First Author: V.Chaudhary CANADA
Co Author(s): W. Lam R. Devenyi J. Teichman M. Mak F. Farrokhyar J. Barbosa
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Since genetic markers have been implicated in the onset and progression of Age Related Macular Degeneration (AMD), it is plausible that polymorphisms may also explain variability is treatment response. Herein, we sought to evaluate the pharmacogenetic relationship between CFH haplotypes or single nucleotide polymorphisms (SNPs) at rs2230199 (C3), rs10490824 (ARMS2), and the mtDNA with treatment response in a wAMD cohort.
Single-centred, prospective cohort study
60 treatment naïve patients with choroidal neovascularization secondary to AMD were genotyped for CFH haplotypes, SNP rs2230199 (C3), SNP rs10490824 (ARMS2), and the mtDNA A4917G marker using the Macula Risk test. After receiving three consecutive monthly loading doses of ranibizumab, all study participants were treated on a pro re nata schedule for 10 additional months. The primary outcome was a gain of 15 or more letters at the 12 month endpoint in patients with risk alleles or haplotypes for AMD compared to those without. Secondary outcome measures identified the association between genetic dispositions and change in VA or central macular thickness.
No significant associations were observed between genetic dispositions and treatment outcomes.
CFH haplotypes, SNP rs2230199 (C3), SNP rs10490824 (ARMS2), and the mtDNA A4917G marker are not implicated in wAMD treatment response to ranibizumab.