Verteporfin

Verteporfin is a prescription drug used for the treatment of subfoveal choroidal neovascularization (subfoveal CNV). The fovea is a small area in the retina of the eye that contains a concentration of cones (see diagram). The fovea is needed for proper vision. The choroid lies just beneath the fovea. Subfoveal CNV is a growth of blood vessels into the choroidal layer that interferes with vision. The Food and Drug Administration approved verteporfin April 12, 2000. Verteporfin I sold under the bran name Visudyne by Novartis.

Source:Wikimedia Commons: Diagram of an eye. The fovea (p) is part of the retina (e) the choroid (d) lies just beneath the fovea. In subfoveal choroidal neovascularization new blood vessels form in the choroid and disrupts vision. Verteporfin prevents these blood vessels from growing a = optic nerve, b = optic disc, c = sclera, d = choroid, e = retina, f = zonular fibres, g = posterior chamber, h = iris, i = pupil, j = cornea, k = anterior chamber, l = ciliary muscle, m = lens, n = suspensory ligament, o = vitreous humour, p = fovea Source:Wikimedia Commons

Uses

Verteporfin is used to treat subfoveal CNV that is caused by the following:

• age-related macular degeneration
• myopia (near sightedness)
• histoplasmosis infection in the eye

How Verteporfin is Taken

Verteporfin therapy is a two-step process requiring intravenous (IV) administration of the drug (15 mg) followed by the application of red light to the affected eye via a laser. The laser is used to activate Verteporfin after it enters the eye. This procedure may need to be repeated several times depending on the degree of blood vessel formation in the fovea.

How Verteporfin Works

Subfoveal CNV is the growth of new blood vessels in the choroid layer of the retina, a region just below the fovea (see diagram above). These new blood vessels negatively affect the function of the fovea and ultimately hinder vision. After injection, verteporfin travels to the eye where it is activated by a laser. This activation causes the formation of oxygen free radicals. Free radicals are molecules that cause damage to proteins and cells. These oxygen radicals damage the lining of the newly formed blood vessels in the choroid. This damage promotes platelet aggregation, clot formation, and constriction of the blood vessels. Clotting and constriction causes the new blood vessels to shrink and die. This improves the function of the fovea and, in turn, improves vision.

How the Body Affects Verteporfin

Verteporfin is metabolized to a minor degree by enzymes in the liver and blood. Its half-life, or time needed for the concentration of the drug in the blood to be reduced by half, is 5–7 hours. The majority of verteporfin is excreted in feces.

Side Effects

One of the most common side effects of verteporfin is headache. Other common side effects occur at the site of infusion (injection site reactions):

• pain
• edema (swelling around the injection site)
• inflammation
• the injection "seeping out" of the vein
• rashes
• bleeding
• discoloration

Some other common side effects involve vision:

• blurriness
• flashes of light
• decreased ability to discern objects

These events occurred in approximately 10%–30% of patients enrolled in clinical trials.

Risks and Precautions

Treatment with verteporfin causes temporary sensitization to light. Avoidance of sunlight or bright indoor lights for the 5 days following therapy reduces the risk of damage to the skin or eyes.

Verteporfin is partly metabolized in the liver. However, the influence of liver impairment or obstruction of the bile ducts on the effectiveness or safety of verteporfin is not known.

Verteporfin has been found in human breast milk. The concentration of verteporfin in breast milk has been reported to be up to 66% of the corresponding blood levels in the mother. Because of the potential for serious side effects in nursing infants, some individuals may choose to postpone treatment or not nurse an infant while receiving verteporfin.

Drug Interactions

Based on its mechanism of action, verteporfin has the potential to interact with many drugs. The interaction may influence the effectiveness of verteporfin. A list of drugs that may interact with verteporfin, as well as the potential result of the interaction, is below:

• Calcium channel blockers (e.g., nifedipine), polymyxin B or radiation therapy could enhance the rate of verteporfin uptake into the lining of blood vessels
• Other drugs that sensitize the skin or eyes to light (e.g., tetracyclines, sulfonamides, some antipsychotics, some antidiavetics, some diuretics, and griseofulvin) could increase the sensitivity of the skin to light
• drugs that quench active oxygen radicals (e.g., ethanol, mannitol) could reduce the effectiveness of verteporfin
• Drugs that decrease clotting, constriction of blood vessels, or platelet aggregation (e.g., warfarin) could decrease the effectiveness of verteporfin

Clinical Trials

Two studies were conducted in patients with subfoveal CNV secondary to age-related macular degeneration. ^[1] These studies combined enrolled 609 patients. Effectiveness was measured as maintenance of visual acuity (ability to discern objects). Acuity was determined on an eye chart. Verteporfin was effective in maintaining vision at both the 1-year and 2-year endpoints of the study.

One study looked at the effectiveness of verteporfin in 120 patients with subfoveal CNV secondary to myopia. ^[2] verteporfin was effective in maintaining vision at the 1-year endpoint but not at the 2-year endpoint of the study. ^[3]

Another trial looked at the effectiveness of verteporfin in maintaining vision in 26 patients with subfoveal CNV secondary to histoplasmosis infection in the eye.^[4] More than half of the patients improved by at least six letters on an eye chart.

References

1. ↑ Bressler NM, Arnold J, Benchaboune M, et al. Verteporfin therapy of subfoveal choroidal neovascularization in patients with age-related macular degeneration: additional information regarding baseline lesion composition's impact on vision outcomes-TAP report No. 3. Arch Ophthalmol. 2002 Nov;120(11):1443-54. Abstract | Full Text | [ http://archopht.ama-assn.org/cgi/reprint/120/11/1443 PDF]
2. ↑ Barbazetto I, Burdan A, Bressler NM, et al. Photodynamic therapy of subfoveal choroidal neovascularization with verteporfin: fluorescein angiographic guidelines for evaluation and treatment--TAP and VIP report No. 2. Arch Ophthalmol. 2003 Sep;121(9):1253-68 Abstract | PDF
3. ↑ Rosenfeld PJ, Saperstein DA, Bressler NM, et al. Ophthalmology. 2004 Sep;111(9):1725-33. Abstract
4. ↑ Rosenfeld PJ, Saperstein DA, Bressler NM, et al. Photodynamic therapy with verteporfin in ocular histoplasmosis: uncontrolled, open-label 2-year study. Ophthalmology. 2004 Sep;111(9):1725-33. Abstract

External Links

AgingEye.com

FDA: Patient Information Sheet