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Reversible Nyctalopia and Retinopathy in a Patient With Metastatic Cancer Treated With Anti–Heat Shock Protein 90 Therapy

Marion R. Munk, MD, PhD1,2; Joshua Fernandes, MD2; Marilyn Mets, MD2; Jyoti D. Patel, MD3; Melissa L. Johnson, MD3; Lee M. Jampol, MD2
[+] Author Affiliations
1Department of Ophthalmology, Medical University of Vienna, Vienna, Austria
2Department of Ophthalmology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois
3Division of Hematology/Oncology, Department of Internal Medicine, Feinberg School of Medicine, Northwestern University, Chicago, Illinois
JAMA Ophthalmol. 2014;132(7):899-901. doi:10.1001/jamaophthalmol.2014.409.
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Cancer-associated retinopathy is an autoimmune disease in which autoantibodies trigger retinal tissue destruction.1 Patients with cancer-associated retinopathy may develop visual acuity or visual field loss, photopsias, photophobia, and/or nyctalopia.1 Drug-induced toxic effects can also cause photoreceptor damage and corresponding visual symptoms.2 We describe a patient with nyctalopia during treatment of non–small cell lung cancer with AUY922, a heat shock protein 90 (HSP90) inhibitor.3

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Figure.
Photoreceptor Status in a Patient Treated With a Heat Shock Protein 90 Inhibitor

Central (A) and superior (B) horizontal B-scans of the right eye of a patient with metastatic non–small cell lung cancer and positive anti–α-enolase antibodies with anti–heat shock 90 therapy (AUY922). These spectral-domain optical coherence tomographic scans are representative of the photoreceptor status in each single B-scan of the volume scan, and the left eye was virtually identical. Arrows indicate the location of photoreceptor damage and following improvement. At initial presentation, the right eye had a distorted ellipsoid zone and external limiting membrane, indicating severe photoreceptor damage; centrally, the fovea was relatively preserved (A). One month after cessation of the study drug, the external limiting membrane and ellipsoid zone were still disintegrated and mottled but began to be differentiable, indicating photoreceptor recovery. Two months after cessation of the study drug, the integrity of the respective layers had further improved. Five months after cessation, further photoreceptor layer recovery was seen, although the hyperreflective bands were still irregular. Eight months after cessation, there was further improvement; despite some irregularities, the external limiting membrane and ellipsoid zone seemed integrated again. Fifteen months after cessation, there was further improvement in the integrity of the hyperreflective bands; respective layers were well integrated, but there were still some irregularities.

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