Hata, M., Yamashiro, K., Oishi, A., et al.
网膜 内皮 血管瘤
摘要：目的：旨在探讨抗血管内皮生长因子（VEGF）治疗视网膜血管瘤性增生过程中视网膜色素上皮（retinal pigment epithelial，RPE）萎缩的发生率及危险因素。方法：这项研究包括46只初治性视网膜血管瘤性增生眼。所有患者均接受雷珠单抗或阿柏西普注射治疗。评估彩色眼底摄影，光谱域光学相干断层扫描和眼底自发荧光检查进行RPE萎缩诊断。分析ARMS2 A69S和CFH I62V的基线特征和基因多态性与RPE萎缩发展和进展的相关性。结果：雷珠单抗治疗的21只基线时无RPE萎缩眼中，5只眼（23.8％）在12个月时发生RPE萎缩。20只使用阿柏西普但没有RPE萎缩眼中，12个月时10只眼（50.0％）出现RPE萎缩。基线时的折光性玻璃膜疣与12个月时的RPE萎缩相关（P = 0.014），RPE萎缩区域的进展速度与基底膜下脉络膜厚度呈负相关（R = -0.595，P = 0.019）。基因多态性与视网膜色素上皮萎缩无关。结论：抗VEGF治疗视网膜血管瘤性增生12个月后，视网膜色素上皮萎缩发生率为36.6％。基线时折光性玻璃疣的存在被确定为RPE萎缩发展的新显著风险因素。
PURPOSE:To investigate the incidence rate and risk factors for development of retinal pigment epithelial (RPE) atrophy during anti-vascular endothelial growth factor (anti-VEGF) treatment for retinal angiomatous proliferation.METHODS:This study included 46 eyes with treatment-naive retinal angiomatous proliferation. All patients were treated with ranibizumab or aflibercept injections. Color fundus photography, spectral-domain optical coherence tomography, and fundus autofluorescence were evaluated for RPE atrophy diagnosis. Baseline characteristics and gene polymorphisms of ARMS2 A69S, and CFH I62V were analyzed for association with development and progression of RPE atrophy.RESULTS:Among 21 eyes treated with ranibizumab without preexisting RPE atrophy at baseline, 5 eyes (23.8%) developed RPE atrophy at 12 months. Among 20 eyes treated with aflibercept without preexisting RPE atrophy at baseline, 10 eyes (50.0%) developed RPE atrophy at 12 months. Refractile drusen at baseline was associated with RPE atrophy development at 12 months (P = 0.014), and the progression rate of RPE atrophy area was negatively correlated with subfoveal choroidal thickness at baseline (R = -0.595, P = 0.019). Gene polymorphisms were not associated with RPE atrophy.CONCLUSION:Retinal pigment epithelial atrophy developed in 36.6% during 12 months after anti-VEGF treatment for retinal angiomatous proliferation. The presence of refractile drusen at baseline was identified as a novel significant risk factor for RPE atrophy development.