Age-Related Macular Degeneration

A Primer for the Primary Care Provider

Kyle N. Klingler, MD; Sophie J. Bakri, MD


June 11, 2012

In This Article

Treatment of AMD

Treatment depends on both the type and the severity of AMD. Patients with early AMD have a low 5-year risk for progression to advanced AMD.[3] These patients do not require treatment, but they should have regular dilated examinations to monitor disease progression.

Patients with intermediate AMD have been found to have an increased risk for progression to advanced AMD over 5 years. Supplementation with antioxidants and zinc can reduce this risk by 25%.[3]

In patients with advanced AMD in 1 eye, the risk for progression to advanced disease in the fellow eye can be reduced by taking antioxidant and zinc supplements.[3] These are commonly referred to as "AREDS" supplements because their efficacy was established by the National Eye Institute's Age-Related Eye Disease Study. The ongoing AREDS2 trial is investigating the effects of other supplements, such as lutein, zeaxanthin, and omega-3 fatty acids, on the progression of AMD.

Treatment of patients with wet AMD has made significant progress in recent years. In the past, the fibrovascular lesions have been treated with laser photocoagulation or photodynamic therapy. These treatments slowed progression of disease but generally resulted in further loss of visual acuity.

Today, the neovascularization associated with wet AMD can be halted with antiangiogenesis drugs injected directly into the vitreous cavity of the eye. These molecules are specifically designed to bind to vascular endothelial growth factor (VEGF) or its receptor and block the angiogenesis cascade. VEGF inhibitors improve visual outcomes compared with previous treatments and have become first-line therapy for wet AMD.[1] These drugs effectively cause regression of choroidal neovascularization; however, they are not able to repair the break in the retinal basement membrane, nor are they able to eliminate the source of VEGF. As VEGF continues to be produced within the eye and the anti-VEGF molecules begin to be metabolized, the balance will shift once again toward neovascularization. Consequently, these drugs are not a cure for AMD, and effective treatment requires lifelong monitoring and frequent dosing. Research continues in an attempt to define the optimal treatment schedule and find more potent and effective antiangiogenesis molecules. Compounds with different mechanisms of action for both dry and wet AMD are being developed.


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