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A. I. Den Hollander, D. Smailhodzic, H. A. Khan, A. Omar, A. Y. Zhang, B. Kirchhof, J. Chen, C. B. Hoyng, R. K. Koenekoop, S. Fauser; Pharmacogenetic Studies of Ranibizumab Treatment in Neovascular Age-Related Macular Degeneration. Invest. Ophthalmol. Vis. Sci. 2010;51(13):1283. doi: https://doi.org/.
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To determine whether the response to ranibizumab treatment is associated with genotypes in several genes known to be involved in age-related macular degeneration (AMD).
Blood samples of 246 neovascular AMD patients were collected who received ranibizumab treatment at monthly intervals. DNA was collected after informed consent. Patients were included with visual impairment (best corrected visual acuity of 1.3 to 0.2 logmar) due to an active primary choroidal neovascularization associated with AMD. Exclusion criteria were a subretinal hemorrhage involving the fovea and previous intravitreal drug delivery. Best corrected visual acuities (BCVA) were measured before treatment and after the third injection. In an initial analysis, 60 patients of this cohort were genotyped for 12 SNPs in nine genes previously associated with AMD.
After three ranibizumab injections, fifty (20%) patients experienced a decrease in baseline BCVA ranging from -0.2 to -0.8 logmar (we designate these as non-responders), while 82 (33%) patients improved in baseline BCVA ranging from +0.2 to +0.8 logmar (we designate these as responders). Initial genotyping in 60 patients showed that the Y402H risk allele in the complement factor H (CFH) gene is more prevalent among non-responders (55%) than in responders (42%). Genotype analysis of the remaining patient samples is in progress.
Our results suggest that the response to ranibizumab treatment in patients with neovascular AMD differs according to the CFH genotype.
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