Presumed Ocular Histoplasmosis Syndrome Medication

Updated: Sep 20, 2018
  • Author: Lihteh Wu, MD; Chief Editor: C Stephen Foster, MD, FACS, FACR, FAAO, FARVO  more...
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Medication

Medication Summary

Antifungals, such as amphotericin B, are not helpful. Steroids anecdotally have been used in subfoveal CNV by a few observers.

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Corticosteroids

Class Summary

Anecdotal, controversial evidence suggests efficacy in treating subfoveal CNV.

Prednisone (Deltasone, Orasone)

May decrease inflammation by reversing increased capillary permeability and suppressing PMN activity.

Triamcinolone (Kenalog)

Off-label use of triamcinolone.

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Photosensitizers for photodynamic therapy

Class Summary

Reduction of leakage from abnormal, neovascular vessels, resulting in reduced visual loss.

Verteporfin (Visudyne)

A benzoporphyrin derivative monoacid (BPD-MA), consists of equally active isomers BPD-MAC and BPD-MAD, which can be activated by low-intensity, nonthermal light of 689-nm wavelength. After activation with light and in presence of oxygen, verteporfin forms cytotoxic oxygen free radicals and singlet oxygen. Singlet oxygen causes damage to biological structures within range of diffusion. This leads to local vascular occlusion, cell damage, and cell death. In plasma, verteporfin is transported primarily by low-density lipoproteins (LDL). Tumor and neovascular endothelial cells have increased specificity and uptake of verteporfin because of their high expression of LDL receptors. Effect can be enhanced by use of liposomal formulation.

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Anti-VEGF agents

Class Summary

These agents are used to neutralize VEGF expression in ocular angiogenesis.

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.

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.

Bevacizumab (Avastin)

Murine derived monoclonal antibody that inhibits angiogenesis by targeting and inhibiting vascular endothelial growth factor (VEGF). VEGF causes angiogenesis and increases vascular permeability and inflammation. Nonspecific VEGF inhibitor.

Because ranibizumab ($1950/dose) and bevacizumab ($50-75/dose) have an enormous price differential, yet, as many retina physicians feel, comparable effectiveness, a great deal of interest exists in comparing the 2 medications directly. The National Eye Institute has recently funded a large randomized controlled trial to directly compare the safety and efficacy of bevacizumab and ranibizumab in the Comparison of Age-Related Macular Degeneration Treatment Trials (CATT) that is expected to begin enrollment in early 2008 and be completed by 2011.

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.

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