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抗血管内皮生长因子治疗新生血管性年龄相关性黄斑变性后患者的黄斑萎缩进展研究

Abdelfattah NS, Zhang H, Boyer DS, et al.

期刊名称:Retina

卷期:2016年第36卷第10期

摘要

目的:本研究旨在确定采用抗血管内皮生长因子治疗新生血管性年龄相关性黄斑变性超过2年后患者的黄斑萎缩(MA)进展频率,并量化该结果。研究方法:将46名确诊为湿性年龄相关性黄斑变性患者的54只眼(患者的平均年龄为86.7±6.8岁,其中女性占53.7%)纳入本项回顾性研究。将接受光动力治疗或激光治疗的患者眼排除在外。我们对基线处及治疗2年后的所有患者眼进行Cirrus谱域光学相干断层扫描成像检测,扫描模式为黄斑区512×128三维立方扫描。采用美国食品和药物管理局的cleared Advanced RPE分析软件获得每个三维数据集的光学相干断层扫描眼底图像,该分析软件通过分割面部脉络膜图像的反射率增加区域来自动识别黄斑萎缩区域。分割误差由经过训练的Doheny影像报告中心的分级人员采用一种标准化分级方案进行手动校正。并电脑计算患者在基线处及随访第2年的黄斑萎缩患病率及扩大率。随时间变化的基线人口统计学因素、类型及抗血管内皮生长因子注射次数与黄斑萎缩的发展和扩大相关。研究结果:我们注意到有32只眼在基线处存在黄斑萎缩(59.3%),并且这些患者眼在接下来的2年中发生了黄斑萎缩进展。在基线处无黄斑萎缩的28只眼睛中,2年后有6只眼发生了MA进展(在基线处无黄斑萎缩眼中占21.4%)。值得注意的是,在整个研究过程中有22只眼从未发生过黄斑萎缩(占总患者眼的40.7%)。在基线处有黄斑萎缩的眼中,MA的年增长率为0.89±0.93mm。我们采用多元回归分析来评估性别、年龄、吸烟状况、药物注射和注射次数对MA的影响。除总注射次数(R = 0.3,P<0.01)外,所有研究变量不能明显地预测MA发展或进展(F [ 0.73,13 ] = 0.378,P = 0.86,R = 0.05)。但该研究也不能考察较小的影响因素。研究结论:采用抗血管内皮生长因子治疗湿性年龄相关性黄斑变性前后,患者的黄斑萎缩均较为常见。在开始抗血管内皮生长因子治疗后,新型光学相干断层扫描技术确定的黄斑萎缩频率(第2年为21%)与CATT、IVAN、和HARBOR报道的频率接近。MA扩大的几率与注射次数呈正相关,但没有出现该几率大于所报道的在无脉络膜新生血管情况下黄斑萎缩扩大几率的案例。

PURPOSE:To define the frequency and quantify the progression of macular atrophy (MA) in patients with neovascular age-related macular degeneration undergoing treatment with antivascular endothelial growth factor therapy for >2 years.METHODS:Fifty-four eyes of 46 patients (86.7 ± 6.8 years, 53.7% women) diagnosed with wet age-related macular degeneration were included in this retrospective study. Eyes that received photodynamic therapy or laser treatment were excluded. All eyes were imaged at baseline and after 2 years with the Cirrus spectral domain optical coherence tomography using a 512 × 128 macular cube scan protocol centered on the fovea. Optical coherence tomography en face fundus images were obtained for each 3-dimensional data set using the U.S. Food and Drug Administration-cleared Advanced RPE Analysis software, which automatically identifies atrophic areas by segmenting regions of increased reflectivity in en face choroidal slab images. Segmentation errors were manually corrected by trained Doheny Image Reading Center graders using a standardized grading protocol. The prevalence rates of atrophy at baseline and at 2-years follow-up and enlargement rates were computed. Baseline demographic factors and types and numbers of antivascular endothelial growth factor injections received over time were correlated with the development and enlargement of atrophy.RESULTS:Macular atrophy was noted at baseline in 32 (59.3%) eyes and progressed in all eyes over the next 2 years. Among the 28 eyes without atrophy at baseline, MA developed by 2 years in 6 eyes (21.4% of eyes without MA at baseline). Of note, 22 eyes (40.7% of overall cohort) never developed atrophy during the course of the study. Among eyes with atrophy at baseline, the annual growth rate of MA was found to be 0.89 ± 0.93 mm. A multiple regression analysis was performed to evaluate the influence of gender, age, smoking status, medication injected, and number of injections on MA. Except for the number of total injections (R = 0.3, P < 0.01), the studied variables could not significantly predict development or progression of MA (F [0.73, 13] = 0.378, P = 0.86, R = 0.05). However, the study was not powered to detect small effects.CONCLUSION:Macular atrophy is a frequent finding in eyes with wet age-related macular degeneration both before and after antivascular endothelial growth factor therapy. The frequency of new optical coherence tomography-defined atrophy (21% at 2 years) after starting therapy was close to the rates reported in CATT, IVAN, and HARBOR. The rate of MA enlargement was positively correlated with the number of injections, but did not appear to be greater than that reported for atrophy in the absence of choroidal neovascularization.


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