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Choroidal Rupture Medication

  • Author: Lihteh Wu, MD; Chief Editor: Hampton Roy, Sr, MD  more...
 
Updated: Mar 08, 2016
 
 

Anti-VEGF agents

Class Summary

Vascular endothelial growth factor (VEGF) is essential for angiogenesis. Inhibitors of VEGF that bind to the receptor of VEGF-A isoforms prevent its interaction with Flt-1 and KDR on the endothelial cell surface, and therefore decreases cell proliferation and new blood vessel formation.

Ranibizumab (Lucentis)

 

Recombinant humanized IgG1-kappa isotype monoclonal antibody fragment designed for intraocular use. Indicated for neovascular (wet) age-related macular degeneration (ARMD). In clinical trials, about one third of patients had improved vision at 12 mo that was maintained by monthly injections. Binds to VEGF-A, including biologically active, cleaved form (ie, (VEGF110). VEGF-A has been shown to cause neovascularization and leakage in ocular angiogenesis models and is thought to contribute to ARMD disease progression. Binding VEGF-A prevents interaction with its receptors (ie, VEGFR1, VEGFR2) on surface of endothelial cells, thereby reducing endothelial cell proliferation, vascular leakage, and new blood vessel formation.

Pegaptanib (Macugen)

 

Selective vascular endothelial growth factor (VEGF) antagonist that promotes vision stability and reduces visual-acuity loss and progression to legal blindness. VEGF causes angiogenesis and increases vascular permeability and inflammation, all which contribute to neovascularization in age-related wet macular degeneration.

Bevacizumab (Avastin)

 

Murine derived monoclonal antibody that inhibits angiogenesis by targeting and inhibiting vascular endothelial growth factor (VEGF). Used investigationally for ARMD secondary to choroidal neovascularization.

Aflibercept (Eylea)

 

Fusion protein of key domains from human VEGF receptors 1 (VEGFR1) and 2 (VEGFR2) with human IgGFc designed for intraocular use. Indicated for neovascular (wet) age-related macular degeneration (ARMD) and macular edema secondary to central retinal vein occlusion. Binds to VEGF-A, including biologically active, cleaved form (ie, (VEGF110) and placental growth factor. VEGF-A has been shown to cause neovascularization and leakage in ocular angiogenesis models and is thought to contribute to ARMD disease progression. Binding VEGF-A prevents interaction with its receptors (ie, VEGFR1, VEGFR2) on surface of endothelial cells, thereby reducing endothelial cell proliferation, vascular leakage, and new blood vessel formation.

 
 
Contributor Information and Disclosures
Author

Lihteh Wu, MD Asociados de Macula Vitreo y Retina de Costa Rica

Lihteh Wu, MD is a member of the following medical societies: American Academy of Ophthalmology, American Society of Retina Specialists, Association for Research in Vision and Ophthalmology, Club Jules Gonin, Macula Society, Pan-American Association of Ophthalmology, Retina Society

Disclosure: Received income in an amount equal to or greater than $250 from: Bayer Health; Quantel Medical; Heidelberg Engineering.

Coauthor(s)

Dhariana Acón, MD Ophthalmologist, Caja Costarricense Seguro Social, Hospital de Guapiles, Costa Rica

Disclosure: Nothing to disclose.

Specialty Editor Board

Simon K Law, MD, PharmD Clinical Professor of Health Sciences, Department of Ophthalmology, Jules Stein Eye Institute, University of California, Los Angeles, David Geffen School of Medicine

Simon K Law, MD, PharmD is a member of the following medical societies: American Academy of Ophthalmology, Association for Research in Vision and Ophthalmology, American Glaucoma Society

Disclosure: Nothing to disclose.

Steve Charles, MD Director of Charles Retina Institute; Clinical Professor, Department of Ophthalmology, University of Tennessee College of Medicine

Steve Charles, MD is a member of the following medical societies: American Academy of Ophthalmology, American Society of Retina Specialists, Macula Society, Retina Society, Club Jules Gonin

Disclosure: Received royalty and consulting fees for: Alcon Laboratories.

Chief Editor

Hampton Roy, Sr, MD Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences

Hampton Roy, Sr, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, Pan-American Association of Ophthalmology

Disclosure: Nothing to disclose.

Additional Contributors

Russell P Jayne, MD Consulting Vitreoretinal Surgeon, The Retina Center at Las Vegas

Russell P Jayne, MD is a member of the following medical societies: American Medical Association, American Society of Cataract and Refractive Surgery, American Society of Retina Specialists

Disclosure: Nothing to disclose.

Acknowledgements

Teodoro Evans, MD Consulting Surgeon, Vitreo-Retinal Section, Clinica de Ojos, Costa Rica

Disclosure: Nothing to disclose.

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A 23-year-old man was in a motor vehicle accident 2 months before his presentation. His visual acuity is 20/400, and an afferent pupillary defect is present. Traumatic optic neuropathy and choroidal rupture are observed. This is a red-free photograph. (Courtesy of Jorge Gutierrez, MD.)
Mid-phase fluorescein angiogram in a 23-year-old man who was in a motor vehicle accident 2 months before his presentation. (Courtesy of Jorge Gutierrez, MD.)
Late-phase fluorescein angiogram in a 23-year-old who man was in a motor vehicle accident 2 months before his presentation. (Courtesy of Jorge Gutierrez, MD.)
 
 
 
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