aaron S, Murray Timothy G

机构信息

Miami Ocular Oncology & Retina, Miami, FL, USA.

出版信息

J Vitreoretin Dis. 2022 Jun 3;6(4):332-336. doi: 10.1177/24741264221092908. eCollection 2022 Jul-Aug.

Abstract

PURPOSE

This work presents a case of secondary maculopathy associated with the use of erdafitinib (Balversa) for the management of bladder urothelial carcinoma with bony metastasis.

METHODS

A case report is presented.

RESULTS

A 58-year-old Hispanic man presented with blurry vision 3 weeks after starting erdafitinib for the management of bony metastases associated with urothelial carcinoma. A comprehensive evaluation identified multiple areas of subretinal fluid induced by erdafitinib. Throughout treatment, the ocular condition progressed, causing worsening of vision; this led to discontinuation of the drug. Discontinuation was associated with visual and anatomic function improvement.

CONCLUSIONS

Fibroblast growth factor receptor (FGFR) plays a major role in maintaining mature and premature retinal pigment epithelium cells. Drugs that inhibit the FGFR pathway block the activation of the mitogen-activated protein kinase pathway, leading to synthesis of antiapoptotic proteins. Erdafitinib is associated with ocular toxicity and leads to multifocal pigment epithelial detachments associated with secondary subretinal fluid.

摘要

目的

本研究报告了1例使用厄达替尼(Balversa)治疗伴有骨转移的膀胱尿路上皮癌时出现的继发性黄斑病变。

方法

本文呈现了1例病例报告。

结果

一名58岁的西班牙裔男性在开始使用厄达替尼治疗与尿路上皮癌相关的骨转移3周后出现视力模糊。全面评估发现了由厄达替尼引起的多个视网膜下液区域。在整个治疗过程中,眼部病情进展,导致视力恶化,这使得药物停用。停药后视力和解剖功能得到改善。

结论

成纤维细胞生长因子受体(FGFR)在维持成熟和未成熟视网膜色素上皮细胞方面起主要作用。抑制FGFR途径的药物会阻断丝裂原活化蛋白激酶途径的激活,导致抗凋亡蛋白的合成。厄达替尼与眼部毒性有关,并导致与继发性视网膜下液相关的多灶性色素上皮脱离。

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本文引用的文献

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Effect of inhibition of the FGFR-MAPK signaling pathway on the development of ocular toxicities.
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