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Chloroquine and Hydroxychloroquine
Published in M. Lindsay Grayson, Sara E. Cosgrove, Suzanne M. Crowe, M. Lindsay Grayson, William Hope, James S. McCarthy, John Mills, Johan W. Mouton, David L. Paterson, Kucers’ The Use of Antibiotics, 2017
Retinal toxicity is a potentially serious complication of longterm CQ and HCQ use. Although the mechanism of toxicity is uncertain, the binding of CQ and HCQ to melanin in the retinal pigment epithelium (RPE) likely contributes. CQ- or HCQ-induced retinal toxicity is characterized by bull’s-eye maculopathy, a ring of RPE depigmentation with fovea sparing. Although visual acuity may be excellent, paracentral visual scotomas may develop. With continued drug exposure, the area of functional disturbance and RPE atrophy spreads into the fovea, with resultant loss of visual acuity, and eventually the entire fundus may be involved. Visible bull’seye maculopathy is generally irreversible and may progress after the drug has been ceased. Delayed-onset retinopathy has also been reported, many years after cessation of CQ or HCQ (Martin et al., 1978; Ehrenfeld et al., 1986; Kazi et al., 2013).
Antimalarials
Published in Sarah H. Wakelin, Howard I. Maibach, Clive B. Archer, Handbook of Systemic Drug Treatment in Dermatology, 2015
Early retinopathy with antimalarials takes the form of a non-specific fine pigmentary stippling in the macular area and loss of the foveal light reflex. This may develop into irreversible bull’s eye maculopathy and widespread retinal pigment epithelial atrophy, associated with a central scotoma, loss of visual acuity and peripheral visual field loss. Corneal deposits, and impairment of accommodation are reversible, dose related side-effects.
Ocular Manifestations of Neuronal Ceroid Lipofuscinoses
Published in Seminars in Ophthalmology, 2021
Rohan Bir Singh, Prakash Gupta, Akash Kartik, Naba Farooqui, Sachi Singhal, Sukhman Shergill, Kanwar Partap Singh, Aniruddha Agarwal
In majority of the patients, the onset of ocular symptoms occurs late in the disease at an average age of 4–5 years. Though recent studies have shown that retinal changes can be detected very early in the disease, overpowering neurological manifestations could be the cause of delayed diagnosis of ocular symptoms.41 The patients present with inability to fixate on a point, inability to follow objects, decreased pupillary reactivity to light, or complete visual impairment. Ocular involvement is usually symmetric and has been considered to be in synergy with the neurological impairment when quantified on the LINCL severity scale.14,41,53,54 Recent studies have shown that though previously thought otherwise, retinal degeneration and neuronal degeneration occur independently.55 The manifestations are usually limited to the posterior segment, and no anterior segment manifestation has been reported in the literature. The fundoscopic examination findings may range from no abnormality to the destruction of retinal structures and fulminant bull’s eye maculopathy.
Heterozygous CRX R90W mutation-associated adult-onset macular dystrophy with phenotype analogous to benign concentric annular macular dystrophy
Published in Ophthalmic Genetics, 2020
Caleb C Ng, William M Carrera, H. Richard McDonald, Anita Agarwal
Bull’s-eye maculopathy is a distinct ophthalmoscopic finding where there is circumferential degeneration of the retinal pigment epithelium around a relatively normal central foveola. Drug toxicity, retinal and macular dystrophies, and age-related macular degeneration have been associated with this finding (1,2). Patients with largely asymptomatic bilateral bull’s eye maculopathy and no prior exposure to inciting agents, like hydroxychloroquine, are thought to have benign concentric annular macular dystrophy (BCAMD) (3). However, retinal and macular dystrophies can be associated with a plethora of genetic mutations of varying phenotypes. We report a case of adult-onset macular dystrophy due to a heterozygous CRX R90 W mutation with a phenotype analogous to BCAMD, and review the literature regarding CRX macular dystrophy with preserved visual acuity.
Bull’s eye maculopathy caused by a novel IMPG-1 mutation
Published in Ophthalmic Genetics, 2019
Ana González-Gómez, Jose Lorenzo Romero-Trevejo, Antonio García-Ben, Jose Manuel García-Campos
The best corrected visual acuity (BCVA) was 1/2 in the right eye and 2/3 in the left eye. Intraocular pressure and anterior segment were unremarkable. Ophthalmoscopy showed a bilateral and annular alteration of the retinal pigment epithelium (RPE) surrounding an intact central macula. Optic coherence tomography (OCT) revealed a central and annular atrophy of the RPE, with increased choroidal hyperreflectivity, that respected the foveal region. A generalized thinning of the macular thickness and the ganglion cell layer were also observed. Autofluorescence detected a central area of normal fluorescence surrounded by a concentric, perifoveal, and hyperautofluorescent area. Fluorescein angiography confirmed the bull’s-eye maculopathy. Electrophysiological testing described a nonspecific rod and cone dysfunction (Figure 1). Campimetry showed a bilateral central scotoma affecting the central 5 degrees. Considering all these findings, a clinical diagnosis of plausible BCAMD was established. Blood samples were taken for genetic sequencing and comparison with reference sequences. It revealed a heterozygous mutation of the IMPG-1 gene that affected the IVS11 + 2T>C zone (c.1212 + 2 T > C) in the chromosome 6. Patient’s parents were also genetically checked, but they did not carry this mutation.