title: Wet age-related macular degeneration.
abstract: Age-related macular degeneration (AMD) is the leading cause of irreversible visual loss in industrialized nations for those age 65 and above. The majority of patients with severe visual loss suffer from the wet form of AMD wherein there is choroidal neovascularization (CNV) and associated manifestations such as retinal pigment epithelial detachment, subretinal hemorrhages, and fibrovascular disciform scarring. The main focus on understanding the pathogenesis of CNV has been on the hypothesis that the diffuse thickening of Bruch's membrane predisposes it to develop cracks and in-growth of new vessels from choriocapillaries with associated low-grade inflammatory response. Currently, three types of treatments (laser photocoagulation, photodynamic therapy, and anti-Vascular Endothelial Growth Factor (VEGF) therapy) have been demonstrated to limit or delay loss of vision in patients. Only a minority of cases show stabilization of vision and a small proportion of cases show significant improvement in vision. This highlights the need for more and better pharmacologic or other interventions, with the goal of lowering recurrence rates and preventing the development of CNV in order to achieve better functional outcomes.
authors.affiliation: Department of Ophthalmology, University of California, Irvine, 118 Med Surge I, Irvine, CA 92697, USA.
authors.forename: Amol D
authors.initials: AD
authors.lastname: Kulkarni
authors.forename: Baruch D
authors.initials: BD
authors.lastname: Kuppermann
mesh_terms: D020256:Choroidal Neovascularization / Q000209:etiology / Q000503:physiopathology / Q000628:therapy*; D006801:Humans; D008268:Macular Degeneration / Q000209:etiology / Q000503:physiopathology / Q000628:therapy*; D013508:Ophthalmologic Surgical Procedures; D010778:Photochemotherapy; D011878:Radiotherapy; D012307:Risk Factors; D042461:Vascular Endothelial Growth Factor A / Q000502:physiology
chemical_list: C467484:VEGFA protein, human; D042461:Vascular Endothelial Growth Factor A