Reduced Macular Pigment Optical Volume Is Linked to High-Risk OCT Biomarkers and Lower Contrast Sensitivity Function in iAMD

在iAMD患者中,黄斑色素光学体积减少与高风险OCT生物标志物和较低的对比敏感度功能相关。

阅读:1

Abstract

PURPOSE: To investigate relationships among macular pigment optical volume (MPOV), optical coherence tomography (OCT) biomarkers, and contrast sensitivity (CS) measured by the quantitative contrast sensitivity function (qCSF) test in intermediate age-related macular degeneration (iAMD). METHODS: Sixty-five eyes from 34 patients with OCT-confirmed iAMD, visual acuity (VA) >20/100, and no confounding comorbidities underwent same-day qCSF testing (area under the logarithmic CS function [AULCSF], contrast acuity [CA], and CS at 1-18 cycles per degree [cpd]), MPOV imaging, and macular OCT. OCT features evaluated within the central 3-mm circle included outer nuclear layer (ONL) thickness, retinal pigment epithelium (RPE) volume, subretinal drusenoid deposits, hyporeflective drusen cores (hDCs), intraretinal hyperreflective foci, and incomplete RPE and outer retinal atrophy (iRORA). MPOV was quantified at 1°, 2°, and 9° eccentricities (plateau set at 9°). Generalized linear mixed-effects models assessed associations of MPOV with OCT biomarkers and qCSF metrics. RESULTS: Lower MPOV values were associated with reduced ONL thickness (β*, 0.343-0.424; all P < 0.01), presence of hDCs (β*, -0.80 to -0.60; all P < 0.01), and iRORA at 1° (β*, -0.43; P = 0.03). MPOV at all eccentricities was associated with lower AULCSF (β*, 0.32-0.45), CA (β*, 0.38-0.48), and CS at 3 cpd and 6 cpd (β*, 0.39-0.69; all P < 0.05), but not with VA (β*, 0.10-0.28; all P > 0.05). CONCLUSIONS: MPOV was significantly associated with high-risk OCT biomarkers and qCSF-derived CS metrics in iAMD, highlighting its potential role as a biomarker of structural integrity and functional impairment not captured by standard VA testing.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。