Abstract
Purpose: To identify the effects of prolonged type 2 diabetes (T2DM) on macular microcirculation and the inner retinal layer in diabetic eyes without clinical diabetic retinopathy (DR). Methods: 97, 92, and 57 eyes in the control, patients with T2DM < 10 years (DM group one), and patients with T2DM ≥ 10 years (DM group two) were enrolled. The ganglion cell-inner plexiform layer (GC-IPL) thickness and superficial vessel density (VD) were compared. Linear regression analyses were performed to identify factors associated with VD in T2DM patients. Results: GC-IPL thicknesses in the control, DM group one, and DM group two were 84.58 ± 0.89, 83.49 ± 0.70, and 79.04 ± 0.96 μm, respectively (p < 0.001). The VDs of the full area were 20.32 ± 0.15, 19.46 ± 0.17, and 18.46 ± 0.23 mm−1 (p < 0.001). Post-hoc analyses revealed that the VDs of the full area was significantly different in the control vs. DM group one (p = 0.001), control vs. DM group two (p < 0.001), and DM group one vs. DM group two (p = 0.001). Multivariate linear regression analyses revealed that DM duration (p = 0.037), visual acuity (p = 0.013), and GC-IPL thickness (p < 0.001) were significantly associated with the VD of T2DM patients. Conclusions: We confirmed GC-IPL thinning and decreased superficial VD in the macular areas using OCTA in T2DM patients. Patients with T2DM ≥ 10 years exhibited significantly more severe macular microcirculation impairment compared to patients with T2DM < 10 years and normal controls.
Highlights
Type 2 diabetes (T2DM) is a major global health problem that is increasing in prevalence due to lifestyle changes [1,2,3,4]
Previous studies have found that retinal damage caused by T2DM could result in thinning of the ganglion cell-inner plexiform layer (GC-IPL) and peripapillary retinal nerve fiber layer in T2DM patients without clinical diabetic retinopathy (DR) [9,10,11]
Visual acuity showed a significant difference among the groups (p = 0.027), but this difference disappeared on post-hoc analyses
Summary
Type 2 diabetes (T2DM) is a major global health problem that is increasing in prevalence due to lifestyle changes [1,2,3,4]. DR, which is the leading cause of blindness in the working-age population, is known to be associated with ischemic damage on retina following to change in the microvasculature [6,7,8] Such retinal damage is found in patients without clinical DR. Previous studies have found that retinal damage caused by T2DM could result in thinning of the ganglion cell-inner plexiform layer (GC-IPL) and peripapillary retinal nerve fiber layer (pRNFL) in T2DM patients without clinical DR [9,10,11] Such inner retinal thinning reflects diabetic retinal neurodegeneration, an early event in DR pathogenesis activated by pathologic pathways such as polyols, hexosamine, or oxidative stress [12,13]. With the development of devices that are able to observe retinal microvasculature and retinal perfusion in detail, various studies on retinal microvasculature damage in patients with T2DM have been reported
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