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    Background: Age-related macular degeneration is the leading cause of blindness in the developed world. The number of persons with vision loss from age-related macular degeneration is projected to increase dramatically over the next few decades. Therefore, effective therapeutic and prophylactic agents are greatly needed. Objective: This article will discuss some of the newer treatment strategies that may help to reduce the incidence of visual loss from age-related macular degeneration. Some of these therapies and strategies can be implemented today, while many are hypothetical based on current laboratory data and ongoing clinical trials. Methods: A review of the literature and ongoing clinical trials was undertaken. Conclusion: Current therapies using antioxidants for prevention of the progression of age-related macular degeneration and anti-vascular endothelial growth factor therapies for neovascular age-related macular degeneration have given us tools for tackling this disease better and reducing the number of patients with vision loss. Combinations of some of the existing treatments and new forms of therapy may yet further decrease the treatment burden in the future.
    Pharmacotherapy
    Citations (14)
    Age-related macular degeneration is the leading cause of irreversible loss of vision in the west, accounting for up to 50% of all blind registrations. With an ageing population age-related macular degeneration will have a discernible impact on society and the NHS. This article outlines our current level of understanding of age-related macular degeneration and treatment strategies.
    Degeneration (medical)
    Population Ageing
    In Brief Purpose: To determine whether there is an association between response to intravitreal anti-vascular endothelial growth factor agents and genotype in patients with neovascular age-related macular degeneration. Methods: Analysis of the current literature evaluating pharmacogenetics of treatment response in patients with neovascular age-related macular degeneration. Results: Studies have demonstrated associations between various genotypes and response to intravitreal anti-vascular endothelial growth factor agents. Lower-risk genotypes of the CFH, ARMS2, HTRA1, and VEGF-A genes may be associated with improved visual outcomes. Additionally, frequency of injections may be associated with certain genotypes. Conclusion: Genetic background may influence an individual's response to treatment of neovascular age-related macular degeneration. Further studies to investigate biologic pathways of neovascular age-related macular degeneration and gene products that are directly involved might lead to better understanding of contribution of various genes to treatment response. A review of studies examining pharmacogenetics of treatment response to anti-vascular endothelial growth factor therapy in neovascular age-related macular degeneration.
    Pharmacogenomics
    To compare 25-hydroxyvitamin D (25OHD) levels in patients with neovascular age-related macular degeneration (NVAMD) with patients with nonneovascular age-related macular degeneration and control patients.Medical records of all patients diagnosed with age-related macular degeneration and tested for serum 25OHD level at a single medical center were reviewed. Control patients were selected from patients diagnosed with pseudophakia but without age-related macular degeneration. The lowest 25OHD level available for each patient was recorded.Two hundred sixteen patients with nonneovascular age-related macular degeneration, 146 with NVAMD, and 100 non-age-related macular degeneration control patients were included. The levels of 25OHD (mean ± SD) were significantly lower in NVAMD patients (26.1 ± 14.4 ng/mL) versus nonneovascular age-related macular degeneration (31.5 ± 18.2 ng/mL, P = 0.003) and control (29.4 ± 10.1 ng/mL, P = 0.049) patients. The prevalence of vitamin D insufficiency (<30 ng/mL 25OHD), deficiency (<20 ng/mL), and severe deficiency (<10 ng/mL) were highest in the NVAMD group. The highest quintile of 25OHD was associated with a 0.35 (95% confidence interval, 0.18-0.68) odds ratio for NVAMD.This is the largest study to compare 25OHD levels in patients with the different clinical forms of age-related macular degeneration. Mean 25OHD levels were lower and vitamin D deficiency was more prevalent in NVAMD patients. These associations suggest that further research is necessary regarding vitamin D deficiency as a potentially modifiable risk factor for the development of NVAMD.