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新生血管性年龄相关性黄斑变性抗血管生成治疗中视网膜色素上皮萎缩的进展

Progression of retinal pigment epithelial atrophy in antiangiogenic therapy of neovascular age-related macular degeneration.

作者信息

Schütze Christopher, Wedl Manuela, Baumann Bernhard, Pircher Michael, Hitzenberger Christoph K, Schmidt-Erfurth Ursula

机构信息

Department of Ophthalmology, Medical University of Vienna, Austria, Vienna, Austria.

Center for Medical Physics and Biomedical Engineering, Medical University of Vienna, Austria, Vienna, Austria.

出版信息

Am J Ophthalmol. 2015 Jun;159(6):1100-1114.e1. doi: 10.1016/j.ajo.2015.02.020. Epub 2015 Mar 10.

DOI:10.1016/j.ajo.2015.02.020
PMID:25769245
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4430174/
Abstract

PURPOSE

To monitor retinal pigment epithelial (RPE) atrophy progression during antiangiogenic therapy of neovascular age-related macular degeneration (AMD) over 2 years using polarization-sensitive optical coherence tomography (OCT).

DESIGN

Prospective interventional case series.

METHODS

setting: Clinical practice.

STUDY POPULATION

Thirty patients (31 eyes) with treatment-naïve neovascular AMD.

OBSERVATION PROCEDURES

Standard intravitreal therapy (0.5 mg ranibizumab) was administered monthly during the first year and pro re nata (PRN; as-needed) during the second year. Spectral-domain (SD) OCT and polarization-sensitive OCT (selectively imaging the RPE) examinations were performed at baseline and at 1, 3, 6, 12, and 24 months using a standardized protocol. RPE-related changes were evaluated using a semi-automated polarization-sensitive OCT segmentation algorithm and correlated with SD OCT and fundus autofluorescence (FAF) findings.

MAIN OUTCOME MEASURES

RPE response, geographic atrophy (GA) progression.

RESULTS

Atrophic RPE changes included RPE thinning, RPE porosity, focal RPE atrophy, and development of GA. Early RPE loss (ie, RPE porosity, focal atrophy) increased progressively during initial monthly treatment and remained stable during subsequent PRN-based therapy. GA developed in 61% of eyes at month 24. Mean GA area increased from 0.77 mm(2) at 12 months to 1.10 mm(2) (standard deviation = 1.09 mm(2)) at 24 months. Reactive accumulation of RPE-related material at the lesion borders increased until month 3 and subsequently decreased.

CONCLUSIONS

Progressive RPE atrophy and GA developed in the majority of eyes. RPE migration signifies certain RPE plasticity. Polarization-sensitive OCT specifically images RPE-related changes in neovascular AMD, contrary to conventional imaging methods. Polarization-sensitive OCT allows for precisely monitoring the sequence of RPE-related morphologic changes.

摘要

目的

使用偏振敏感光学相干断层扫描(OCT)监测新生血管性年龄相关性黄斑变性(AMD)抗血管生成治疗2年期间视网膜色素上皮(RPE)萎缩的进展情况。

设计

前瞻性干预病例系列。

方法

设置

临床实践。

研究人群

30例初治新生血管性AMD患者(31只眼)。

观察程序

第一年每月给予标准玻璃体内注射治疗(0.5mg雷珠单抗),第二年按需给药。在基线以及第1、3、6、12和24个月使用标准化方案进行光谱域(SD)OCT和偏振敏感OCT(选择性成像RPE)检查。使用半自动偏振敏感OCT分割算法评估RPE相关变化,并与SD OCT和眼底自发荧光(FAF)结果相关联。

主要观察指标

RPE反应、地图样萎缩(GA)进展。

结果

萎缩性RPE变化包括RPE变薄、RPE孔隙形成、局灶性RPE萎缩和GA的发展。早期RPE丢失(即RPE孔隙形成、局灶性萎缩)在最初每月治疗期间逐渐增加,在随后的按需治疗期间保持稳定。24个月时61%的眼发生GA。GA平均面积从12个月时的0.77mm²增加到24个月时的1.10mm²(标准差=1.09mm²)。病变边界处RPE相关物质的反应性积聚在第3个月前增加,随后减少。

结论

大多数眼中出现进行性RPE萎缩和GA。RPE迁移表明RPE具有一定的可塑性。与传统成像方法相反,偏振敏感OCT可特异性成像新生血管性AMD中RPE相关变化。偏振敏感OCT能够精确监测RPE相关形态学变化的序列。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/11cb/4430174/9f04c0d5485e/gr11.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/11cb/4430174/e81b62cf6ac1/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/11cb/4430174/0ad1c524b398/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/11cb/4430174/dc6fb215e5dd/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/11cb/4430174/59583d74f536/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/11cb/4430174/de88d8f8799f/gr7.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/11cb/4430174/6d09a2975792/gr10.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/11cb/4430174/9f04c0d5485e/gr11.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/11cb/4430174/7ad9c60e4613/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/11cb/4430174/0a18fbd4f3a2/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/11cb/4430174/e81b62cf6ac1/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/11cb/4430174/0ad1c524b398/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/11cb/4430174/dc6fb215e5dd/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/11cb/4430174/59583d74f536/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/11cb/4430174/de88d8f8799f/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/11cb/4430174/61391549dd0c/gr8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/11cb/4430174/880ecb6d58d0/gr9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/11cb/4430174/6d09a2975792/gr10.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/11cb/4430174/9f04c0d5485e/gr11.jpg

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