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抗 VEGF 药物和地塞米松植入物治疗糖尿病黄斑水肿患者后 SD-OCT 可检测到的高反射焦点的行为。

Behavior of SD-OCT Detectable Hyperreflective Foci in Diabetic Macular Edema Patients after Therapy with Anti-VEGF Agents and Dexamethasone Implants.

机构信息

Department of Ophthalmology, Charité Universtätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin and Berlin Institute of Health, Germany.

Berlin Institute of Health (BIH), Berlin, Germany.

出版信息

J Diabetes Res. 2021 Apr 13;2021:8820216. doi: 10.1155/2021/8820216. eCollection 2021.

DOI:10.1155/2021/8820216
PMID:33937416
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8060103/
Abstract

PURPOSE

Diabetic macular edema (DME) is the most common cause of blindness in the working-age population. Spectral-domain optical coherence tomography (SD-OCT) allows detection and monitoring of the edema and a detailed analysis of the retinal structure. Hyperreflective foci (HF) are small, circumscribed lesions on OCT, and their origin is yet to be determined. Our study was aimed to shed light on HF pathophysiology, by analyzing their number and location in DME patients at baseline and after therapy.

METHODS

A prospective, observational study on 59 eyes of 51 DME patients who were treated with antivascular endothelial growth factor (VEGF) therapy (VEGF group, = 40 eyes) or dexamethasone implant (DEX group, = 19). HF and hard exudates (HE) were discriminated by their appearance on fundus photographs and their size on OCT. Quantity and location of HF and HE were analyzed at baseline and after therapy.

RESULTS

DME decreased in 75% of patients in the VEGF (455.5 m vs. 380.8 m, = 0.02) and in 95% of patients in the DEX group (471.6 m vs. 381.9 m, = 0.007). The number of foci decreased in 62.5% of patients after anti-VEGF (130.6 vs. 111.1, = 0.07) and in 68% of patients after dexamethasone injection ((123.4 vs. 94.9, = 0.02) 5.1). A subgroup of 15% of eyes, all treated with anti-VEGF, showed accumulation of larger HF in outer retinal layers to visible HE during DME resolution, whereas smaller HF, found in all retinal layers, remained unchanged. There was a trend towards a dynamic shift of the foci from inner to outer retinal layers.

CONCLUSION

The dynamic rearrangement of the small HF and their slightly greater reduction after anti-inflammatory therapy suggest inflammatory cells as their origin, whereas larger HF in the outer retinal layers correspond to microexudates. Furthermore, we found a more favourable outcome in patients with HF after treatment with dexamethasone implants compared to anti-VEGF agents.

摘要

目的

糖尿病性黄斑水肿(DME)是工作年龄人群失明的最常见原因。频域光相干断层扫描(SD-OCT)可检测和监测水肿,并对视网膜结构进行详细分析。高反射病灶(HF)是 OCT 上的小而局限的病变,其起源尚不清楚。我们的研究旨在通过分析 DME 患者基线和治疗后的 HF 数量和位置,阐明 HF 的病理生理学。

方法

对 51 例 DME 患者的 59 只眼进行前瞻性观察研究,这些患者接受了抗血管内皮生长因子(VEGF)治疗(VEGF 组,=40 只眼)或地塞米松植入(DEX 组,=19 只眼)。通过眼底照片上的外观和 OCT 上的大小来区分 HF 和硬性渗出物(HE)。在基线和治疗后分析 HF 和 HE 的数量和位置。

结果

VEGF 组 75%(455.5μm 比 380.8μm,=0.02)和 DEX 组 95%(471.6μm 比 381.9μm,=0.007)的 DME 减少。抗 VEGF 治疗后,62.5%(130.6 比 111.1,=0.07)和地塞米松注射后 68%(123.4 比 94.9,=0.02)的患者病灶数量减少。在 15%的眼亚组中,所有接受抗 VEGF 治疗的眼均在外视网膜层出现较大 HF 积聚,可见 HE 在 DME 消退过程中,而所有视网膜层中的较小 HF 保持不变。病灶有从内向外层视网膜动态转移的趋势。

结论

小 HF 的动态重新排列及其在抗炎治疗后略有减少表明其起源是炎症细胞,而外层视网膜中的较大 HF 则对应于微渗出物。此外,我们发现 HF 患者在接受地塞米松植入物治疗后的结果比接受抗 VEGF 药物治疗的结果更有利。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e3a/8060103/918dddca5b34/JDR2021-8820216.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e3a/8060103/74cedc51845c/JDR2021-8820216.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e3a/8060103/250ee05825ef/JDR2021-8820216.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e3a/8060103/e727248c5e14/JDR2021-8820216.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e3a/8060103/50cb6bc42c85/JDR2021-8820216.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e3a/8060103/aacaf9b8e495/JDR2021-8820216.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e3a/8060103/918dddca5b34/JDR2021-8820216.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e3a/8060103/74cedc51845c/JDR2021-8820216.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e3a/8060103/250ee05825ef/JDR2021-8820216.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e3a/8060103/e727248c5e14/JDR2021-8820216.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e3a/8060103/50cb6bc42c85/JDR2021-8820216.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e3a/8060103/aacaf9b8e495/JDR2021-8820216.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e3a/8060103/918dddca5b34/JDR2021-8820216.006.jpg

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