Abstract
Diabetic macular edema (DME) represents the most common cause of vision loss in patients affected by diabetes mellitus. Although the pathophysiology of DME is not wholly understood, vascular endothelial growth factor (VEGF) has been identified as a key contributor to the development of DME. In addition, latest information suggests that acute and chronic inflammatory changes occur, contributing to the DME pathogenesis. The current therapeutic approach for DME is mainly based on the administration of anti-VEGF molecules. In particular, VEGF-inhibitors that have been studied for diabetic retinopathy include pegaptanib, ranibizumab, bevacizumab, and aflibercept. The present review analyzes the main characteristics of each molecule, describing the most important results of clinical trails.
MeSH terms
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Aptamers, Nucleotide / administration & dosage
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Aptamers, Nucleotide / adverse effects
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Aptamers, Nucleotide / therapeutic use*
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Bevacizumab / administration & dosage
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Bevacizumab / adverse effects
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Bevacizumab / therapeutic use*
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Diabetic Retinopathy / drug therapy*
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Diabetic Retinopathy / metabolism
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Humans
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Macular Edema / drug therapy*
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Macular Edema / metabolism
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Randomized Controlled Trials as Topic
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Ranibizumab / administration & dosage
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Ranibizumab / adverse effects
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Ranibizumab / therapeutic use*
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Receptors, Vascular Endothelial Growth Factor / administration & dosage
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Receptors, Vascular Endothelial Growth Factor / adverse effects
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Receptors, Vascular Endothelial Growth Factor / therapeutic use*
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Recombinant Fusion Proteins / administration & dosage
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Recombinant Fusion Proteins / adverse effects
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Recombinant Fusion Proteins / therapeutic use*
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Treatment Outcome
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Vascular Endothelial Growth Factor A / antagonists & inhibitors*
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Visual Acuity / drug effects
Substances
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Aptamers, Nucleotide
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Recombinant Fusion Proteins
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VEGFA protein, human
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Vascular Endothelial Growth Factor A
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aflibercept
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pegaptanib
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Bevacizumab
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Receptors, Vascular Endothelial Growth Factor
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Ranibizumab