Abstract
Purpose: The aim was to investigate the effect and underlying mechanism of anti-vascular endothelial growth factor (anti-VEGF) in diabetic macular edema (DME) by optical coherence tomography angiography (OCTA).Methods: Twenty-five eyes in 18 treatment-naïve patients with DME were included. All eyes were imaged by OCTA at baseline and 1 week after monthly intravitreal aflibercept injection (IAI). Visual acuity was measured as best corrected visual acuity (BCVA). Additional parameters were evaluated by OCTA, including central macular thickness (CMT), the number of hyperreflective foci (HRF), foveal avascular zone (FAZ), vessel density (VD) in the deep capillary plexus (DCP), the en-face area of cystoid edema in DCP segmentation, and subretinal fluid (SRF) height.Results: The mean time between baseline and final follow-up by OCTA was 79.24 ± 38.15 (range, 28–163) days. Compared with baseline, BCVA was increased significantly after the 3rd IAI, while CMT was decreased significantly from the 1st IAI. SRF height and the area of cystoid edema in DCP segmentation were decreased significantly after the 2nd IAI compared with baseline. The number of HRF was decreased significantly after the 1st IAI (8.87 ± 9.38) compared with baseline (11.22 ± 10.63). However, FAZ’s area and perimeter as well as VD in DCP showed no significant changes post-treatment.Conclusion: Anti-VEGF is effective in treating DME, improving visual acuity and decreasing macular edema. The decreased HRF indicates anti-inflammatory effects of aflibercept to deactivate retinal microglia/macrophages. The decreased cystoid edema and SRF height indicated improved drainage function of Müller glial cells and retinal pigment epithelium after IAI.
Highlights
Diabetic macular edema (DME), a major cause of central visual loss in patients with diabetic retinopathy, has a prevalence of 4.8% and seriously affects the patient’s quality of life (Varma et al, 2014)
Most DME patients significantly benefit from antiVEGF treatment, about 31–66% still show poor response to monthly anti-vascular endothelial growth factor (VEGF) treatment (Bressler et al, 2018), indicating that beyond VEGF, other pathogenic factors are involved in the pathogenesis of DME, including microglial activation, and retinal Müller glia (RMG) and retinal pigment epithelium (RPE) dysfunction
We retrospectively investigated 25 eyes in 18 treatment-naïve patients with DME before and after treatment with special focus on the changes of hyperreflective foci (HRF), cystoid edema, and subretinal fluid (SRF) as assessed by Optical coherence tomography angiography (OCTA)
Summary
Diabetic macular edema (DME), a major cause of central visual loss in patients with diabetic retinopathy, has a prevalence of 4.8% and seriously affects the patient’s quality of life (Varma et al, 2014). The dysfunction of retinal Müller glia (RMG) and retinal pigment epithelium (RPE) results in cystoid edema and subretinal fluid accumulation (Daruich et al, 2018). The exact pathophysiological mechanism of DME remains unclear, it is currently assumed that macular edema results from an imbalance between fluid entry and fluid exit driven by the Starling equation (Daruich et al, 2018). Anti-VEGF drugs, including bevacizumab (Avastin), ranibizumab (Lucentis), aflibercept (Eylea), and conbercept (Lumitin), are potent in the treatment of DME. Most DME patients significantly benefit from antiVEGF treatment, about 31–66% still show poor response to monthly anti-VEGF treatment (Bressler et al, 2018), indicating that beyond VEGF, other pathogenic factors are involved in the pathogenesis of DME, including microglial activation, and RMG and RPE dysfunction
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