Literature DB >> 30324420

Novel clinical findings in autosomal recessive NR2E3-related retinal dystrophy.

Vittoria Murro1, Dario Pasquale Mucciolo2, Andrea Sodi1, Ilaria Passerini3, Dario Giorgio1, Gianni Virgili1, Stanislao Rizzo1.   

Abstract

PURPOSE: To evaluate the clinical phenotype of autosomal recessive NR2E3-related retinal dystrophy.
METHODS: We retrospectively studied 11 patients carrying out at least 2 NR2E3 mutations; they had undergone comprehensive ophthalmological examination, fundus photography, optical coherence tomography, electrophysiological testing, and visual field at the Regional Reference Center for Hereditary Retinal Degenerations of the Eye Clinic in Florence.
RESULTS: Five females and six males with a diagnosis of NR2E3-related retinal dystrophy were included in the study. All patients complained of nyctalopia. Visual acuity ranged from 0.00 logMAR to hand motion. Two patients presented bull's eye maculopathy, and one of these was characterized by a triple hyper-autofluorescent ring at the fundus autofluorescence examination. Three patients showed small yellowish dots and spots at the mid-periphery. One patient was characterized by widespread subretinal drusenoid deposits (SDD) at the posterior pole. Four patients showed vitreous abnormalities. Optical coherence tomography (OCT) examinations detected variable degrees of abnormal retinal lamination and schitic changes. Seven patients were compound heterozygous and four were homozygous for mutations in NR2E3.
CONCLUSIONS: Our study confirmed high variable phenotype in autosomal recessive NR2E3-related retinal dystrophy. Bull's eye maculopathy, subretinal drusenoid deposits, and foveal hypoplasia represent novel clinical findings in NR2E3-related retinal dystrophy. Macular involvement was detectable in all the patients, and the abnormal foveal avascular zone (FAZ) supports the role of NR2E3 in retinal development.

Entities:  

Keywords:  Autosomal recessive disease; Foveal hypoplasia; Goldmann-Favre; NR2E3; Retinal dystrophy; Retinitis pigmentosa; Subretinal drusenoid deposits

Mesh:

Substances:

Year:  2018        PMID: 30324420     DOI: 10.1007/s00417-018-4161-z

Source DB:  PubMed          Journal:  Graefes Arch Clin Exp Ophthalmol        ISSN: 0721-832X            Impact factor:   3.117


  77 in total

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4.  Mutation of a nuclear receptor gene, NR2E3, causes enhanced S cone syndrome, a disorder of retinal cell fate.

Authors:  N B Haider; S G Jacobson; A V Cideciyan; R Swiderski; L M Streb; C Searby; G Beck; R Hockey; D B Hanna; S Gorman; D Duhl; R Carmi; J Bennett; R G Weleber; G A Fishman; A F Wright; E M Stone; V C Sheffield
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Authors:  S Gerber; J M Rozet; S I Takezawa; L C dos Santos; L Lopes; O Gribouval; C Penet; I Perrault; D Ducroq; E Souied; M Jeanpierre; S Romana; J Frézal; F Ferraz; R Yu-Umesono; A Munnich; J Kaplan
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Authors:  Dror Sharon; Michael A Sandberg; Rafael C Caruso; Eliot L Berson; Thaddeus P Dryja
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1.  Optical coherence tomography (OCT) features of cystoid spaces in choroideremia (CHM).

Authors:  Vittoria Murro; Dario Pasquale Mucciolo; Dario Giorgio; Andrea Sodi; Ilaria Passerini; Giacomo Bacci; Sara Bargiacchi; Gianni Virgili; Stanislao Rizzo
Journal:  Graefes Arch Clin Exp Ophthalmol       Date:  2019-10-26       Impact factor: 3.117

2.  Novel Pathogenic Sequence Variants in NR2E3 and Clinical Findings in Three Patients.

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3.  A mutation in CRX causing pigmented paravenous retinochoroidal atrophy.

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