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S. V. Reddy, T. H. Tezel, H. J. Kaplan, S. Schaal; Functional and Anatomical Response of Idiopathic Macular Telangiectasis Type II to Intravitreal Anti-VEGF Treatment With Bevacizumab. Invest. Ophthalmol. Vis. Sci. 2010;51(13):2218.
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© ARVO (1962-2015); The Authors (2016-present)
To investigate the functional and anatomical response of idiopathic macular telangiectasis type II (IMT type II) to intravitreal bevacizumab therapy.
Twelve eyes of 12 patients diagnosed with idiopathic IMT type II and treated with intravitreal Avastin injections at every 12 weeks were included in the present study. Retinal thickness measurements from nine central optical coherence tomography (OCT) sectors were standardized according to a diurnal variation norms obtained from an age-matched control group.Anatomical response to bevacizumab was then plotted as significant variation of macular volume (=Standardized volumetric change index (SVCI)) after each bevacizumab (2.5 mg/100 µL) injection. Functional outcome was assesd by plotting the logMAR variation of the visual acuity during the course of the treatment.
The standardized macular volume change after intravitreal bevacizumab injection fit to a dumping sine curve (r=0.9 , p=0.06 ). The maximum anatomical effect of bevacizumab was observed at 10.8 weeks and the average time for the fluid to recur within the macula was 16.8 weeks. The average initial visual acuity was 20/42 ± 20/26. Vision improved to average of 20/25 at 3.5 weeks after the first injection; however returned back to 20/46 at 9.7 weeks. This cycle (r=0.86, p=0.04) continued with a diminished amplitude throughout the follow-up period. The average final visual acuity at 36 weeks was 20/39 ± 20/24. Three patients (23%) improved >2 lines whereas one 7.7% decreased.
Anatomical and functional benefit from anti-VEGF treatment implies a definitive role of VEGF in the pathogenesis of IMT type II. However, the response to intravitreal anti-VEGF therapy was less obvious than the tradional response seen in AMD patients, indicating the role of other confounding pathological pathways in the pathogenesis of IMT type II.
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