Purpose:
To determine whether genetic factors that influence age-related macular degeneration (AMD) have early pharmacogenetic effect on the treatment of exudative AMD with ranibizumab.
Methods:
Changes in central retinal thickness (CRT) after initial three monthly dosing of intravitreal ranibizumab were observed and percentiles of CRT were calculated. Genotypes of polymorphisms in known AMD susceptibility loci (CFH, AMRS2, HTRA1, VEGFA and KDR) were determined, and their frequencies were compared. Changes in visual acuity (VA) during three month were also used as secondary outcome measure.
Results:
Of the 146 eyes included in the study, 120 completed monthly CRT assessment using optical coherence tomography. Based on the change in CRT, two groups were established: 90 eyes were assigned to the good tomographic responders (75th percentile) and 30 eyes to the poor tomographic responders (25th percentile). There was no significant difference in mean baseline CRT between the groups. There was no significant association between allelic and genotypic distributions of each polymorphism and the change of CRT in both groups of tomographic responders. We defined the good functional responder as patients who showed improved BCVA after treatment. Again, there was no significant association between types of polymorphism and the change of BCVA in both groups of functional responders.
Conclusions:
In our patient cohort, there was no statistically significant pharmacogenetic association between early response to ranibizumab therapy and genotype in both good and poor responder groups.
Keywords: age-related macular degeneration • genetics • vascular endothelial growth factor