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What are the types of age-related macular degeneration? [ 11/04/14 ]

There are two forms of AMD: dry and wet. It is possible for a person to suffer from both forms and for the disease to progress slowly or rapidly.

Dry macular degeneration is the most common type of AMD. This form, in which the photosensitive cells of the macula slowly break down, is diagnosed in 85 to 90 percent of cases. Yellow deposits called drusen (waste products from metabolism) form and accumulate under the retina, between the retinal pigmented epithelium (RPE) layer and the Bruch's membrane, the blood-retina barrier which supports the retina. Drusen are often found in the eyes of older people, but an increase in the size and number of these deposits is frequently the first sign of macular degeneration. Over time, drusen are associated with deterioration of the macula and the death of RPE and photoreceptor cells, resulting in blurring or a spotty loss of clear, straight-ahead vision.

Dry AMD may advance and cause loss of vision without turning into the wet form of the disease. It is also possible for early-stage dry AMD to change into the wet form of the disease.

Wet macular degeneration is usually preceded by the dry form of the disease. This wet form occurs when the Bruch's membrane begins to break down, usually near drusen deposits, and new blood vessels grow. This growth is called neovascularization. These vessels are very fragile and can leak fluid and blood, resulting in scarring of the macula and the potential for rapid, severe damage. The neovascularization disturbs the natural organization of the light-detecting photoreceptor cells and their associated RPE cells, eventually leading to their death. Straight-ahead vision can become distorted or be lost entirely in a short period of time, sometimes within days or weeks. The wet form accounts for approximately 10 percent of all cases of AMD, but it results in 90 percent of the cases of legal blindness. All wet AMD is considered advanced.

Although there is no cure, are there treatments available for age-related macular degeneration? [ 11/04/14 ]
  • Dry age-related macular degeneration

    Once dry age-related macular degeneration reaches the advanced stage, there is no form of treatment at present to prevent further vision loss. However, there is an intervention measure that could delay and possibly prevent intermediate age-related macular degeneration from progressing to the advanced stage in which vision loss occurs.

    The National Eye Institute’s Age-Related Eye Disease Study (AREDS) found that taking nutritional supplements with a specific high-dose formulation of antioxidants (vitamins C and E and beta-carotene), zinc, and copper delayed or prevented the progression of age-related macular degeneration from the intermediate to the advanced stage.

    A follow-up trial, called AREDS2, was completed in May 2013. In that study, researchers found that the addition of omega-3 fatty acids to the supplements did not improve the formula’s success. The antioxidants lutein and zeaxanthin proved safer than beta-carotene, which increases the risk of lung cancer for smokers or ex-smokers. Thus, the AREDS2 recommendation for the supplement formula is 500 milligrams of vitamin C, 400 international units of vitamin E, 10 milligrams of lutein, 2 milligrams of zeaxanthin, 80 milligrams of zinc, and 2 milligrams of copper.
  • Wet age-related macular degeneration

    Wet AMD can be treated with injections of angiogenesis inhibitors into the eye, with photodynamic therapy, or with laser surgery. None of these treatments will cure wet AMD, but each may slow the rate of vision decline or stop further vision loss. However, the disease and loss of vision may also progress despite treatment. Options should be discussed with a doctor.

    Angiogenesis Inhibitors: Angiogenesis inhibitors work by blocking the activity of vascular endothelial growth factor (VEGF), a protein that promotes blood vessel growth.

    Three treatments for wet AMD using angiogenesis inhibitors—EYLEA®, Lucentis®, and Macugen®—were approved by the U.S. Food and Drug Administration (FDA) in 2011, 2006, and 2004, respectively. There is also a fourth drug, called Avastin®, approved by the FDA as a blood vessel growth inhibitor to treat colorectal and other cancers, that has been used off-label (i.e., for purposes other than the approved uses) by some doctors to treat AMD.

    EYLEA®: After numbing the eye, the doctor injects EYLEA into the clear, jellylike substance (the vitreous) that fills the eye from the lens back to the retina and then monitors the patient's progress. After an initial three-month period of injections every four weeks, EYLEA can be administered every eight weeks.

    In comparison, treatments with the other angiogenesis inhibitors are normally given every four weeks (Lucentis and Avastin) or every six weeks (Macugen). The actual number of injections needed is determined by the physician, taking the individual patient's disease status and response to treatment into consideration.

    The most commonly reported side effects of EYLEA (affecting no more than fi ve percent of patients) include hemorrhage of the conjunctiva (the membrane that covers the white of the eye), eye pain, risk of cataract, vitreous detachment, vitreous floaters (specks or clouds moving in the field of vision), and increased eye pressure. There is a greater risk for endophthalmitis (severe inflammation of the eye interior) and retinal detachments, as can follow any injection into the vitreous.

    Lucentis®: Lucentis is also injected into the vitreous portion of the eye after it has been numbed. Injections are given regularly over a period of time. The frequency and actual number of injections needed are determined by the physician and the individual patient's disease status and response to treatment. Findings from international studies announced in 2012 indicate that an injection every four weeks may be optimal.

    The most commonly reported side effects of Lucentis include hemorrhage of the conjunctiva, floaters, eye pain, increased eye pressure, and inflammation of the eye. Rare but serious adverse events include endophthalmitis, retinal detachment, retinal tear, increased eye pressure, and traumatic cataract.

    Macugen®: Macugen is also injected into the vitreous portion of the eye that has been numbed. It is usually administered every six weeks. The actual number of injections needed is determined by the physician, taking the individual patient's disease status and response to treatment into consideration. Macugen is still available for treatment of wet AMD, but is not used as often as other injectable angiogenesis inhibitors.

    Common side effects of Macugen include inflammation of the eye, blurred vision, other changes in vision, cataracts, bleeding in the eye, swelling of the eye, eye discharge, irritation or discomfort of the eye, and "spots" in vision. Injection can also make the eye susceptible to infection for a period of time.

    Avastin®: Avastin is an FDA-approved cancer therapy drug manufactured by the same company that makes Lucentis. Avastin has been used by doctors as an off-label treatment for AMD. Both drugs are similarly administered. However, Avastin is much less expensive, and many doctors believe these drugs are equally effective against macular degeneration. The National Eye Institute of the National Institutes of Health conducted clinical trials (Comparison of Treatments Trials, or CATT) to study the relative efficacy and safety of Avastin and Lucentis. In May 2011, they reported that Avastin and Lucentis were found to be nearly equally effective in treating AMD.

    In April 2012, CATT findings showed that the best results for maintaining visual acuity are achieved with injections every four weeks, with comparable results for either Avastin or Lucentis injected monthly. The report showed that receiving doses of either drug "as needed" was less effective for maintaining visual acuity than monthly dosing. Although Avastin was associated with a greater number of serious adverse events than Lucentis, the researchers could not determine whether these differences were due to statistical chance or to real differences between the safety profiles of the two drugs.

    Drug Safety Issues

    Avastin®, a drug approved for cancer treatment, must be divided into smaller doses for use as an eye treatment. This is done by licensed "compounding pharmacies." Although use of a compounding pharmacy is an accepted practice, currently the compounded medicines are not individually evaluated by the U.S. Food and Drug Administration.

    The compounding procedure can also introduce the opportunity for bacterial contamination of a drug product. Although rare, there have been illnesses and even deaths due to poorly compounded drugs. Consult with your doctor about how your Avastin and other off-label drugs are prepared.

    For the latest news on this and other drug safety issues, visit the news updates section of our website.

    Photodynamic Therapy: Photodynamic therapy (PDT) is most effective in a subtype of wet AMD called predominantly classic subfoveal choroidal neovascularization, in which blood vessel growth and leakage in the fovea—the small region in the center of the macula—are well defined. It should be noted that PDT is rarely used now that there are drugs (EYLEA, Lucentis, Macugen, and Avastin) that specifically block the vessel-promoting VEGF protein. During the PDT procedure, a drug called Visudyne® is injected into the arm. The drug courses through the body and is absorbed by the fragile, leaking blood vessels in the eye.

    Because Visudyne is activated by light, the doctor directs a low-intensity laser at the retina for a little over a minute. This activates the Visudyne, allowing it to destroy the abnormal vessels. One treatment normally takes about twenty minutes and is relatively painless.

    The most common side effects of PDT include headache, injection site reaction, and blurred or reduced vision. Because the drug is activated by light, it is important to avoid exposing eyes or any part of the skin to sunlight or bright indoor light for up to five days after treatment.

    PDT may help to stabilize vision, but it will not restore lost vision.

    Laser Surgery: Laser photocoagulation surgery was the first treatment used for wet AMD, but it is only an option for a small number of patients. During the outpatient procedure, the eye is numbed, and a high-energy laser heats, seals, and destroys abnormal leaky blood vessels. This can potentially prevent further vision loss, but it results in a permanent blind spot due to scarring.

    Some patients experience mild pain during and/or shortly after the procedure. When successful, laser surgery is done once. However, if new blood vessels grow, surgery may have to be repeated.

    Implantable Miniature Telescope: Approved by the FDA in 2010, the implantable miniature telescope (IMT) may help those with end-stage wet AMD gain back some vision.

    The tiny telescope is inserted into one eye, which then provides central vision while the other eye provides peripheral vision. The telescope projects images over healthy areas of the retina. The IMT can usually be implanted by an eye surgeon during an outpatient surgical visit. After surgery, patients must participate in a structured vision rehabilitation program to learn how to perform daily activities using the device.
If diagnosed with age-related macular degeneration, what questions should I ask my doctor? [ 11/04/14 ]
  • Do I have wet macular degeneration or dry?
  • Do I have it in one eye or both eyes?
  • What stage of the disease do I have?
  • How often should I come in for check-ups?
  • What is the Amsler grid and how often should I perform a test with it at home?
  • Are there things that I can do to delay disease progression?
  • What are the current treatments for macular degeneration?
  • Are there lifestyle changes that I should make?
  • Should I alter my diet?
  • Do my current medications affect disease progression?
  • Should I begin to take vitamin supplements?
  • Will vitamin supplementation interfere with medications, or vice versa?
  • Are there any experimental treatments for macular degeneration?
What is age-related macular degeneration (AMD)? [ 11/04/14 ]

AMD is a common eye disease associated with aging that gradually destroys sharp, central vision. The retina is the very thin tissue that lines the back of the eye and contains the light-sensing cells that send visual signals to the brain. Sharp, clear, 'straight ahead' vision is processed by the macula, which is the central part of the retina. When the macula is damaged, many daily activities such as driving, reading and recognizing faces become increasingly difficult.

How many people are estimated to have age-related macular degeneration (AMD)? [ 11/04/14 ]

Age-related macular degeneration (AMD) is a major cause of visual impairment in the U.S. Age-related macular degeneration (AMD) is a major cause of visual impairment in the United States. As many as 11 million Americans have some form of macular degeneration, including both early and later stages of the wet and dry forms. More than two million people, aged 50 and older, are living with the most advanced forms of the disease.

How is age-related macular degeneration (AMD) diagnosed? [ 11/04/14 ]

To help diagnose AMD, an eye care professional will perform a dilated eye exam to view the retina and optic nerve for damage, a visual acuity test to measure sight from various distances and a fundoscopy to examine the back of the eye. If wet AMD is suspected, fluorescein angiography, in which dye is used to detect leaking blood vessels, may also be performed. The patient might be asked to look at Amsler grid; if the straight lines on the grid appear wavy or distorted, AMD may be developing.

What new research is being conducted to find a cure for age-related macular degeneration (AMD)? [ 11/04/14 ]

Researchers continue to explore environmental, genetic and dietary factors that may contribute to developing AMD. New treatment strategies are also being explored, including retinal cell transplants, drugs to prevent or slow down the progress of the disease, radiation therapy, gene therapies, a computer chip implanted in the retina (may help simulate vision) and agents to prevent the growth of new blood vessels under the macula.

Is age-related macular degeneration (AMD) hereditary? [ 11/04/14 ]

Age-related macular degeneration (AMD) typically affects individuals over 50 years old. Scientific evidence shows that genes may play a role in the development of nearly three out of four cases of this devastating eye disease.

Several genes are believed to be strongly associated with the risk of developing AMD:

  • Factor H and Factor B genes are responsible for proteins that help regulate inflammation in the part of the immune system that attacks diseased and damaged cells. According to study results published in 2006 by Columbia University, 74 percent of AMD patients carry certain variants in one or both of these genes, and these may significantly increase their risk of developing it.

  • PLEKHA1 – a gene located on chromosome 10; researchers believe it may increase the risk of developing AMD. Like Factors H and B, PLEKHA1 appears to be involved in the cellular processes related to inflammation.

  • LOC387715 – A certain variation of this gene appears to increase the risk of developing AMD. This risk is further heightened if a person with this gene variation also smokes.

  • HTRA1 – Scientists have identified a link between a mutation in this gene and the development of AMD. Specifically, the HTRA1 mutation is thought to be associated with the formation of drusen (yellow deposits of waste products under the retina that are often a sign of dry AMD), and may also promote the growth of fragile new blood vessels typical of wet AMD.

  • Complement C3 – Researchers have found that a variant in this gene increases the risk of developing the wet and dry forms of AMD. This gene plays an important role in the immune system, leading scientists to believe that inflammation is a vital part of the AMD disease process.

Other gene candidates are being studied to determine their role in AMD. While there is definitely a strong genetic component to this disease, it is highly likely that its development is due to a combination of multiple factors including gene mutations or variations and environmental factors such as sunlight exposure, diet and smoking.

Can you get age-related macular degeneration (AMD) in only one eye or does it usually occur in both? [ 11/04/14 ]

It is possible to develop AMD in only one eye. However, as the disease progresses both eyes may become affected. If an individual has macular degeneration in one eye, he or she is more likely to develop it in the other eye than someone who does not.

Can vitamin supplements help treat dry age-related macular degeneration? [ 11/04/14 ]

Once dry age-related macular degeneration reaches the advanced stage, there is no form of treatment at present to prevent further vision loss. However, there is an intervention measure that could delay and possibly prevent intermediate age-related macular degeneration from progressing to the advanced stage in which vision loss occurs.

The National Eye Institute’s Age-Related Eye Disease Study (AREDS) found that taking nutritional supplements with a specific high-dose formulation of antioxidants (vitamins C and E and beta-carotene), zinc, and copper delayed or prevented the progression of age-related macular degeneration from the intermediate to the advanced stage.

A follow-up trial, called AREDS2, was completed in May 2013. In that study, researchers found that the addition of omega-3 fatty acids to the supplements did not improve the formula’s success. The antioxidants lutein and zeaxanthin proved safer than beta-carotene, which increases the risk of lung cancer for smokers or ex-smokers. Thus, the AREDS2 recommendation for the supplement formula is 500 milligrams of vitamin C, 400 international units of vitamin E, 10 milligrams of lutein, 2 milligrams of zeaxanthin, 80 milligrams of zinc, and 2 milligrams of copper.

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Disclaimer: The information provided in this section is a public service of the BrightFocus Foundation, and should not in any way substitute for the advice of a qualified healthcare professional and is not intended to constitute medical advice. Although we take efforts to keep the medical information on our website updated, we cannot guarantee that the information on our website reflects the most up-to-date research. Please consult your physician for personalized medical advice; all medications and supplements should only be taken under medical supervision. The BrightFocus Foundation does not endorse any medical product or therapy.

Some of the content in this section is adapted from other sources, which are clearly identified within each individual item of information.

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