Abstract
The wet form of age related macular degeneration (AMD), known also as exudative or neovascular, is characterized by the formation of a pathological choroidal neovascular membrane (CNV) responsible for most cases of severe blindness. Vascular endothelial growth factor (VEGF) is a homodimeric glycoprotein acting as a growth factor selective for endothelial cells; it regulates angiogenesis and enhances vascular permeability and plays a leading role in this disorder. The consistent association between CNV and increased VEGF-A expression provides a strong reason for exploring the therapeutic potential of anti-VEGF agents in the treatment of neovascular AMD. The importance of VEGF for the development of AMD-related CNV has led to the development of a strategy able to block its pathologic effects. The rationale is that a blockade of VEGF actions could be effective in arresting choroidal angiogenesis and also reducing the vascular permeability, which is frequently the main cause of visual acuity deterioration. However, VEGF has also important functions in vascular physiology. The effects of anti-VEGF therapy may inhibit these functions. Herein we report the systemic adverse events secondary to intravitreal administration of these compounds, i.e. the main cardiovascular effects (thrombosis, hemorrhage, hypertension, proteinuria), as well as the less frequent cerebrovascular accidents, myocardial infarction, transient ischemic attacks, deep vein thrombosis, pulmonary embolism and thrombophlebitis.
Keywords: Anti-VEGFage related macular degeneration, bevacizumab, ranibizumab, pegaptanib, side effects, hypertension, stroke, proteinuria, bleeding
Current Vascular Pharmacology
Title: Systemic Adverse Drug Reactions Secondary to Anti-VEGF Intravitreal Injection in Patients with Neovascular Age-Related Macular Degeneration
Volume: 9 Issue: 5
Author(s): Francesco Semeraro, Francesco Morescalchi, Francesco Parmeggiani, Barbara Arcidiacono and Ciro Costagliola
Affiliation:
Keywords: Anti-VEGFage related macular degeneration, bevacizumab, ranibizumab, pegaptanib, side effects, hypertension, stroke, proteinuria, bleeding
Abstract: The wet form of age related macular degeneration (AMD), known also as exudative or neovascular, is characterized by the formation of a pathological choroidal neovascular membrane (CNV) responsible for most cases of severe blindness. Vascular endothelial growth factor (VEGF) is a homodimeric glycoprotein acting as a growth factor selective for endothelial cells; it regulates angiogenesis and enhances vascular permeability and plays a leading role in this disorder. The consistent association between CNV and increased VEGF-A expression provides a strong reason for exploring the therapeutic potential of anti-VEGF agents in the treatment of neovascular AMD. The importance of VEGF for the development of AMD-related CNV has led to the development of a strategy able to block its pathologic effects. The rationale is that a blockade of VEGF actions could be effective in arresting choroidal angiogenesis and also reducing the vascular permeability, which is frequently the main cause of visual acuity deterioration. However, VEGF has also important functions in vascular physiology. The effects of anti-VEGF therapy may inhibit these functions. Herein we report the systemic adverse events secondary to intravitreal administration of these compounds, i.e. the main cardiovascular effects (thrombosis, hemorrhage, hypertension, proteinuria), as well as the less frequent cerebrovascular accidents, myocardial infarction, transient ischemic attacks, deep vein thrombosis, pulmonary embolism and thrombophlebitis.
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Cite this article as:
Semeraro Francesco, Morescalchi Francesco, Parmeggiani Francesco, Arcidiacono Barbara and Costagliola Ciro, Systemic Adverse Drug Reactions Secondary to Anti-VEGF Intravitreal Injection in Patients with Neovascular Age-Related Macular Degeneration, Current Vascular Pharmacology 2011; 9 (5) . https://dx.doi.org/10.2174/157016111796642670
DOI https://dx.doi.org/10.2174/157016111796642670 |
Print ISSN 1570-1611 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-6212 |
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