A comparison of macular ganglion cell complex thickness in diabetic patients with and without diabetic retinopathy using SD-OCT
DOI:
https://doi.org/10.18203/2320-6012.ijrms20242613Keywords:
Diabetic retinopathy, Spectral domain optical coherence tomography, RNFL thickness, Diabetic mellitus, GCL IPL thicknessAbstract
Background: Diabetic retinopathy (DR) is a leading cause of visual impairment in working-age individuals. Retinal neurodegeneration due to pro-inflammatory cytokines and inflammation precede the clinical signs of DR. Preserving the integrity of the retinal ganglion cell (RGC) is essential for maintaining visual function.
Methods: This prospective, cross-sectional study involved 120 subjects, divided into three groups: 40 normal controls (G1), 40 diabetics without retinopathy (G2), and 40 diabetics with retinopathy (G3). Measurements of ganglion cell-inner plexiform layer (GC-IPL) and retinal nerve fibre layer (RNFL) thickness were taken for each participant. Data were analyzed using ANOVA and/or unpaired t-tests, and Pearson’s correlation was used to evaluate the linear correlation between variables, with a significance threshold of p<0.05.
Results: The mean GC-IPL thickness was 84.81±5.02 µm for normal controls, 73.3±12.48 µm for diabetics without retinopathy, and 67.18±14.58 µm for diabetics with retinopathy (overall p<0.001). The mean RNFL thickness was 100.35±4.14 µm for normal controls, 85.80±14.04 µm for diabetics without retinopathy, and 80.25±21.03 µm for diabetics with retinopathy (overall p<0.001). There was no significant correlation between GC-IPL thickness and HbA1c levels (p>0.05).
Conclusions: Diabetic patients, both with and without DR, exhibited significant reductions in GC-IPL and RNFL thickness compared to controls, indicating neuro retinal changes precede vascular changes in DR. However, the correlation between RNFL/GC-IPL thickness and diabetes duration or HbA1c levels was not significant. Optical coherence tomography (OCT) is thus a useful non-invasive tool for early detection of neuronal loss before clinical signs of retinopathy.
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