First Author: M.Losada SPAIN
Co Author(s): N. Manresa J. Mulero J.M. Sanchez P. Zafrilla 0 0 0 0 0 0 0 0 0
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Anti-VEGF therapies have been shown to be remarkably effective in preventing vision loss from neovascular and exudative complications of retinal diseases particularly in AMD. Different authors have observed among beneficiaries newly diagnosed as having exudative AMD, the introduction of anti-VEGF therapy reduced vision loss by 41% and onset of severe vision loss and blindness by 46%. However, inhibition of VEGF pathway may disturb the homeostatic maintenance of normal vasculature and ROS. The aim of this study was to analyze the effect of antiangiogenic treatments on total antioxidant status and antioxidant enzymes in patients with age related macular degeneration.
A total of 43 patients with exudative AMD with no previous anti-VEGF treatment (age group of 55–82 years with the mean age of 71 years) were recruited for the study. The following parameters were determined: total antioxidant activity and the activity of endogenous antioxidant enzymes.
Total antioxidant status (TAS) in plasma was measured by ORAC method. The oxygen radical absorbance capacity was determined as described by Dávalos et al. with slight modifications. For the quantitative determination of glutathione peroxidase in the blood the Ransel commercial kit was used. This method is based on that of Plagia and Valentine. Glutathione peroxidase (GPx) catalyses the oxidation of Glutahione (GSH) by cumene hydroperoxide. Absorbancy reduction was measured al 340 nm for 2 min and the GPx activity was expressed as U/L of sample. Determination of glutathione reductase was achieved using the procedure described by Anderson et al. 100 μL of serum was added to the mixture of 0.1 EDTA, 0.1 mM NADPH in 50 mM HEPES/KOH (pH=8) buffer. The reaction was initiated by adding 100 μL reduced glutathione 1 mM (final volume 1mL) and the reduction of NADPH at 340 nm was monitored for 3 min. Enzymatic activity was expressed as U/L The analisis of erythrocite superoxide dismutase activity was performed using Randox (Randox, Crumlin, UK). The activities were measured enzymatically at 37ºC on a Varian spectrometer (mod. Cary Bio-50 UV-Vis) at 505 nm. Randox provided standards. SOD activity was expressed as U/g Hb of sample.
Average values of antioxidant activity at baseline in patients treated with Pegaptanib sodium are 166,6±20,4 µM Trolox and 202,4±27,4 µM Trolox in patients treated with Ranibizumab. After anti-VEGF therapy, the dates were not significantly different (151,2 ±16,5 µM Trolox) in patients treated with Pegaptanib and (193,7±122,1 µM Trolox) in patients treated with Ranibizumab. Average values of gluthatione peroxidase at baseline was 7149,1± 2120 U/L in patients treated with Pegabtanib and at 6 months these values not showed significant changes 6549,1± 1511 U/L. Patients treated with Ranibizumab showed no changes in average values of gluthatione peroxidase at baseline (7328,1± 1954 U/L) and after intravitreal therapy with Ranibizumab (6728,1± 1846 U/L). Average values of gluthation reductase activity are higher in patients treated with Pegabtanib than in patients treated with Ranibizumab (54.1± 3.4 U/L± vs 50.6±2.9 U/L). After antiangiogenic therapies these values decrease slightly but there were no significant differences (52.6± 2.4 U/L Pegabtanib vs 48.7± 2.7 U/L Ranibizumab). Values activity are of superoxide dismutase higher in patients treated with Pegabtanib than in patients treated with Ranibizumab (885.8± 25.4 Ug/Hb vs 815.8± 75.8 Ug/Hb). After antiangiogenic therapies these values decrease but there were no significant differences.
There wasn’t statistically significant difference in any of parameters studied after treatment with both Pegaptanib and Ranibizumab in patients with AMD.