中度葡萄膜炎相关囊样黄斑水肿的光学相干断层血管造影。

Q2 Medicine
Leila Alizadeh Ghavidel, Farideh Mousavi, Hesam Sadat Hashemi, Masood Bagheri
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引用次数: 0

摘要

背景:囊样黄斑水肿(CME)是葡萄膜炎患者永久性视力损害的主要原因,特别是在中度葡萄膜炎(IU)患者中。本研究旨在比较IU伴黄斑无反应性CME和无黄斑水肿患者黄斑微血管的变化。方法:在本病例对照研究中,使用AngioVue OCT-A系统的光谱域光学相干断层扫描血管成像(OCT-A),对55只IU患者的黄斑微血管结构进行评估,包括血管密度、中央凹无血管区(FAZ)测量和血管形态学变化。我们将患者分为以下两组:病例组,包括30只与IU相关的无反应性CME,对照组,包括25只无黄斑水肿的IU眼。结果:病例组和对照组的参与者年龄分布(P = 0.753)和性别分布(P = 0.124)相似。与对照组相比,病例组全身毛细血管浅丛血管密度显著降低(P = 0.027),凹旁区血管密度显著降低(P = 0.001)。然而,两组在中央凹浅血管密度、深毛细血管丛血管密度、FAZ面积、FAZ周长、FAZ循环指数、FAZ周围300µm宽环内的中央凹血管密度方面,差异均无统计学意义(P > 0.05)。两组OCT-A总览图上的血管形态学改变,如毛细血管丛、毛细血管扩张或微动脉瘤,并无差异。结论:与无黄斑水肿的患者相比,iu相关性无反应性CME患者的平均浅表毛细血管丛血管密度较低。我们观察到SCP患者比DCP患者有更多的囊腔。视网膜内微囊性改变和局部缺血可能是无反应性CME的根本原因。未来对健康、匹配对照的前瞻性纵向研究有必要证实我们的发现。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Optical coherence tomography angiography in intermediate uveitis-related cystoid macular edema.

Optical coherence tomography angiography in intermediate uveitis-related cystoid macular edema.

Background: Cystoid macular edema (CME) is the leading cause of permanent visual impairment in patients with uveitis, particularly in patients with intermediate uveitis (IU). This study was aimed at comparing the changes in the macular microvasculature in patients with IU with uveitic non-responsive CME and without macular edema.

Methods: In this case-control study, 55 eyes of patients with IU were assessed for macular microvascular structures, including vascular density, foveal avascular zone (FAZ) measurement, and vascular morphological changes, using spectral-domain optical coherence tomography angiography (OCT-A) with the AngioVue OCT-A system. We divided patients into the following two groups: the case group, including 30 eyes with IU-related non-responsive CME, and the control group, including 25 eyes with IU without macular edema.

Results: Participants in the case and control groups had comparable age (P = 0.753) and sex (P = 0.124) distributions. Superficial capillary plexus vessel density in the case group was significantly decreased in the whole image (P = 0.027) and the parafoveal area (P = 0.001) compared to the control group. However, there were no statistically significant differences between the two groups in terms of foveal superficial vessel density, deep capillary plexus vessel density, FAZ area, FAZ perimeter, FAZ acircularity index, or foveal vessel density in a 300-µm-wide annulus around the FAZ (all P > 0.05). Vascular morphological changes, such as the capillary tuft, telangiectatic vessels, or micro-aneurism, were not different in the overview images of the OCT-A printout between the two groups.

Conclusions: The mean superficial capillary plexus vessel density was lower in eyes with IU-related nonresponsive CME than in those without macular edema. We observed more cystoid spaces in SCP than in DCP. Microcystic changes in the inner retina and ischemia may be the underlying cause in eyes with nonresponsive CME. Future prospective longitudinal studies with healthy, matched controls are warranted to confirm our findings.

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