Antiangiogenic approaches to age-related macular degeneration today.
Intravitreal ranibizumab reduces the risk of visual acuity loss and increases the chance of visual acuity gain compared with no treatment or photodynamic therapy for selected cases of subfoveal choroidal neovascularization (CNV) in age-related macular degeneration (AMD). Although intravitreal ranibizumab did not result in substantial improvement (15 or more letters on an ETDRs chart) in the majority of cases treated in the MARINA (Minimally classic/occult trial of the Anti-VEGF antibody Ranibizumab in the treatment of Neovascular AMD) or ANCHOR (Anti-VEGF Antibody for the Treatment of Predominantly Classic CHORoidal Neovascularization in AMD) trials, few cases experienced substantial visual acuity loss. The most serious known risk of treatment, endophthalmitis, although rare, is always a possibility. Intravitreal bevacizumab might be considered when ranibizumab is not available because of regulatory or financial constraints, and it might be considered in place of ranibizumab even without financial constraints if noninferiority trials show that bevacizumab is almost as good as-or is better than-ranibizumab. Systemic risks of intravitreal ranibizumab or bevacizumab are unknown, although trials have ruled out moderate or large systemic risks for ranibizumab. This therapy should be considered when initiating therapy for lesions that are subfoveal, and predominantly CNV when the lesion composition on fluorescein angiography (FA) is predominantly classic, or when there is presumed recent disease progression and the lesion composition is minimally classic or occult with no classic. Optical coherence tomography, FA, or both also might be of value to assist with decisions regarding continuation of treatment after it has been initiated. However, to date, there is little consistent information to suggest that utilizing these imaging modalities to consider withholding treatment before 2 years has been shown confidently to result in outcomes as good as monthly treatment. Extrapolation of these recommendations should be done with caution when considering the treatment of subfoveal CNV that is not predominantly CNV, such as predominantly blood lesions or lesions that are predominantly scar, as well as lesions associated with very low levels of visual acuity or those owing to causes other than AMD. A subsequent review in this series discusses other therapies for CNV being considered in the future.
The Wilmer Eye Institute, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21287, USA. nbressler@jhmi.edu
Neil M
NM
Bressler
D000465:Algorithms; D020533:Angiogenesis Inhibitors / Q000009:adverse effects / Q000627:therapeutic use*; D000818:Animals; D002986:Clinical Trials as Topic; D003661:Decision Support Techniques; D006801:Humans; D008268:Macular Degeneration / Q000188:drug therapy* / Q000503:physiopathology; D010778:Photochemotherapy; D042461:Vascular Endothelial Growth Factor A / Q000037:antagonists & inhibitors; D014792:Visual Acuity / Q000502:physiology
D020533:Angiogenesis Inhibitors; D042461:Vascular Endothelial Growth Factor A