Comparative Effectiveness of Treatments for Open-Angle Glaucoma: A Systematic Review for the U.S. Preventive Services Task Force
ABSTRACT Glaucoma is an acquired degeneration of the optic nerve and a leading cause of blindness worldwide. Medical and surgical treatments that decrease intraocular pressure may prevent visual impairment and blindness.
To compare the effectiveness of medical, laser, and surgical treatments in adults with open-angle glaucoma with regard to decreasing intraocular pressure and preventing optic nerve damage, vision loss, and visual impairment.
MEDLINE, CENTRAL, and an existing database for systematic reviews (through 2 March 2011); MEDLINE, EMBASE, LILACS, and CENTRAL for primary studies (through 30 July 2012).
English-language systematic reviews; randomized, controlled trials; and quasi-randomized, controlled trials for most outcomes and observational studies for quality of life and harms.
Two investigators abstracted or checked information about study design, participants, and outcomes and assessed risk of bias and strength of evidence.
High-level evidence suggests that medical, laser, and surgical treatments decrease intraocular pressure and that medical treatment and trabeculectomy reduce the risk for optic nerve damage and visual field loss compared with no treatment. The direct effect of treatments on visual impairment and the comparative efficacy of different treatments are not clear. Harms of medical treatment are primarily local (ocular redness, irritation); surgical treatment carries a small risk for more serious complications.
Heterogeneous outcome definitions and measurements among the included studies; exclusion of many treatment studies that did not stratify results by glaucoma type.
Medical and surgical treatments for open-angle glaucoma lower intraocular pressure and reduce the risk for optic nerve damage over the short to medium term. Which treatments best prevent visual disability and improve patient-reported outcomes is unclear.
Agency for Healthcare Research and Quality.
- SourceAvailable from: Peter J Little
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- "Glaucoma is one of the leading causes of blindness worldwide . Glaucoma is characterized by retinal ganglion cell (RGC) degeneration and loss of visual field and it occurs with or without elevated intraocular pressure (IOP) . "
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ABSTRACT: Cellular aging occurs by the lifelong accumulation of oxidative damage leading to neuronal apoptosis, termed 'neurodegeneration', and the functional deficits of aging. Loss of visual function is one of the most important quality of life measures for older adults. We discuss recent clinical and laboratory advances in the neuroprotective treatment of the aging eye with particular emphasis on the three major ocular neurodegenerative conditions: glaucoma, age-related macular degeneration (AMD), and diabetic retinopathy (DR).Missouri medicine 11/2012; 110(5):429-36.
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ABSTRACT: Dedicator of cytokinesis 3 (Dock3), a new member of the guanine nucleotide exchange factors for the small GTPase Rac1, promotes axon regeneration following optic nerve injury. In the present study, we found that Dock3 directly binds to the intracellular C-terminus domain of NR2B, an N-methyl-D-aspartate (NMDA) receptor subunit. In transgenic mice overexpressing Dock3 (Dock3 Tg), NR2B expression in the retina was significantly decreased and NMDA-induced retinal degeneration was ameliorated. In addition, overexpression of Dock3 protected retinal ganglion cells (RGCs) from oxidative stress. We previously reported that glutamate/aspartate transporter (GLAST) is a major glutamate transporter in the retina, and RGC degeneration due to glutamate neurotoxicity and oxidative stress is observed in GLAST-deficient (KO) mice. In GLAST KO mice, the NR2B phosphorylation rate in the retina was significantly higher compared with Dock3 Tg:GLAST KO mice. Consistently, glaucomatous retinal degeneration was significantly improved in GLAST KO:Dock3 Tg mice compared with GLAST KO mice. These results suggest that Dock3 overexpression prevents glaucomatous retinal degeneration by suppressing both NR2B-mediated glutamate neurotoxicity and oxidative stress, and identifies Dock3 signaling as a potential therapeutic target for both neuroprotection and axonal regeneration.Cell Death and Differentiation advance online publication, 12 July 2013; doi:10.1038/cdd.2013.91.Cell death and differentiation 07/2013; 20(9). DOI:10.1038/cdd.2013.91 · 8.39 Impact Factor