title: [Treatment of neovascular age-related macular degeneration with antiangiogenic drugs].
abstract: Age-related macular degeneration (ARMD) remains a leading cause of blindness in the western world. Several clinical forms of the disease are recognized, whereas choroidal neovascularization (CNV) represents an important manifestation suitable for treatment. The treatment of CNV has been a major focus of research in the past decades, and the first evidence-based established therapy was laser photocoagulation, which reduces the risk of visual loss in extrafoveal lesions. In the late 90's photodynamic therapy has been established as an efficient method for the treatment of predominantly classic and occult CNV. Additional therapies such as macular translocation, submacular surgery, and indocyanine-mediated prothrombosis are currently under investigation in large-scale clinical trials. Molecular biology has recently provided a better comprehension of the pathogenesis of ARMD, and vascular endothelial growth factor (VEGF) was recognized as key mediator in the angiogenesis of CNV-formation. Therefore, the pharmacological approach rose as a key research area to treat CNV. The first FDA-approved agent for CNV-therapy is aptamer pegaptanib sodium (Macugen), which inactivates the key angiogenic isoform VEGF165. Additional VEGF-blockers such as ranibizumab RhuFab V2 (Lucentis) and bevacizumab (Avastin) are under evaluation in major clinical studies. Impressive results of intravitreal bevacizumab were released recently. Moreover, the steroid-derived anecortave acetate as well as the corticosteroid triamcinolone acetate have been proposed as methods for treatment of wet-ARMD. This paper presents the rationale and principles of the pharmacologic antiangiogenic therapy for CNV in ARMD.
authors.affiliation: Departamento de Retina, Serviço de Oftalmologia, Hospital Regional São José, Instituto de Olhos Florianópolis - Centro Oftalmológico - Florianópolis (SC) - Brasil. edubrodriguess@yahoo.com.br
authors.forename: Eduardo Büchele
authors.initials: EB
authors.lastname: Rodrigues
authors.forename: Eglas Emanuel
authors.initials: EE
authors.lastname: Rossi
authors.forename: Astor
authors.initials: A
authors.lastname: Grumann Junior
authors.forename: Carsten H
authors.initials: CH
authors.lastname: Meyer
authors.forename: Allen C
authors.initials: AC
authors.lastname: Ho
mesh_terms: D020533:Angiogenesis Inhibitors / Q000494:pharmacology / Q000627:therapeutic use*; D000911:Antibodies, Monoclonal / Q000494:pharmacology / Q000627:therapeutic use*; D061067:Antibodies, Monoclonal, Humanized; D052157:Aptamers, Nucleotide / Q000494:pharmacology / Q000627:therapeutic use; D000068258:Bevacizumab; D020256:Choroidal Neovascularization / Q000188:drug therapy* / Q000209:etiology; D002986:Clinical Trials as Topic; D006801:Humans; D008028:Light Coagulation; D008268:Macular Degeneration / Q000188:drug therapy* / Q000209:etiology; D000069579:Ranibizumab; D015861:Retinal Neovascularization / Q000188:drug therapy* / Q000209:etiology; D016896:Treatment Outcome; D042461:Vascular Endothelial Growth Factor A / Q000187:drug effects; D014792:Visual Acuity / Q000187:drug effects
chemical_list: D020533:Angiogenesis Inhibitors; D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D052157:Aptamers, Nucleotide; D042461:Vascular Endothelial Growth Factor A; C495058:pegaptanib; D000068258:Bevacizumab; D000069579:Ranibizumab