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Natsumi Takahashi, Matthew S J Katz, Solly Elmann, Bert M Glaser; Vitreous VEGF Receptor Levels Rise Following Treatment of CNV in Eyes with wet AMD. Invest. Ophthalmol. Vis. Sci. 2016;57(12):5774.
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© ARVO (1962-2015); The Authors (2016-present)
Vitreous levels of VEGF Receptor 2 Y1175 have been previously shown to be elevated in eyes with wet AMD that respond to anti-VEGF treatment compared to non-responders. Feeder Vessel Treatment (FV Rx) of CNV has been found to cause rapid closure and regression of CNV in eyes with wet AMD that is sustained much longer than treatment with anti-VEGF. We therefore studied how the more sustained effect of FV Rx might affect VEGF Receptor 2 Y1175 levels in the vitreous over time.
Sequential vitreous aspirates (50-120μL) were obtained from 20 eyes of 19 patients treated for nAMD with intravitreal injection of bevacizumab between 12/1/07 and 11/1/13 in an IRB approved study. During the course of treatment, these eyes had Feeder Vessel Treatment (FVTx) resulting in rapid and sustained reduction of CNV. All vitreous samples were investigated utilizing RPPM (Reverse Phase Protein Microarray) technology. VEGFR2 Y1175 as well as VEGF A levels were measured in Relative Intensity Units and fold changes were calculated.
Compared to pre FV Rx levels VEGFR2 Y1175 levels increased by 9.2% in samples collected from 1-4 weeks following FV Rx and increased by 36.2% in samples collected 5-10 weeks following FV Tx. In contrast, within 30 min of FV Rx, VEGFR2 Y1175 levels decrease by 25.8%. VEGF A levels did not demonstrate a remarkable change following treatment.
Vitreous VEGF Receptor 2 Y1175 levels in eyes with wet AMD are elevated in relation to treatment by two different modalities, anti-VEGF and FV Rx. It is interesting that vitreous VEGF A levels did not show remarkable changes in response to treatment. The lack of change in VEGF A is consistent with previous studies. These findings suggest that VEGF Receptor 2 Y1175 might play an important role in the pathogenesis of CNV in wet AMD. Further study of this biomarker may yield an improved understanding of CNV.
This is an abstract that was submitted for the 2016 ARVO Annual Meeting, held in Seattle, Wash., May 1-5, 2016.
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