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Age-related macular degeneration (AMD):

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AMD is the primary cause of severe irreversible visual loss in persons over the age of fifty, affecting 1.75 million people in the United States alone. The prevalance of AMD is reported to increase from 1% at the age of 55 to 15% at the age of 80. It is a very complex, multi-factoral disease, whose cause and underlying pathways for development are poorly understood. Increasing age is the most important risk factor in developing AMD. The incidence increases with each successive decade of life after the age of 50. Other risk factors include a positive family history, female gender, Caucasian race, cigarette smoking, obesity and high blood pressure.

There are two forms of AMD. In the dry type, aging may reduce the amount of nourishment that the retina receives, allowing for the formation of abnormal deposits of breadown materials from the metabolism in the retinal tissue itself. It has also been linked to decreased dietary intake of a number of vitamins and minerals such as Zinc, Vitamin A, Vitamin C, Vitamin E, Lutein and Zeaxanthin. The dry form makes up 80-90% of all cases of AMD and the only viable treatment at the present time is the intake of vitamin supplementation in the form of Ocuvite or I-Caps with Lutein and Zeaxanthin. These are taken by mouth twice a day.

The dry form of AMD can lead to the wet form, depending on its severity. Dry AMD is characterized by the presence of deposits under the retina called drusen. The severity of the dry AMD is determined by the size and number of drusen present. Patients with minimal drusen are at very low risk (about 1.3% over a 5-year period of time) for developing severe and irreversible blindness. Patients with intermediate size of drusen present run about an 18% risk of progressing into the advanced stages of AMD over five years. To be classified as having advanced AMD, a patient must have developed the abnormal blood vessel complex underneath the retina itself and/or atrophy involving the macula of the eye, which is responsible for central visual acuity. A patient having these features in one eye have an approximately 43% chance of developing the component in the other eye over a 5-year period of time as well.

If a patient smokes there are special formulations that leave out the Beta-Carotene because studies suggest that active cigarette smokers or those who have just recently stopped smoking have an increased risk of developing lung cancers with the Beta-Carotene component. These special formulations are perfectly safe.

Obviously, vitamin and mineral intake along with a balanced diet that includes green vegetables is advantageous in retarding the development of AMD. In addition, one low dose 81mg aspirin daily is recommended, if there are no contraindications to aspirin therapy.

The second form of AMD is the wet form. This form comprises only about 10-20% of the cases but is responsible for 90% of patients who develop severe and irreversible blindness. In wet AMD, a bundle of abnormal blood vessels grow from the middle layer of the eye into and under the retinal tissue. In a short time, this leads to leaking of fluid and hemorrhaging underneath the retina in the dead center space of the retina that one reads with. As the process continues without treatment, these abnormal vascular membranes known as choroidal neovascular membranes will destroy the very important photo receptors of the retina, leading to the formation of a fibrotic scar in the macular portion of the retina and ultimately leading to irreversible blindness.

There have been quantum leaps in medical and surgical treatments of the wet form of AMD. Prior to any medication being available for treatment, laser photocoagulation was used to treat many forms of the disease. If the wet AMD was dead center under the macula, no treatment was available for many years. Then PDT (Photodynamic Therapy) was developed. A chemical agent called Verteporfin is injected into the veins. In conjunction with the laser treatment, this chemical did prove to occlude (or close) the small abnormal vessels in the neovascular membranes. Initially, only about 25% of these lesions were treatable with the laser or PDT. Most recently, about 35% can be treated.

However, PDT appears to damage the small normal blood vessels in the middle layer of the eye that nourishes the outer layer of the retina and keeps it viable and functional. This was not known initially when the treatment became available. This damage is associated with leaking blood vessels as seen within the first four to six hours after treatment. This leakage does resolve slowly by the end of the first week, as the small blood vessels become occluded and no longer leak. Even though the abnormal blood vessel membranes have been occluded, the normal small blood vessels that nourish that part of the retina that we read with have also become occluded. Thrombosis (closure) of these small normal blood vessels helps stimulate further development of new abnormal blood vessels and a vicious cycle follows. The occlusion of these small blood vessels reaches a maximum at about one week following PDT treatment and then resolves by 3 months in 50% of patients but persists in the remaining 50%. The more treatments an individual has, the more occlusion of the blood vessels takes place.

At the present time, studies are being conducted that are attempting to decrease the intensity of the laser and hopefully change the effect on the normal blood vessels while still occluding the abnormal blood vessels that have grown and started to leak and bleed.

In the last two years, pharmacological agents have become available for the treatment of wet AMD. They have proven to be quite effective, but not curative. The first to be approved by the FDA and become available was Macugen. It works by selectively binding and inhibiting the VEGF 165 released by some of the occular tissues. VEGE 165 is one of the substances responsible for the development of the abnormal new blood vessels bundles that cause the damage.

There are a number of other VEGF particles in the eye that are responsible for stimulating these new vessels, and Macugen only targets one of them. It has been proven about as effective as PDT treatment but without the side effects of the occlusion of the small blood vessels that the retina needs for its viability. Macugen does not occlude any vessels. Its primary function is to stop the new blood vessels from growing and becoming more of a problem, but it does cure wet AMD.

Avastin is a medication that Moulton Eye Clinic is using for treatment of wet AMD and other diseases of the retina. It attacks all forms of VEGF. Avastin is currently being used off-label, which means that it has not received FDA approval but can still be used for the neovascular (wet) form of AMD. It is quite effective and safe, much more so than Macugen and PDT. Unlike PDT or laser, Avastin does not damage or destroy any of the normal small blood vessels necessary for proper nourishment of the retinal tissue. Side effects withiin the eye are not yet known. Currently, no toxicity or damage to tissue has been reported. Avastin, like Macugen and Lucentis, is injected into the eye on an outpatient basis in our clinic under topical anesthesia. It is readily available and much less expensive than Macugen and the other treatment options.

Studies demonstrate the safety and effecacy of these intraocular injections for wet AMD but long-term effects are not known at this time. Patients are advised that they may need a minimum of one to two years of therapy before they realize the benefits of the injections. Injections every four to six weeks can be expected.
It has been our experience that results with the initial injection of Avastin for wet AMD have been very impressive, those being stabilization or improvement of visual acuity and decreased edema (swelling) of the retina.

Another medication called Lucentis will become available soon following FDA approval. It is designed to target all of the forms of VEGF, not just one. The patients treated with Lucentis experienced a mean improvement in vision as compared to other treatment modalities used in the past. It was the first to show actual improvement in visual acuity overall until Avastin became the primary treatment of choice.

The development of these anti-VEGF agents, that is Macugen, Lucentis and Avastin, represent an important advance in the treatment of wet AMD. The PDT laser treatment has proven to slow the loss of visual acuity in patients with wet AMD. Macugen also slows the loss. Lucentis appears to have actually improved vision in some patients based on numerous studies. In clinical experience of almost all retinal surgeons in the country as well as our own experience, Avastin also may improve vision by blocking all forms of VEGF.

The process, whether wet or dry, leads to impairment of central visual functions such as reading, driving, face recognition and other daily functions that depend on fine visual acuity. At the present time, there is no cure for macular degeneration, wet or dry. Obviously, a complete eye examination is critical in diagnosing the presence of macular degeneration and its different stages of severity.

Patients can check themselves at home using small grid paper. Testing one eye at a time, focus on a mark in the center of the paper. Any distortion of the lines should be reported to an Ophthalmologist as soon as possible, because it indicates the possible development of the wet form of AMD. The sooner the patient is diagnosed with the wet form, the sooner treatment can begin, thus resulting in better results. We ask our patients to tape the grid paper to the refrigerator door where they can see it daily and test each eye separately with glasses on if worn.

Even though the central vision may become distorted, blurred or wavy, the peripheral, or side, vision usually stays normal. In advanced stages of AMD, dry or wet, the patient may not be able to perform functions that require good central vision such as reading, sewing, driving, watching TV, etc.

AMD is a disease that should be treated early with a sense of urgency. It is also a chronic disease, which means that it is important to get examinations and treatment at regular intervals. There is no cure for AMD, but keeping up with your treatment regimen is absolutely critical to help slow and control the visual loss.
Outside of the doctor’s office, a patient can maintain as much vision as possible by:

  • Not smoking since cigarette smoking is a definite risk factor for developing AMD.
  • Taking vitamin and mineral supplements as discussed is also very important.
  • Controlling blood pressure and diabetes.
  • Wearing polarized sunglasses to block out harmful sunlight.
  • Eating foods rich in antioxidants such as fruits, dark green leafy vegetables and carrots.