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Sonja Gudrun Prager, Magdalena Schuster, Christoph Mitsch, Jan Lammer, Christoph D Scholda, Ursula Schmidt-Erfurth, DRRG Vienna; Thinning of the central neurosensory retina during anti-VEGF treatment of diabetic retinopathy.. Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):1736.
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Intravitreally injected anti-VEGF drugs were proven to be effective in the treatment of diabetic macular edema (DME) and other exudative macular diseases such as neovascular age-related macular degeneration (AMD). Recently, concerns have been raised that continuous VEGF inhibition could disturb the neuroprotective role of VEGF in the human eye, since neurosensory degeneration is a hallmark of diabetic disease and patients with DME are usually treated repeatedly with anti-VEGF agents over years. The purpose was to examine the frequency of central retinal thickness (CRT) thinning below 200 µm in patients treated for vision threatening diabetic retinopathy (DR) and if CRT thinning affects visual function.
Data of all outpatient visits at the subspecialty unit of diabetic retinopathy at the department of ophthalmology, Medical University Vienna between January and November 2014 were included in a retrospective analysis. All patients with CRT of less than 200 µm on SD-OCT (Cirrus, Zeiss) were reviewed in regards to their demographics, visual acuity and treatments received before CRT thinning.
In total, 1529 visits of 578 patients were reviewed. In 112 (16%) eyes of 93 patients (mean±SD age 66±13 years, 47 females) CRT was less than 200 µm (158±40 µm) and mean best-corrected visual acuity (BCVA) was 0.4±0.3 Snellen Equivalents. There was no significant correlation found between BCVA and low CRT, despite an overall higher rate of central retinal thinning as compared to other macular disease under treatment.
Conclusion: CRT thinning below 200 µm does not seem to be a reliable biomarker for visual function in patients treated for vision threatening DR However, distinct analysis of individual neurosensory layers may identify disease- and treatment related neurodegeneration.
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