Switching of an inhibitor of vascular endothelial growth factor in the treatment of resistant to ranibizumab neovascular form of age-related macular degeneration. Case study
Authors: Ivanova Nanuli V , Rasin Oleg G , Savchenko Aleksey V , Litvinenko Olga A 
Published: June 2017

Aim: To analyze the spontaneous reattachment of retinal pigment epithelium (RPE) after replacing the anti-VEGF drug - ranibizumab, with aflibercept in the treatment of neovascular AMD based on the example given in our clinical study. Material and methods. We carried out a retrospective analysis of the patient’s history with exudative detachment of RPE due to choroidal neovascularization in age-related macular degeneration. This patient was treated with anti-angiogenic treatment in the form of monthly IVI ranibizumab. At the time of treatment, the visual acuity of the left eye was 0.3 with sph + 1,5D = 0,5, in the fundus of the eye there was a high exudative detachment of RPE in the macular region common to the vascular arcades. The edges were determined by the detachment of the neuroepithelium and abundance of hard drusen. Using optical coherence tomography, (OCT) we saw that the center of the macula of the left eye had a high detachment of RPE, local detachment of the neuroepithelium at the edge of the RPE detachment and an abundance of hard drusen. The foveola was flattened, and beneath it, the RPE was detached in the center - thickness of 247 microns (m). After the seventh injection of ranibizumab, we used OCT to assess the condition of the retina. The retinas condition was almost the same as before. The thickness in the central zone was 251 m, detachment of neuroepithelium was not seen, the dome of the RPE detachment circuit was unchanged and visual acuity improved to 0.7 with a maximum correction. We then replaced ranibizumab with another anti-angiogenic drug - aflibercept. Results and discussion. Two weeks on from our control examination, we noticed there was a smooth bubble detachment of the RPE and a retinal prominence over the choroidal neovascular membrane area (CNM). The OCT scan indicated minimal RPE detachment, resorption of the exudate, presence of subretinal spindle - shaped formation near the temporal side (CNM? Scar?). Retinal thickness was 178 m at the fixation point. Intravitreal injections were stopped. Visual acuity increased to 0.8 and remained stable for 5 months, but there were signs of renewed activity of choroidal neovascularization. According to OCT, the thickness in the central parts of the retina increased to 230 m, there were intraretinal cysts and increased spindle - shaped formation under the RPE. After 10 months of IVI aflibercept, acute vision decreased to 0.5, the thickness at the point of fixing increased to 250 m, subretinal formation increased and oozing of fluid was observed mainly parafoveal, which explains the high visual acuity. We then administered IVI ranibizumab. Two weeks later, the retinal thickness was 169 m, visual acuity improved to 0.8, but 1 month later we found that the retinal thickness had increased once more and decreased to 0.7. After 3 months after IVI ranibizumab, retinal thickness at the fixation point reached 286 m and visual acuity dropped to 0.5. Conclusion. In our practice, we face patients with neovascular AMD, who respond badly to ranibizumab. For such patients, it is important to replace ranibizumab with a better, more therapeutically effective anti-VEGF drug with anti-vaso proliferative properties. Aflibercept is an effective substitute for ranibizumab which was shown in this clinical case.