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Management of age-related macular degeneration
Age-related macular degeneration (AMD) is a multifactorial disorder with heterogeneous clinical features. Based on clinical and multimodal imaging studies, AMD has been classified with a great extent of consensus into early-stage, that is, from medium- to large-sized drusen and retinal pigmentary abnormalities and late-stage, that is, atrophic and neovascular. At different stages, multiple cell types of retina and choroid, as well as immune cells, interact and participate in pathophysiological events at the macular region. In the macular milieu, dysregulated events in the oxidative stress/ROS generation, bioenergetic homeostasis, complement, inflammation, angiogenesis, and extracellular matrix metabolism contribute to AMD pathogenesis over the disease course. To date, increasing genetic susceptibility loci have been identified, of which the most important ones are in the CFH and ARMS2 genes. The interplay between genetic factors and environmental factors has been gradually elucidated through new findings and the advent of new technologies. Based on the mechanistic understanding, slowing down the dry AMD progression by dietary antioxidants and zinc and preventing vision loss in patients with wet AMD by intravitreal anti-VEGF therapy have been achieved. However, it must be admitted that there is no cure for AMD yet. In this chapter, we are introducing the proven therapies for AMD patients at different stages and discussing some experimental therapies used in the real world clinical practice.
Management of dry AMD
Education on modifiable risk factors
There is no effective treatment for dry AMD to date. Therefore, the management for patients with dry AMD has focused on the prevention of vision loss and maintenance of the remaining visual functions. Smoking and diet habits are considered as important modifiable risk factors for AMD. Evidences exist that patients smoking longer than 40 years are likely to develop AMD two to four times more than nonsmokers of the same age groups. Therefore, for this influential risk factor, patients should be educated at each visit to refrain from smoking to preventing further visual loss. A high intake of certain fats, such as saturated fats, transfats, and omega-6 fatty acids, has been associated with a twofold increase in the prevalence of intermediate AMD, whereas monounsaturated fats were potentially protective. It has been recognized that modifiable factors, such as cigarette smoking and high-fat diet, can convert oxidative stress into a pathological role in AMD development. The negative impact of oxidative stress-related impaired cytoprotective functions of retinal pigment epithelium (RPE) may be the mechanistic bases of these detrimental risk factors.
Self-monitoring by Amsler grid
An Amsler grid should be provided to all AMD patients for self-monitoring purposes at home on a regular basis. Patients should be instructed to seek physicians’ advice urgently if any changes on Amsler grid test are noticed such as metamorphopsia and scotoma.
Dietary antioxidants and zinc
Age-related eye disease study (AREDS) and other previous epidemiologic studies pointed out a possible role for antioxidants in reducing the risk of cancer, cardiovascular disease, and eye disease. In addition, a small, randomized clinical trial suggested that pharmacologic doses of zinc provide some protection against vision loss from AMD. In Chapters 7 and 8 of this book, the possible pathogenic role of oxidative stress and ROS generation in AMD development has been discussed. The AREDS now called AREDS1 and the follow-up AREDS2 using high-dose antioxidant vitamins and minerals in dry AMD patients on a regular basis were applied. The results showed that both AREDS1 and AREDS2 formulations can decrease the risk of the development of advanced AMD in patients with dry AMD. Therefore, AREDS2 recommended that the individuals (>55 years old), who have one or more following clinical features, should take the AREDS2 supplements. The indications of AREDS2 are as follows: (1) extensive intermediate drusen (>63–125 μm); (2) at least one large druse (>125 μm); (3) geographic atrophy in one or both eyes; and (4) late stage of AMD in one eye. The formulation used in AREDS1 consisted of vitamin C, vitamin B, the β-carotene form of vitamin A, and 80 mg daily of zinc with copper to prevent zinc-induced copper deficiency. However, a high dose of zinc is potentially associated with genitourinary tract problems. Previous data also showed that 25 mg of zinc may be the maximal level that is absorbed. Additionally, β-carotene could increase the incidence of lung cancer in current and former smokers. Therefore, AREDS2 changed β-carotene and lowered zinc dose (from 80 to 25 mg daily) and tested whether alternative supplementations could enhance the outcome. Based on AREDS2, the carotenoid lutein and zeaxanthin are a safe alternative to β-carotene for peoples who had a smoking history. Comparing AREDS1 and AREDS2 formulations, the result of slowing down AMD progression by AREDS2 is probably superior. The result showed an 18% reduction in risk of advanced AMD above that conferred by the AREDS1 regimen. AREDS2 data demonstrated that lutein and zeaxanthin supplements added to the original AREDS1 formulation were associated with a statistically significant but modestly reduced (26%) risk of AMD. AREDS2 also showed that omega-3 fatty acids added to the formulation did not enhance outcome. The study of AREDS2 formulation with reduced potential side effects of a high dose of zinc showed a statistically significant benefit in AMD progression.
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