Age-related macular degeneration (AMD) affects 13 to 14 million North Americans, a number that is expected to increase by 50 percent over the next few decades. Most cases of AMD (90 percent) are classified as early or intermediate stages of the disease. Early signs include retinal pigment changes that affect the macula; however, intermediate AMD presents with more extensive clinical features and may be considered a high-risk form of early AMD. Advanced AMD is not as common as the early and intermediate stages, but it does affect 7 percent of persons who are 75 years or older. It is divided into neo-vascular (wet) and atrophic (dry) subtypes.

The cause of AMD is not known, but heredity and cardiovascular disease may play roles in the development of this disease. Because the disease affects central vision, AMD impacts a patient’s ability to perform daily activities such as driving, reading, and watching television. It also limits social interaction and impairs facial recognition and spatial orientation. The loss of these functions also may account for the high rate of depression (almost one third) in patients with AMD.

Treatment is limited, but strategies are evolving. Smoking cessation and reducing cardiovascular risk factors are recommended. Patients who have AMD in the intermediate stage may benefit from high-dose antioxidant vitamins and zinc supplements. Meanwhile, ongoing trials are evaluating unproven agents such as lutein and zeaxanthin.

Thermal laser photocoagulation has been replaced by verteporfin photodynamic therapy to treat the wet subtype of advanced AMD. The former treatment destroyed retinal tissue with the neovascular formation it targeted. The photodynamic therapy works by activating a photodynamic dye that occludes abnormal vessels. When it is injected directly into the eye, another agent, pegaptanib (Macugen), targets vascular endothelial growth factor, a peptide that stimulates angiogenesis. A study of this agent showed that the intervention resulted in less visual loss than with usual care. Unproven treatments include corticosteroids and surgical removal of angiogenic vessels. Other than these treatments to slow late visual decline, effective interventions and restoration of visual loss remain elusive.

The authors conclude that the use of glasses and magnification aids may be helpful, and patients with AMD should be treated for depression.

editor’s note: In a recent study, researchers found that carriers of the CFH Y402H allele were at higher risk of all stages of AMD compared with those without the allele, with homozygotes being at higher risk than heterozygotes.¹ They also confirmed the toxic effect of smoking. Homozygous CFH Y402H patients who smoked had a much higher risk of late AMD than did nonsmoking patients without the allele. Inflammation may play a role in this effect because greater C-reactive protein levels and erythrocyte sedimentation rates were associated with a greater risk of disease in CFH Y402H carriers. Smoking cessation may be preventive, and future interventions may target inflammation in genetically susceptible persons.—c.w.