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Management of choroidal neovascularisation in late onset retinal degeneration
Author(s) -
WIRYASAPUTRA S,
YONG SO
Publication year - 2014
Publication title -
acta ophthalmologica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.534
H-Index - 87
eISSN - 1755-3768
pISSN - 1755-375X
DOI - 10.1111/j.1755-3768.2014.f068.x
Subject(s) - macular degeneration , ophthalmology , medicine , retinal , choroidal neovascularization , retinal degeneration , retina , optometry , neuroscience , psychology
Purpose Late onset retinal degeneration is a hereditary condition characterized by progressive difficulty in dark adaptation and risk of choroidal neovascularisation. This in turn leads to a marked decline in visual acuity. We describe our experience treating a patient with a positive family history of late onset retinal degeneration who developed subfoveal choroidal neovascularisation. Methods Case report. A 57 year old Caucasian lady with a positive family history of late onset retinal degeneration and progressive decline in dark adaptation presented to us with a 1‐week history of blurring of vision. Fundus fluorescein and indocyanine green angiography revealed a subfoveal classic neovascular membrane. Results Our patient was initially treated with intra‐vitreal Ranibizumab and clinical activity of neovascularisation was monitored with serial spectral domain optical coherence tomography and visual acuity. Serial scans revealed recurrence of activity within a month of intra‐vitreal Ranibizumab. With the advent of intra‐vitreal Aflibercept, we offered our patient a change in treatment regime. Treatment with Aflibercept has thus far demonstrated a stabilization of disease activity on spectral domain optical coherence tomography and visual acuity for at least 8 weeks. Conclusion Whilst Ranibizumab and Aflibercept remain off‐label for the treatment of late onset retinal degeneration, this suggests that Aflibercept is possibly more efficacious in the management of choroidal neovascular membranes in late onset retinal degeneration.