
Development of Macular Atrophy in Patients with Wet Age-Related Macular Degeneration Receiving Anti-VEGF Treatment
Author(s) -
Alexander Foss,
Tryfon Rotsos,
Theodoros Empeslidis,
Victor Chong
Publication year - 2021
Publication title -
ophthalmologica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.639
H-Index - 60
eISSN - 1423-0267
pISSN - 0030-3755
DOI - 10.1159/000520171
Subject(s) - macular degeneration , medicine , choroidal neovascularization , choroid , ranibizumab , ophthalmology , atrophy , vascular endothelial growth factor , neovascularization , retina , surgery , bevacizumab , vegf receptors , angiogenesis , chemotherapy , physics , optics
Age-related macular degeneration (AMD) is a leading cause of blindness. Late AMD can be classified into exudative (commonly known as wet AMD [wAMD]) or dry AMD, both of which may progress to macular atrophy (MA). MA causes irreversible vision loss and currently has no approved pharmacological treatment. The standard of care for wAMD is treatment with anti-vascular endothelial growth factors (VEGF). However, recent evidence suggests that anti-VEGF treatment may play a role in the development of MA. Therefore, it is important to identify risk factors for the development of MA in patients with wAMD. For example, excessive blockade of VEGF through intense use of anti-VEGF agents may accelerate the development of MA. Patients with type III macular neovascularisation (retinal angiomatous proliferation) have a particularly high risk of MA. These patients are characterised as having a pre-existing thin choroid (age-related choroidopathy), suggesting that the choroidal circulation is unable to respond to increased VEGF expression. Evidence suggests that subretinal fluid (possibly indicative of residual VEGF activity) may play a protective role. Patients receiving anti-VEGF agents must be assessed for overall risk of MA and there is an unmet medical need to prevent the development of MA without undertreating wAMD.