Medication Summary
The goals of pharmacotherapy are to reduce morbidity and to prevent complications.
Photosensitizers
Class Summary
Effects can induce vascular occlusion.
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.
Antineoplastic Agent, Monoclonal Antibody
Class Summary
Antivascular growth factor inhibitor stops 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.
Ophthalmics, VEGF Inhibitors
Aflibercept intravitreal (Eylea)
EYLEA (aflibercept) is a recombinant fusion protein consisting of portions of human vascular endothelial growth factor (VEGF) receptors 1 and 2 extracellular domains fused to the Fc portion of human IgG1 formulated as an iso-osmotic solution for intravitreal administration. Aflibercept is a dimeric glycoprotein with a protein molecular weight of 97 kilodaltons (kDa) and contains glycosylation, constituting an additional 15% of the total molecular mass, resulting in a total molecular weight of 115 kDa. Aflibercept is produced in recombinant Chinese hamster ovary (CHO) cells.
Afliberceptis a sterile, clear, and colorless to pale yellow solution. EYLEA is supplied as a preservative-free, sterile, aqueous solution in a single-use, glass vial designed to deliver 0.05 mL (50 microliters) of aflibercept (40 mg/mL in 10 mM sodium phosphate, 40 mM sodium chloride, 0.03% polysorbate 20, and 5% sucrose, pH 6.2).
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Progression of angioid streaks. Large subretinal hemorrhage.
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Same eye as in previous image, 11 months later. Partial resolution of subretinal blood. Notice the old subretinal hemorrhage under the fovea and color change to white-yellow.
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Late complication of choroidal neovascularization in angioid streaks. Same eye as in previous images, 5 years later. Notice the extensive scarring and subretinal exudates and dehemoglobinized blood.
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Red-free photograph of the optic nerve and posterior pole showing the cracks in the Bruch membrane. Notice the retinal arteries and veins crossing over the dark red streaks.
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Early fluorescein angiography showing the early hyperfluorescence, window defect, of the angioid streaks.
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Late fluorescein angiography of the same eye as in Media file 2. Notice the staining of the edges of the streaks. Also, staining in the center of the macula is present due to extension of the Bruch membrane crack. When compared to early fluorescein angiography, no active leakage is present.
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Right eye, midphase arteriovenous, showing choriocapillaris atrophic changes. This 45-year-old patient underwent 3 injections of Avastin and one session of half-time photodynamic therapy.
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Same patient as in previous image, a few months before the Avastin injection and half-time photodynamic therapy.
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A 50-year-old man with a 2-month history of blurring vision in the left eye. The color photograph showed subretinal blood and large membrane, extrafoveal in location.
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Early fundus fluorescein angiography showing the hyperfluorescence of the choroidal neovascular membrane of the left eye of the same patient in the previous image.
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Late fundus fluorescein angiography confirming the active choroidal neovascular membrane of the left eye.
