Abstract
Purpose :
To investigate the association between Y402H polymorphism of complement factor H and response to ranibizumab for exudative age-related macular degeneration.
Methods :
Prospective study that included 15 patients with exudative age related macular degeneration. Y402H polymorphism was identified in patients with clinical evidence of choroidal neovascularization and subsequently treated with ranibizumab until inactivation of the neovascular membrane.
The follow-up was 1 year. Polymorphism genotypes were identified and analyzed whether there was a relationship with nonresponders to anti-angiogenic therapy.
Results :
The study was conducted with a total of 15 patients, female gender was the most affected with 60% of cases. The mean age of patients was 78.8 years with a standard deviation of 5.1. The Y402H polymorphism complement factor H, was observed in 50% of our patients, 30% were heterozygotes with a T/C genotype, and 20% homozygotes with C/C genotype.
50% of the patients did not have the mutation by any of the alleles, probably because of the criteria taken from the better visual acuity of 1.3 logMAR.
To analized the response to treatment we consider the final visual acuity and the decrease macular edema measured by OCT. We obtain a statistically significant difference with genotypes in relation to visual acuity, however we did not get a statistically significant difference in relation to decrease macular edema. Secondly variables as time evolution and smoking were analyzed with the final visual acuity, and were statistically significant between the two.
The C allele is associated with larger lesions and greater loss of anatomy pigmented epithelium and neurosensory retina, and visual acuity is worse pre- and post-treatment. The C allele is more significant for the final visual acuity than the antiangiogenic response.
Conclusions :
The genotype plays a more important role in the severity of disease than the response to antiangiogenic treatment.
We realize the role of genetics in the course and severity of illness. We concluded that the patients who are considered as non-responders to treatment can not be explained by Y402H genetic mutation.
This is an abstract that was submitted for the 2016 ARVO Annual Meeting, held in Seattle, Wash., May 1-5, 2016.