Macular degeneration is damage or breakdown of the macula, which is the part of the retina responsible for central vision. When the macula doesn’t function correctly, we experience blurriness or darkness in the center of our vision. Macular degeneration affects both distance and close vision.
Dr. Bergstrom can perform laser surgery, prescribe optical devices or refer you to a low-vision specialist to help fight this disease.
The disease exists in two forms, dry and wet.
Dry macular degeneration is by far the most common (roughly 90% of all cases). However, it is the milder of the two forms, develops gradually, and usually leads to only minor vision loss. Dry macular degeneration tends to occur when yellow fatty particles called drusen accumulate in the retina underneath the macula. This build-up results in thinning and drying-out of the macular cells.
Wet macular degeneration is less common, but the vast majority of severe vision loss cases result from this form. First, abnormal blood vessels form underneath the surface of the retina. Leakage of blood and other fluids from these blood vessels permanently damage the outside cells (which detect incoming light). As these cells are damaged, vision is lost. The primary cause of macular degeneration remains unknown. Macular degeneration typically occurs more frequently in the aging population with patients over 60. Research has shown there are many other factors such as family history, smoking, hypertension, obesity, and/or a high cholesterol, high fat diet that may contribute towards the development of macular degeneration.
Macular degeneration symptoms may include:
Shadows, blurriness, or holes in the center of vision
Straight lines appear wavy
Trouble seeing details both up close and at a distance
Difficulty telling colors apart, especially ones close in hue
Vision can be slow to come back after bright light exposure
Treatment for dry macular degeneration:
Unfortunately, there is no treatment for the dry form of macular degeneration. Those at high risk should schedule a checkup with their ophthalmologist at least once every one to two years, to catch the disease in its infancy. Also, it is thought that dietary supplementation of antioxidants and zinc may help to slow its development. Early detection is very important because once vision is lost there is no treatment to regain it.
Treatments for wet macular degeneration:
Anti-angiogenesis drugs: This treatment has literally revolutionized our treatment of wet macular degeneration in recent years. These inhibit proteins which contribute to abnormal blood vessel growth. They are known as anti-VEGF (anti-vascular endothelial growth factor) drugs. There are a variety of drugs that can be applicable for this purpose, some FDA approved, and some off-label (officially approved for a different application).
Other pharmaceutical treatments: For example, angiostatic treatments, which combat blood vessel growth with steroid injections.
Avastin: Early study results indicate that a potential new age-related macular degeneration (AMD) therapy may improve vision within one week of injection, researchers announced at the Macula Society meeting of international retinal specialists.
Avastin, the drug used in initial studies, works by inhibiting growth of abnormal blood vessels in the back inner part of the eye(retina), a condition that occurs in the “wet” form of AMD. Researchers at the University of Miami’s Bascom Palmer Eye Institute said Avastin substantially reduced blood vessel leakage contributing to vision loss. A larger study is needed to determine if benefits of Avastin as a macular degeneration therapy outweigh risks, said Philip J. Rosenfeld, MD, PhD, associate professor of ophthalmology at the Institute.
Both Avastin and Macugen (the first opthalmic anti-VEGF drug approved by the FDA in December 2004) target a specific type of protein thought to cause abnormal blood vessel growth. Avastin currently has FDA approval for treatment of metastasis colorectal cancer, but not for macular degeneration. The use of Avastin for macular degeneration is “off label.” It is not manufactured to the quality standards for an ophthalmic drug and no ocular safety testing has been done.
The FDA has issued a caution that Avastin, when used to treat cancer patients, has been shown to increase risk of stroke and heart attack. Patients who are receiving blood thinning agents, including aspirin, must be precluded from using Avastin. Any patient with any history of abnormal blood chemistry and urinalysis must be excluded from using the drug, the researchers cautioned.
“A potential advantage of Avastin over other therapies for wet AMD is that vision improvement can occur within one week of treatment,” said Dr. Rosenfeld, the principal investigator of the Bascom Palmer clinical trial. “In addition to the improved vision, Avastin causes a reduction in leakage from the abnormal blood vessels, and we observed a restoration of normal macular anatomy.” Avastin, also known as bevacizumab, is manufactured by Genentech, Inc.
Patients with neovascular or the wet form of macular degeneration are thought to have elevated levels of vascular endothelial growth factor (VEGF) in their affected eyes. VEGF is a protein that causes abnormal blood vessels to grow, leak, bleed and damage the macula resulting in vision loss. New anti-VEGF drugs work by blocking this protein and the formation of abnormal blood vessels that grow in the eye.
“We have been injecting anti-VEGF drugs for the past three years with very encouraging results. Genentech recently released the results from two studies investigating Lucentis for the treatment of wet AMD. In those press releases, it was announced that Lucentis therapy in large multi-center trials improved vision at one year in patients with wet AMD. One of the differences between Lucentis and Avastin is that Lucentis is designed for injection into the eye and Avastin is designed for systemic infusion,” said Dr. Rosenfeld.
Dr. Rosenfeld went on to emphasize that Avastin therapy isn’t a cure and it’s not the right treatment for everyone with wet AMD. Avastin is only for patients in the early stages of the disease and should be used within 6 months to 12 months from the time of onset, said Dr. Rosenfeld. Some people would rather have an injection in the eye than worry about the risks of a systemic drug. What this offers us is a new potential option for patients with wet AMD. It also provides us with additional evidence that VEGF is the mayor factor for blood vessel growth and vision loss in wet AMD.
“We don’t know how many treatments will be needed,” Rosenfeld said. “In this study patients were treated two or three times over a twelve week period. As most patients eyes can be treated with a single infusion into the arm. Avastin is now delivered as an intraocular injection. A larger clinical trial is needed to determine if the benefits of Avastin outweigh the risks.”