Effects of aflibercept for ranibizumab-resistant neovascular age-related macular degeneration and polypoidal choroidal vasculopathy.
OBJECTIVE
To evaluate visual and anatomic outcomes in response to the conversion of treatment in patients with neovascular age-related macular degeneration (AMD) and polypoidal choroidal vasculopathy (PCV) refractory to previous treatment. We also investigated the effect of genetic factors.


METHODS
We recruited patients with AMD or PCV refractory to ranibizumab and initiated aflibercept treatment. Changes in the logarithm of minimum angle of resolution (logMAR) and central retinal thickness (CRT) measured using optical coherence tomography (OCT) 6 months after the conversion were compared between the AMD and PCV groups. We also genotyped each patient for the ARMS2 A69S, CFH Y402H, and I62V alleles, and investigated the association between genotype and treatment response.


RESULTS
Mean age of the participants was 75.6 ± 8.0 years. There were 15 patients with AMD and 26 patients with PCV. While PCV patients gained about 1 line of vision (0.40 ± 0.37 to 0.31 ± 0.40, P = 0.003), AMD patients did not show significant improvement (0.41 ± 0.37 to 0.42 ± 0.39, P = 0.699) despite the decrease in CRT (202.1 ± 113.7 to 131.2 ± 55.7 μm, P = 0.003). The prevalence of dry retina after treatment was higher among PCV patients (80.8 vs 46.7 %, P = 0.024). There was no significant difference between patients with risk and non-risk alleles for ARMS2 A69S, CFH Y402H, and I62V.


CONCLUSIONS
In AMD or PCV patients refractory to ranibizumab, switching to aflibercept is generally effective regardless of patient genotype. PCV patients may benefit more significantly than AMD patients.
Department of Ophthalmology and Visual Sciences, Kyoto University Graduate School of Medicine, 54, Shougoin Kawahara-cho, Sakyo-ku, Kyoto, 606-8507, Japan.
Yu
Y
Kawashima
Akio
A
Oishi
Akitaka
A
Tsujikawa
Kenji
K
Yamashiro
Masahiro
M
Miyake
Naoko
N
Ueda-Arakawa
Munemitsu
M
Yoshikawa
Ayako
A
Takahashi
Nagahisa
N
Yoshimura
D000368:Aged; D000369:Aged, 80 and over; D020533:Angiogenesis Inhibitors / Q000627:therapeutic use*; D020256:Choroidal Neovascularization / Q000188:drug therapy* / Q000235:genetics / Q000503:physiopathology; D017242:Complement Factor H / Q000235:genetics; D004351:Drug Resistance; D057915:Drug Substitution; D005260:Female; D005451:Fluorescein Angiography; D060005:Genotyping Techniques; D006801:Humans; D008297:Male; D020641:Polymorphism, Single Nucleotide; D011127:Polyps / Q000188:drug therapy* / Q000235:genetics; D011446:Prospective Studies; D011506:Proteins / Q000235:genetics; D000069579:Ranibizumab / Q000627:therapeutic use*; D040262:Receptors, Vascular Endothelial Growth Factor / Q000627:therapeutic use*; D011993:Recombinant Fusion Proteins / Q000627:therapeutic use*; D041623:Tomography, Optical Coherence; D042461:Vascular Endothelial Growth Factor A / Q000037:antagonists & inhibitors; D014792:Visual Acuity / Q000502:physiology; D057135:Wet Macular Degeneration / Q000188:drug therapy* / Q000235:genetics / Q000503:physiopathology
C514392:ARMS2 protein, human; D020533:Angiogenesis Inhibitors; C493495:CFH protein, human; D011506:Proteins; D011993:Recombinant Fusion Proteins; C467484:VEGFA protein, human; D042461:Vascular Endothelial Growth Factor A; C533178:aflibercept; D017242:Complement Factor H; D040262:Receptors, Vascular Endothelial Growth Factor; D000069579:Ranibizumab