Short-term changes in retinal pigment epithelium after anti-vascular endothelial growth factor therapy for neovascular age-related macular degeneration evaluated by polarization-sensitive optical coherence tomography
摘要
To characterize changes in retinal pigment epithelium (RPE) melanin distribution after anti-vascular endothelial growth factor (VEGF) therapy for neovascular age-related macular degeneration (nAMD).
MethodsThis prospective study enrolled treatment-naïve nAMD eyes with macular neovascularization (MNV) type 1 and type 2. Eyes were treated with intravitreal faricimab injection every four weeks. Visual acuity and anatomical changes were assessed with multimodal imaging. Polarization-sensitive OCT (PS-OCT) was used to examine the polarimetric entropy, quantitative indicator of melanin distribution, at the RPE segment. Retinal sensitivity was assessed with microperimetry.
ResultsTwelve patients with MNV type 1 and seven eyes with MNV type 2 were included. Faricimab significantly improved visual acuity and central subfield thickness (p = 0.0064, < 0.0001, respectively). In MNV type 1, faricimab significantly increased mean entropy in the overall Early Treatment Diabetic Retinopathy Study (ETDRS) grid area (p = 0.0386). In the per-grid analysis, entropy of type 1 also significantly increased, whereas type 2 showed significant reduction (p = 0.0071, 0.0389, respectively). As MNV type 2 regresses, high-entropy area corresponding to MNV decreased and low-entropy area surrounding them increased (p = 0.019, 0.0058, respectively), suggesting RPE migration onto MNV. RPE entropy was significantly associated with visual acuity or retinal sensitivity after the treatment (p = 0.00475, 0.0307, respectively).
ConclusionsAfter anti-VEGF treatment for type 1 or type 2 MNV, RPE melanin distribution at the MNV and the surrounding area distinctly changed. They were associated with visual function. The present study supported deterioration of visual function in eyes with type 2 MNV after anti-VEGF treatment resulted not only from subretinal scar formation but RPE atrophy surrounding the MNV.