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Hille Van Dijk, Michael David Abramoff, Ferdinand Wit, Mirjam EJ Van Velthoven, Reinier O Schlingemann, Frank D Verbraak; Progressive Thinning of Inner Retinal Layer Thickness Over Time in Diabetic Patients. Invest. Ophthalmol. Vis. Sci. 2014;55(13):4428.
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The purpose of this longitudinal study was to confirm progressive thinning of inner retinal layer thickness - the retinal nerve fiber layer (RNFL) and the ganglion cell layer (GCL) / inner plexiform layer ( GCL+IPL) - in diabetes (type 1), that we have previously shown cross-sectionally, and to study any association between thinning, and presence and change in retinal vasculopathy, as well as hyperglycemia.
Forty-five diabetic patients (type 1) with no or minimal diabetic retinopathy (DR) at inclusion were followed prospectively over 5 years, and macula centered Time Domain Optical Coherence Tomography as well as fundus photographs were collected annually. Iowa Reference Algorithms was used to calculate macular neuroretinal thickness (ganglion cell plus inner plexiform layer (GCL+IPL) and nerve fiber layer (NFL) at each timepoint. An expert graded the fundus photographs for presence or absence of retinopathy at inclusion (DR) and for progression of retinopathy at any timepoint (progDR). Annual change in GCL+IPL and RNFL was analysed using a linear mixed model including the random effects age, gender, duration of diabetes at inclusion, HbA1C, DR and progDR.
Both retinal layers decrease in thickness over time taken into account age, gender, duration of diabetes, HbA1C, DR, and progDR. The macular GCL+IPL thins approximately 0.29 μm , and the macular RNFL thickness 0.25 μm per year. Patients with longer duration of diabetes prior to inclusion have thinner inner retinal layers in the pericentral area at baseline. Neither presence nor progression of vasculopathy is associated with thinning of the inner retinal layers. Also HbA1C was not associated with thinning of the layers.
This study confirms that the thinning of the inner neuroretinal layers in the macula is progressive over time, and that this diabetic retinal neurodegeneration is associated with duration of diabetes. The results also seem to indicate that duration of diabetes is the key factor in this retinal neurodegeneration, irrespective of the amount of vasculopathy. This results would make the hypothesis that diabetic neuropathy is caused by diabetic vasculopathy less likely.
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