Uncontrolled angiogenesis (growth of new blood vessels) is a common finding in many potentially blinding conditions, such as prolif-erative diabetic retinopathy, central retinal vein occlusion, wet age-related macular degeneration (ARMD) and retinopathy of prematurity. Inhibiting their growth offers us the hope of dramatically reducing the number of patients going blind each year. It is thought that the angiogenic response is caused by elevated levels of a cytokine called vascular endothelial growth factor (VEGF) produced by abnormal or ischaemic cells within the eye. Attempts to reduce the levels of VEGF and hence turn off the angiogenic drive have involved intravitreal injections of anti-VEGF antibodies or oligonucleotide aptamers, which bind VEGF, or the intravitreal/sub-Tenon's injection of an anti-angiogenic steroid (triamcinolone). All of these treatments are showing great promise in clinical trials. An alternative mechanism of treatment is the destruction of preformed new vessels. Recently, a new type of treatment for wet ARMD has seen the use of a light-activated dye, injected intravenously, which preferentially locates in the choroidal neovascular membrane (photodynamic therapy). Activation of the dye by light of a specific wavelength causes thrombosis and destruction of blood vessels harbouring the dye. Treatment of patients with one particular subtype of wet ARMD (classic with no occult blood vessels) has shown stabilisation of vision in 60-70% of cases.
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