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光学相干断层扫描生物标志物在接受白内障手术联合玻璃体内注射地塞米松植入物的持续性糖尿病黄斑水肿患者中的预测价值

Predictive Value of Optical Coherence Tomography Biomarkers in Patients with Persistent Diabetic Macular Edema Undergoing Cataract Surgery Combined with a Dexamethasone Intravitreal Implant.

作者信息

Fasolino Giuseppe, Lazaar Maryam, Della Rocca Domenico Giovanni, Oellerich Silke, Ní Dhubhghaill Sorcha

机构信息

Department of Ophthalmology, University Hospital Brussels, Laarbeeklaan 101, 1090 Jette, Belgium.

Department of Medicine and Pharmacy, Vrije Universiteit Brussel (VUB), 1090 Brussels, Belgium.

出版信息

Bioengineering (Basel). 2025 May 21;12(5):556. doi: 10.3390/bioengineering12050556.

DOI:10.3390/bioengineering12050556
PMID:40428175
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12109151/
Abstract

Diabetic macular edema (DME) is the most common cause of vision loss among diabetic patients. The first-line treatments for DME are anti-vascular endothelial growth factor (VEGF)-drugs, while intravitreal steroids are generally reserved for second-line treatment. Limited data exist on the role of optical coherence tomography (OCT) biomarkers as predictors of success in non-responders to anti-VEGF treatment undergoing simultaneous cataract surgery and dexamethasone intravitreal implant (DEX-I). This study was designed as a retrospective analysis of patients with DME who were refractory to anti-VEGF treatment but underwent cataract surgery and received a DEX-I at the time of surgery. All procedures were performed between May 2021 and February 2024. The best-corrected visual acuity (BCVA) and central subfoveal thickness (CST) were recorded at baseline and at 1 week, 1 month, and 3 months. The following OCT-based biomarkers were also collected: ellipsoid zone (EZ) integrity, disorganization of the retinal inner layers (DRIL), CST, and hyperreflective foci (HRF). Correlations between the baseline biomarkers and the anatomical outcome were analyzed using linear mixed models (LMMs). Eleven patients (eighteen eyes) met the inclusion criteria. The mean CST decreased significantly from 469.4 ± 53.8 µm at baseline, to 373.1 ± 34.7 µm at 1 week ( = 0.002) and 354.4 ± 24.1 µm at 1 month ( = 0.011). The mean BCVA improved significantly from 0.47 LogMAR to 0.33 LogMAR at 1 week ( = 0.001), 0.23 LogMAR at 1 month ( < 0.001), and 0.25 LogMAR at 3 months ( < 0.001). Baseline predictors significantly influencing CST included the presence of DRIL, a disrupted/absent EZ, and a higher CST. The administration of DEX-I for DME refractory to anti-VEGF treatment in patients undergoing cataract surgery promoted functional improvements persisting longer than the anatomical ones. Patients presenting with DRIL, disrupted EZ, and higher CST at baseline may be better candidates for the combination of DEX-I and cataract surgery.

摘要

糖尿病性黄斑水肿(DME)是糖尿病患者视力丧失的最常见原因。DME的一线治疗药物是抗血管内皮生长因子(VEGF)药物,而玻璃体内注射类固醇通常用于二线治疗。关于光学相干断层扫描(OCT)生物标志物作为接受白内障手术和玻璃体内注射地塞米松植入物(DEX-I)的抗VEGF治疗无反应者治疗成功预测指标的作用,现有数据有限。本研究旨在对DME患者进行回顾性分析,这些患者对抗VEGF治疗无效,但接受了白内障手术,并在手术时接受了DEX-I。所有手术均在2021年5月至2024年2月期间进行。在基线、1周、1个月和3个月时记录最佳矫正视力(BCVA)和中心凹下厚度(CST)。还收集了以下基于OCT的生物标志物:椭圆体带(EZ)完整性、视网膜内层紊乱(DRIL)、CST和高反射灶(HRF)。使用线性混合模型(LMM)分析基线生物标志物与解剖学结果之间的相关性。11名患者(18只眼)符合纳入标准。平均CST从基线时的469.4±53.8µm显著下降至1周时的373.1±34.7µm(P = 0.002)和1个月时的354.4±24.1µm(P = 0.011)。平均BCVA从基线时的0.47 LogMAR显著提高至1周时的0.33 LogMAR(P = 0.001)、1个月时的0.23 LogMAR(P < 0.001)和3个月时的0.25 LogMAR(P < 0.001)。显著影响CST的基线预测因素包括DRIL的存在、EZ的破坏/缺失以及较高的CST。对于接受白内障手术的抗VEGF治疗难治性DME患者,给予DEX-I可促进功能改善,且功能改善持续时间长于解剖学改善。基线时出现DRIL、EZ破坏和CST较高的患者可能是DEX-I与白内障手术联合治疗的更好候选者。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f522/12109151/0275331f096f/bioengineering-12-00556-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f522/12109151/6f30bbae87a9/bioengineering-12-00556-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f522/12109151/037214634e42/bioengineering-12-00556-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f522/12109151/117e0c552e30/bioengineering-12-00556-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f522/12109151/0275331f096f/bioengineering-12-00556-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f522/12109151/6f30bbae87a9/bioengineering-12-00556-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f522/12109151/037214634e42/bioengineering-12-00556-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f522/12109151/117e0c552e30/bioengineering-12-00556-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f522/12109151/0275331f096f/bioengineering-12-00556-g004.jpg

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