背景:年龄相关性黄斑变性(AMD)是老年人中常见的视网膜退行性疾病。淀粉样沉积物,大脑淀粉样血管病(CAA)的标志,可能参与了AMD的发病机制。由于淀粉样蛋白沉积物可能有助于AMD和CAA的发展,我们假设AMD患者的CAA患病率较高.
目的:比较年龄匹配的AMD患者的CAA患病率。
方法:我们进行了横截面,1:1年龄匹配,2011年至2015年在梅奥诊所接受视网膜光学相干断层扫描和脑MRI检查的≥40岁患者的病例对照研究.主要因变量是可能的CAA,浅表铁质沉着症,脑叶和深部脑微出血(CMBs)。使用多变量逻辑回归评估AMD和CAA之间的关系,并在AMD严重程度之间进行比较(无与早期和晚期AMD)。
结果:我们的分析包括256对年龄匹配的对(AMD126,无AMD130)。在那些有AMD的人中,79(30.9%)患有早期AMD,47(19.4%)患有晚期AMD。平均年龄为75±9岁,两组之间的血管危险因素没有显着差异。AMD患者的CAA患病率较高(16.7%vs10.0%,p=0.116)和浅表铁质沉着症(15.1%vs6.2%,p=0.020),但不是深度CMB(5.2%对6.2%,p=0.426),与没有AMD的人相比。在调整协变量后,晚期AMD与CAA(OR2.83,95%CI1.10-7.27,p=0.031)和浅表铁质沉着(OR3.40,95CI1.20-9.65,p=0.022)的几率增加有关,但不是深CMB(OR0.7,95CI0.14-3.51,p=0.669)。
结论:AMD与CAA和浅表铁质沉着症有关,但与深层CMB无关,与淀粉样蛋白沉积在AMD的发展中起作用的假设一致。需要进行前瞻性研究以确定AMD的特征是否可以作为早期诊断CAA的生物标志物。
BACKGROUND: Age-related macular degeneration (AMD) is a common retinal degenerative disorder among older individuals. Amyloid deposits, a hallmark of cerebral amyloid angiopathy (CAA), may be involved in the pathogenesis of AMD. Since amyloid deposits may contribute to the development of both AMD and CAA, we hypothesized that patients with AMD have a higher prevalence of CAA.
OBJECTIVE: To compare the prevalence of CAA in patients with or without AMD matched for age.
METHODS: We conducted a cross-sectional, 1:1 age-matched,
case-control study of patients ≥40 years of age at the Mayo Clinic who had undergone both retinal optical coherence tomography and brain MRI from 2011 to 2015. Primary dependent variables were probable CAA, superficial siderosis, and lobar and deep cerebral microbleeds (CMBs). The relationship between AMD and CAA was assessed using multivariable logistic regression and was compared across AMD severity (none vs early vs late AMD).
RESULTS: Our analysis included 256 age-matched pairs (AMD 126, no AMD 130). Of those with AMD, 79 (30.9%) had early AMD and 47 (19.4%) had late AMD. The mean age was 75±9 years, and there was no significant difference in vascular risk factors between groups. Patients with AMD had a higher prevalence of CAA (16.7% vs 10.0%, p=0.116) and superficial siderosis (15.1% vs 6.2%, p=0.020), but not deep CMB (5.2% vs 6.2%, p=0.426), compared to those without AMD. After adjusting for covariates, having late AMD was associated with increased odds of CAA (OR 2.83, 95% CI 1.10-7.27, p=0.031) and superficial siderosis (OR 3.40, 95%CI 1.20-9.65, p=0.022), but not deep CMB (OR 0.7, 95%CI 0.14-3.51, p=0.669).
CONCLUSIONS: AMD was associated with CAA and superficial siderosis but not deep CMB, consistent with the hypothesis that amyloid deposits play a role in the development of AMD. Prospective studies are needed to determine if features of AMD may serve as biomarkers for the early diagnosis of CAA.