Fundus Autofluorescence in Neovascular Age-Related Macular Degeneration: A Clinicopathologic Correlation Relevant to Macular Atrophy.

Fundus Autofluorescence in Neovascular Age-Related Macular Degeneration: A Clinicopathologic Correlation Relevant to Macular Atrophy.
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DOI:
10.1016/j.oret.2021.01.012
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发表时间:
2021-11
影响因子:
4.5
通讯作者:
Curcio, Christine A.
Curcio, Christine A.
中科院分区:
其他
文献类型:
--
作者:
Chen, Ling;Messinger, Jeffrey D.;Ferrara, Daniela;Freund, K. Bailey;Curcio, Christine A.

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尽管抗血管生成药物治疗成功,但视网膜色素上皮 (RPE) 和光感受器的黄斑萎缩 (MA) 会导致新生血管性年龄相关性黄斑变性 (nAMD) 患者视力丧失。为了加深对 MA 的理解,强化眼底自发荧光 (FAF) 成像的细胞基础,并为 nAMD 的管理提供信息,我们对一只眼睛进行了组织学分析,采用多模式临床成像和由于 nAMD 导致的明显先前渗出。病例研究和临床病理学相关性。一名白人女性,使用 FAF 和光学相干断层扫描 (OCT) 对 AMD 发现的非活动性视网膜下纤维化(右眼)进行了 9 年的随访,没有检测到视网膜下液体或其他反复渗出,并且在 90 岁死亡之前没有进行玻璃体内注射。死后 6.25 小时保存右眼,后固定在单宁酸锇对苯二胺中,并准备亚微米环氧树脂切片(n = 115),其中 19 个与临床 OCT B 扫描相匹配。光显微形态的高自发荧光 (hyperFAF) 区域归因于先前的渗出(“洪泛区”hyperFAF)、MA 的低自发荧光 (hypoFAF) 斑点以及不明显的 FAF 区域。在 9 年的随访中,洪泛区 hyperFAF 一直可见,随着时间的推移,其中有几个 hyperFAF 萎缩点不断扩大。 hyperFAF 模式对应于 OCT 上的外层视网膜萎缩 (ORA) 以及组织学上变形但连续的 RPE 上的光感受器丧失。洪泛区内的hypoFAF斑点对应于OCT上的完全视网膜色素上皮(RPE)和外层视网膜萎缩(cRORA)以及组织学上的光感受器和RPE的损失。相比之下,不显着的 FAF 区域显示出连续的 RPE,并伴有全长光感受器和厚的外核层。 FAF 成像的这种直接临床病理学相关性对于 nAMD 来说是首次。 FAF 是一种投影图像,涉及光感受器的光信号调制以及 RPE 中的发射信号源。 HyperFAF 归因于渗出性洪泛区,意味着连续 RPE 上的光感受器损失。 MA 中的 HypoFAF 表示两个细胞层均丢失。 FAF 成像应使用 OCT 提供的多层视角进行解释,以获得最大价值。预防 nAMD 渗出可能会保护光感受器。对患有新生血管性年龄相关性黄斑变性的眼睛的组织学分析表明,过度自发荧光意味着光感受器的丧失,这归因于先前的渗出和视网膜色素上皮连续层的光学暴露。
Macular atrophy (MA) of retinal pigment epithelium (RPE) and photoreceptors leads to vision loss in neovascular age-related macular degeneration (nAMD) despite successful treatment with anti-angiogenic agents. To enhance understanding of MA, fortify the cellular basis of fundus autofluorescence (FAF) imaging, and inform management of nAMD, we performed histological analysis of an eye with multimodal clinical imaging and apparent prior exudation due to nAMD. Case study and clinicopathologic correlation. A white woman in whom AMD findings of inactive subretinal fibrosis (right eye) were followed for 9 years using FAF and optical coherence tomography (OCT), with no detectable subretinal fluid or other recurrent exudation, and no intravitreal injections before death at age 90 years. The right eye was preserved 6.25 hours after death, post-fixed in osmium tannic acid paraphenylenediamine, and prepared for sub-micrometer epoxy resin sections (n=115), with 19 matched to clinical OCT B-scans. Light microscopic morphology of a hyperautofluorescent (hyperFAF) area attributed to prior exudation (“floodplain” hyperFAF), hypoautofluorescent (hypoFAF) spots of MA, and areas of unremarkable FAF. Floodplain hyperFAF was visible throughout the 9 years follow-up, with several hypoFAF atrophic spots expanding within it over time. The hyperFAF pattern corresponded to outer retinal atrophy (ORA) on OCT and photoreceptor loss over dysmorphic yet continuous RPE in histology. The hypoFAF spots inside the floodplain corresponded to complete retinal pigment epithelium (RPE) and outer retinal atrophy (cRORA) on OCT and loss of both photoreceptors and RPE in histology. In contrast, areas of unremarkable FAF showed continuous RPE accompanied by full-length photoreceptors and a thick outer nuclear layer. This direct clinicopathologic correlation for FAF imaging is the first for nAMD. FAF is a projection image that involves optical signal modulation by photoreceptors as well as emission signal sources in RPE. HyperFAF attributed to an exudative floodplain signifies loss of photoreceptors over continuous RPE. HypoFAF in MA signifies loss of both cell layers. FAF imaging should be interpreted with the multilayer perspective provided by OCT for maximal value. Prevention of exudation in nAMD may preserve photoreceptors. Histologic analysis of an eye with neovascular age-related macular degeneration reveals that hyperautofluorescence signifies loss of photoreceptors, attributed to prior exudation, and optical unmasking of a continuous layer of retinal pigment epithelium.
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