Centre for Vision Research, Department of Ophthalmology, and Westmead Millennium Institute, University of Sydney, Sydney, Australia.
Centre for Vision Research, Department of Ophthalmology, and Westmead Millennium Institute, University of Sydney, Sydney, Australia; Centre for Eye Research Australia, Melbourne University, Melbourne, Australia.
Ophthalmology. 2014 Apr;121(4):917-25. doi: 10.1016/j.ophtha.2013.10.043. Epub 2013 Dec 12.
To assess the 15-year incidence and progression of reticular drusen and associations of this lesion with age-related macular degeneration (AMD) risk factors.
Population-based cohort.
Blue Mountains Eye Study participants (n = 3654) 49 years of age and older attended baseline examinations; of these, 75.8%, 76.7%, and 56.1% of survivors attended 5-year, 10-year, and 15-year follow-up examinations, respectively.
Color retinal photographs were obtained and comprehensive questionnaires were administered at each visit, and DNA samples were genotyped. Fundus autofluorescence images were not available. Reticular drusen identified from photographs were confirmed with side-by-side grading using the Wisconsin AMD grading protocol. Incidence was assessed using Kaplan-Meier product limit survival methods, controlling for competing risk of death. Associations between smoking, fish consumption, serum lipids, systemic and dietary factors, the CFH single nucleotide polymorphism (SNP) rs1061170 and ARMS2 SNP rs10490924, and the 15-year incidence of reticular drusen were analyzed in discrete logistic regression models. Generalized estimating equation models were used to analyze eye-specific relationships between these risk factors and 5-year progression from reticular drusen to late AMD.
Incidence and progression of reticular drusen.
The 15-year cumulative incidence of reticular drusen was 4.0% (n = 95). Increasing age (per decade increase; odds ratio [OR], 3.4; 95% confidence interval [CI], 2.6-4.4), female sex (OR, 2.0; 95% CI, 1.3-3.2), and presence of risk alleles of CFH-rs1061170 (OR, 1.8; 95% CI, 1.3-2.4) or ARMS2-rs10490924 (OR, 3.0; 95% CI, 2.1-4.4) were associated with higher reticular drusen incidence. Current smoking at baseline predicted higher reticular drusen incidence (OR 2.1, 95% CI 1.0-4.5) after adjusting for age, sex, CFH-rs1061170 and ARMS2-rs10490924 polymorphisms. Of 118 eyes with reticular drusen, 40 (33.9%) developed late AMD over 5 years. A higher proportion of eyes with reticular drusen located outside versus within the macular area progressed to late AMD (50.0% vs. 37.8%). Dietary lutein-zeaxanthin intake was associated with decreased likelihood of progression from reticular drusen to late AMD (adjusted OR, 0.5; 95% CI, 0.3-1.0).
Known AMD risk factors were associated with greater long-term risk of reticular drusen. Neither total area nor central location of reticular drusen predicted 5-year progression to late AMD. Increased consumption of lutein-zeaxanthin predicted a lower risk of progression.
评估网状玻璃膜疣的 15 年发生率和进展情况,以及该病变与年龄相关性黄斑变性(AMD)危险因素的关系。
基于人群的队列研究。
参加蓝山眼研究的 3654 名 49 岁及以上的参与者参加了基线检查;其中,75.8%、76.7%和 56.1%的幸存者分别参加了 5 年、10 年和 15 年的随访检查。
在每次就诊时均获取彩色视网膜照片并进行全面问卷调查,并进行 DNA 基因分型。未获得眼底自发荧光图像。使用威斯康星州 AMD 分级方案对照片中确定的网状玻璃膜疣进行并排分级以确认。采用 Kaplan-Meier 乘积限生存方法评估发病率,同时控制死亡的竞争风险。采用离散逻辑回归模型分析吸烟、鱼类摄入、血清脂质、全身和饮食因素、CFH 单核苷酸多态性(SNP)rs1061170 和 ARMS2 SNP rs10490924 与网状玻璃膜疣 15 年发生率之间的关系。采用广义估计方程模型分析这些危险因素与 5 年内从网状玻璃膜疣向晚期 AMD 进展的眼部特异性关系。
网状玻璃膜疣的发生率和进展情况。
网状玻璃膜疣的 15 年累积发生率为 4.0%(n=95)。年龄每增加 10 年(比值比[OR],3.4;95%置信区间[CI],2.6-4.4)、女性(OR,2.0;95%CI,1.3-3.2)、CFH-rs1061170 风险等位基因(OR,1.8;95%CI,1.3-2.4)或 ARMS2-rs10490924(OR,3.0;95%CI,2.1-4.4)存在与更高的网状玻璃膜疣发生率相关。在调整年龄、性别、CFH-rs1061170 和 ARMS2-rs10490924 多态性后,基线时的吸烟状态预测了更高的网状玻璃膜疣发生率(OR 2.1,95%CI 1.0-4.5)。在 118 只患有网状玻璃膜疣的眼中,有 40 只(33.9%)在 5 年内发展为晚期 AMD。位于黄斑区外而非黄斑区内的眼进展为晚期 AMD 的比例更高(50.0%比 37.8%)。网状玻璃膜疣位于黄斑区外而非黄斑区内的眼进展为晚期 AMD 的比例更高(50.0%比 37.8%)。饮食中叶黄素-玉米黄质摄入量与从网状玻璃膜疣进展为晚期 AMD 的可能性降低有关(调整后的 OR,0.5;95%CI,0.3-1.0)。
已知的 AMD 危险因素与网状玻璃膜疣的长期高风险相关。网状玻璃膜疣的总面积和中央位置均不能预测 5 年内进展为晚期 AMD。叶黄素-玉米黄质摄入量增加可降低进展为晚期 AMD 的风险。