Céline Faure1,2, Michel Paques3,4, Isabelle Audo5,3,4. 1. Unité d'électrophysiologie, Centre hospitalier national d'ophtalmologie des Quinze-Vingts, 28, rue de Charenton, 75571, Paris, France. celinefaureoph@gmail.com. 2. Ramsay Générale de santé, Hôpital Privé Saint Martin, 18, rue des Roquemonts, 14050, Caen, France. celinefaureoph@gmail.com. 3. INSERM U968, CNRS, UMR 7210, Institut de la Vision, Sorbonne Universités, UPMC Univ Paris 06, Paris, France. 4. Département hospitalo-universitaire ViewMaintain, Inserm-Direction de l'hospitalisation et de l'organisation des soins-Centre d'Investigations cliniques (DHOS CIC) 1423, Centre hospitalier national d'ophtalmologie des Quinze-Vingts, 75012, Paris, France. 5. Unité d'électrophysiologie, Centre hospitalier national d'ophtalmologie des Quinze-Vingts, 28, rue de Charenton, 75571, Paris, France.
Abstract
PURPOSE: The purpose of this study is to report a case of ritonavir-related retinal toxicity followed over a year. Electrophysiological features and multimodal imaging, including adaptive optics, are provided and discussed. METHODS: Electrophysiological recordings and multimodal imaging were performed and repeated over 1 year. RESULTS: Fundus examination revealed crystalline maculopathy in conjunction with pigment disruption. Spectral domain optical coherence tomography displayed thinning of the macula without cysts. Autofluorescence imaging revealed a mixed pattern of complete loss of the autofluorescence in the area of retinal pigment deposit and an increased transmission of the autofluorescence in the area of retinal thinning. Fluorescein angiography ruled out parafoveal telangiectasia. Indocyanine green angiography was not contributive. Increased spacing of the macular cone mosaic, crystal deposits and pigment migrations were seen with adaptive optics. Full-field electroretinogram was slightly reduced for both eyes, especially in the light-adapted responses, and mfERG confirmed bilateral maculopathy. Functional and structural abnormalities did not change with follow-up besides constant pigmentary changes monitored with adaptive optics. CONCLUSION: Ritonavir-related retinal toxicity is a maculopathy with peculiar features including crystalline and pigment migration associated with central or temporofoveolar thinning and inconstant macular telangiectasia. Despite drug cessation, retinal remodelling continues to progress.
PURPOSE: The purpose of this study is to report a case of ritonavir-related retinal toxicity followed over a year. Electrophysiological features and multimodal imaging, including adaptive optics, are provided and discussed. METHODS: Electrophysiological recordings and multimodal imaging were performed and repeated over 1 year. RESULTS: Fundus examination revealed crystalline maculopathy in conjunction with pigment disruption. Spectral domain optical coherence tomography displayed thinning of the macula without cysts. Autofluorescence imaging revealed a mixed pattern of complete loss of the autofluorescence in the area of retinal pigment deposit and an increased transmission of the autofluorescence in the area of retinal thinning. Fluorescein angiography ruled out parafoveal telangiectasia. Indocyanine green angiography was not contributive. Increased spacing of the macular cone mosaic, crystal deposits and pigment migrations were seen with adaptive optics. Full-field electroretinogram was slightly reduced for both eyes, especially in the light-adapted responses, and mfERG confirmed bilateral maculopathy. Functional and structural abnormalities did not change with follow-up besides constant pigmentary changes monitored with adaptive optics. CONCLUSION:Ritonavir-related retinal toxicity is a maculopathy with peculiar features including crystalline and pigment migration associated with central or temporofoveolar thinning and inconstant macular telangiectasia. Despite drug cessation, retinal remodelling continues to progress.
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