Department of Ophthalmology, Perelman School of Medicine, University of Pennsylvania, Philadelphia.
Duke Eye Center, Duke University Medical Center, Durham, North Carolina.
JAMA Ophthalmol. 2014 Aug;132(8):915-21. doi: 10.1001/jamaophthalmol.2014.1019.
Although anti-vascular endothelial growth factor treatment of neovascular age-related macular degeneration (AMD) results in improved vision overall, loss of substantial vision can occur. Understanding the processes that lead to loss of vision may lead to preventive strategies.
To determine the incidence, characteristics, causes, and baseline predictors of sustained visual acuity loss after 2 years of treatment with ranibizumab or bevacizumab for neovascular AMD.
DESIGN, SETTING, AND PARTICIPANTS: A cohort study within a randomized clinical trial of participants in the Comparison of Age-Related Macular Degeneration Treatments Trials (CATT).
Participants were randomly assigned to treatment with ranibizumab or bevacizumab and to 2 years of monthly or as needed injections or monthly injections for 1 year and as needed injections the following year.
Sustained visual acuity loss, defined as loss of 15 or more letters from baseline at weeks 88 and 104.
Among 1030 participants, 61 eyes (5.9%) developed sustained visual acuity loss in 2 years. Within this group, visual acuity decreased gradually over time, with a mean decrease of 2, 19, and 33 letters from baseline at 4 weeks, 1 year, and 2 years, respectively. At 2 years, eyes with sustained visual acuity loss had more scarring (60.0% vs 41.4%, P = .007), more geographic atrophy (GA) (31.6% vs 20.7%, P = .004), larger lesions (16 vs 8 mm2, P < .001), and higher proportions of intraretinal fluid (82.5% vs 51.0%, P < .001), subretinal hyperreflective material (84.5% vs 44.2%, P < .001), retinal thinning (43.3% vs 23.0%, P < .001), and thickening (20.0% vs 12.1%, P < .001). Likely causes of sustained visual acuity loss included foveal scarring (44.3%), pigmentary abnormalities (27.9%), and foveal GA (11.5%). Baseline factors independently associated with a higher incidence of sustained visual acuity loss were the presence of nonfoveal GA (odds ratio [OR], 2.86; 95% CI, 1.35-6.08; P = .006), larger area of choroidal neovascularization (OR for a >4-disc area vs ≤1-disc area, 3.91; 95% CI, 1.70-9.03; P = .007), and bevacizumab treatment (OR, 1.83; 95% CI, 1.07-3.14; P = .03).
Sustained visual acuity loss was relatively rare in CATT. The development of foveal scar, pigmentary abnormalities, or GA contributed to most of the sustained visual acuity loss. Risk was 3% higher among eyes treated with bevacizumab. Treatment that targeted the prevention of scarring or GA may improve vision outcomes.
clinicaltrials.gov Identifier: NCT00593450.
尽管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（AMD）总体上可改善视力，但仍可能出现大量视力丧失。了解导致视力丧失的过程可能会导致预防策略的出现。
确定雷珠单抗或贝伐单抗治疗新生血管性 AMD 2 年后持续性视力丧失的发生率、特征、原因和基线预测因素。
设计、地点和参与者：参与者为比较年龄相关性黄斑变性治疗试验（CATT）中的随机临床试验的队列研究。
参与者被随机分配接受雷珠单抗或贝伐单抗治疗，并接受每月或按需注射或每月注射 1 年，随后每年按需注射。
持续性视力丧失，定义为在第 88 周和第 104 周时与基线相比视力丧失 15 个或更多字母。
在 1030 名参与者中，61 只眼（5.9%）在 2 年内出现持续性视力丧失。在这一组中，视力逐渐下降，分别在 4 周、1 年和 2 年时与基线相比，平均视力下降 2、19 和 33 个字母。在 2 年时，持续性视力丧失的眼睛有更多的瘢痕（60.0%比 41.4%，P =.007）、更多的地理性萎缩（GA）（31.6%比 20.7%，P =.004）、更大的病变（16 毫米比 8 毫米²，P <.001）、更多的视网膜内液（82.5%比 51.0%，P <.001）、视网膜下高反射物质（84.5%比 44.2%，P <.001）、视网膜变薄（43.3%比 23.0%，P <.001）和增厚（20.0%比 12.1%，P <.001）。持续性视力丧失的可能原因包括中心凹瘢痕（44.3%）、色素异常（27.9%）和中心凹 GA（11.5%）。与持续性视力丧失发生率较高相关的基线因素包括存在非中心凹 GA（优势比[OR]，2.86；95%置信区间，1.35-6.08；P =.006）、脉络膜新生血管面积较大（与 ≤1 个视盘面积相比，>4 个视盘面积的 OR，3.91；95%置信区间，1.70-9.03；P =.007）和贝伐单抗治疗（OR，1.83；95%置信区间，1.07-3.14；P =.03）。
在 CATT 中，持续性视力丧失相对少见。中心凹瘢痕、色素异常或 GA 的发展导致了大部分持续性视力丧失。接受贝伐单抗治疗的眼睛风险增加 3%。针对预防瘢痕或 GA 的治疗可能会改善视力结果。
clinicaltrials.gov 标识符：NCT00593450。
