Age-related macular degeneration (AMD)
- Dry AMD
- Wet AMD
Most people with AMD have the dry type of the disease. In this type, there are deposits, called drusen, under the retina, or degeneration of the layers under the retina (atrophy) with loss of photoreceptor function. Vision can range from minimal changes with the presence of drusen to severe loss with advanced atrophy. Dry macular degeneration can progress to wet AMD. There is no treatment for dry type of AMD, but prevention of progression to wet AMD is possible with a healthy diet and AREDS multivitamins.
The following combination of multivitamins and zinc was shown to have a 25% treatment benefit in the Age-Related Eye Disease Study (AREDS):
500 milligrams of vitamin C
400 International Units of vitamin E
15 milligrams of beta-carotene (or 25,000 International Units of vitamin A)
80 milligrams of zinc as zinc oxide,
2 milligrams of copper as cupric oxide
It is recommended that smokers use a formulation without beta-carotene as high doses of beta-carotene has been linked to increased risk of lung cancer.
A second phase of the AREDS was recently initiated to investigate the roles of lutein, zeaxanthin, and omega-3 fatty acids.
A recent study conducted in Rotterdam, Netherlands, and published in the Journal of the American Medical Association in December, 2005, showed that individuals who had above average dietary intake of Vitamins C and E, beta-carotene, and zinc reduced their risk of AMD by 35%. These vitamins and zinc can be obtained by consuming a healthy diet:
Vitamin E: whole grains, vegetable oil, eggs and nuts
Zinc: meat, poultry, fish, whole grains and dairy products
Beta-carotene: vegetables such as carrots, kale and spinach
Vitamin C: citrus fruits and juices, green peppers, broccoli, and potatoes
Omega 3 Fatty Acids
Recent evidence suggests that Omega 3 Fatty acids may be protective in patients with AMD. Omega 3 fatty acids are present in many nutrients table.
Wet AMD refers to the presence of fluid or blood under the macula due to the formation of abnormal blood vessels under the retina (choroidal neovascularization). With wet AMD, vision can rapidly decline and it is this type that is responsible for severe vision loss. Early detection and treatment are critical for preventing further loss of vision. Unfortunately, the disease is a chronic problem with a high rate of recurrence, and patients generally require multiple treatments over time. Fortunately, new treatment modalities are improving our ability to preserve vision for longer periods of time.
The treatment of wet AMD has evolved over the last 20 years. The treatment options include laser, photodynamic therapy with or without injection of steroid into the eye, and injections of anti-VEGF drugs (Macugen®, Avastin, or Lucentis™) into the eye.
In the 1980s and up until the advent of photodynamic therapy, thermal laser was used to destroy the abnormal new blood vessel complex. This technique was better than no treatment at all but patients were left with an immediate decrease in vision and a dark spot in their vision when treated with laser. Nowadays, laser is used only for those lesions that are located away from the center of the macula or around the optic nerve.
This treatment involves an intravenous infusion of a light-sensitive drug (visudyne) followed by directing a non-thermal laser beam to the abnormal blood vessel complex. Visudyne preferentially binds to components of the abnormal blood vessels and the “cold” laser light photoactivates the drug and causes these vessels to shut down. Recurrences do occur following this treatment, and the average number of treatments is 3 in the 1st year, 2 in the 2nd year, and 1 in the 3rd year after diagnosis of wet AMD. Injection of a steroid called kenalog is typically used in conjunction with PDT.
In wet AMD, there is upregulation of vascular endothelial growth factor (VEGF). Anti-VEGF drugs block VEGF from binding to receptors on blood vessels and cause regression of the abnormal new blood vessel complex. Currently, there are 3 such drugs available.
This is the first FDA-approved anti-VEGF drug and has shown to be efficacious in preventing further loss of vision in patients with wet AMD. This drug is injected in the eye every 6 weeks. In studies comparing this treatment to no treatment at all, 70% of treated eyes versus 55% of untreated eyes lost less than 3 lines of vision at 1 year. There is a 15% treatment benefit, and treated eyes lose less vision over 2 years than untreated eyes.
This drug was approved by the FDA in June 2006 for the treatment of wet AMD. It is an antibody fragment that binds VEGF. This drug is injected into the eye every 4 weeks. In studies comparing treatment to no treatment, 94.5% of treated eyes versus 62.2% of untreated eyes lost less than 3 lines of vision at 1 year. Furthermore, 25 to 33% of patients gained vision with treatment.
This drug is FDA-approved for the treatment of colon cancer. It is a full-length antibody against VEGF and is a bigger molecule compared to Lucentis, which is a fragment antibody. It has been successfully used off-label for treatment of wet AMD for nearly 1 year with no reported safety concerns. Treatment involves injections every 4 weeks until the abnormal blood vessel complex resolves and the patient is then followed periodically to watch for recurrences. Resolution of the abnormal blood vessel complex after 1 or 2 treatments has been shown in retrospective studies.