Disease relevance of Glaucoma, Open-Angle

• Genetic heterogeneity of primary open angle glaucoma and ocular hypertension: linkage to GLC1A associated with an increased risk of severe glaucomatous optic neuropathy [1].
• METHODS: Patients treated with latanoprost for open-angle glaucoma or ocular hypertension were randomly assigned to refill their prescriptions either at the Doheny Eye Institute clinic or a local pharmacy [2].
• CONCLUSIONS: Female reproductive factors do not appear to influence age-related cataract, open-angle glaucoma, macular degeneration or myopia significantly in rural south India [3].
• The sensitivities of an S and an M cone pathway were assessed in patients with retinitis pigmentosa, insulin-dependent diabetes mellitus and open-angle glaucoma using Stiles two-color increment threshold technique [4].
• PARTICIPANTS: Ten eyes (five primary open-angle glaucoma, four chronic angle-closure glaucoma, one nanophthalmos) of nine patients with a mean age of 68.5+/-12.0 years (range, 43-83 years) [5].

High impact information on Glaucoma, Open-Angle

• Clinical features associated with mutations in the chromosome 1 open-angle glaucoma gene (GLC1A) [6].
• Myopia was present in 59% of the ocular hypertensives and 73% of the primary open-angle glaucoma patients, of whom 39% had more than 6 diopters of myopia [7].
• Timolol in the treatment of open angle glaucoma [8].
• CYP1B1 mutations involved cases of juvenile open-angle glaucoma, as well as cases of congenital glaucoma [9].
• Apolipoprotein E-promoter single-nucleotide polymorphisms affect the phenotype of primary open-angle glaucoma and demonstrate interaction with the myocilin gene [10].

Chemical compound and disease context of Glaucoma, Open-Angle

• Defects in cortisol-metabolizing enzymes in primary open-angle glaucoma [11].
• This system may provide an acute model in which to study the pathogenic mechanisms involved in steroid glaucoma and primary open angle glaucoma [12].
• Levobunolol is a potent non-selective beta-adrenoceptor blocking agent used for the topical treatment of increased intraocular pressure in patients with chronic open angle glaucoma or ocular hypertension [13].
• Metipranolol is a non-selective beta-adrenoceptor blocking agent used for the topical treatment of elevated intraocular pressure in patients with chronic open angle glaucoma or ocular hypertension [14].
• PURPOSE: To assess the level of plasma glutathione in patients with untreated primary open-angle glaucoma [15].

Biological context of Glaucoma, Open-Angle

• Mutations in the MYOC gene may lead to juvenile open-angle glaucoma with high intraocular pressure, and are detected in about 4% of people with adult onset glaucoma [16].
• Myocilin is a secreted glycoprotein that is mutated in some forms of primary open-angle glaucoma (POAG), and patients with the Tyr437His mutation have severe phenotypes [17].
• Genetic polymorphisms in the angiotensin II receptor gene and their association with open-angle glaucoma in a Japanese population [18].
• Total biologic plasma glucocorticoid activity of normal, ocular hypertensive, and open-angle glaucoma patients was compared using a glucocorticoid receptor-based competitive binding assay [19].
• We also report that melanosomes in the DBA/2J strain, the parental strain of the Hermansky-Pudlak syndrome strain sandy, are abnormal, indicating that aberrant biogenesis of melanosomes may play a part in the pathogenesis of pigmentary glaucoma observed in these mice [20].

Anatomical context of Glaucoma, Open-Angle

• Using the DBA/2J mouse as an animal model of human pigmentary glaucoma, we demonstrated for the first time that the expression of the IL-18 protein and gene in the iris/ciliary body and level of IL-18 protein in the aqueous humor of DBA/2J mice are dramatically increased with age [21].
• Myocilin is mutated in some forms of primary open angle glaucoma and affected patients show very high intraocular pressures because of an increase in resistance to aqueous humor outflow [22].
• PURPOSE: Glucocorticoid-induced ocular hypertension (the steroid response) may result in optic nerve damage that very closely mimics the pathologic course of primary open angle glaucoma (POAG) [23].
• It has been suggested that the trabecular meshwork may be involved in the pathogenesis of open-angle glaucoma, and some authors have pointed out that disorders of the extracellular matrix components may play a role; nevertheless, nothing is known about the normal metabolism of connective tissue molecules in this particular tissue [24].
• Ultrastructural immunocytochemical analysis of elastin in the human lamina cribrosa. Changes in elastic fibers in primary open-angle glaucoma [25].

Gene context of Glaucoma, Open-Angle

• MYOC mutations included cases of juvenile glaucoma with or without pigmentary glaucoma and mixed-mechanism glaucoma [9].
• Herein, we report mapping of a new adult-onset primary open-angle glaucoma (POAG) locus on 5q22.1 (GLC1G) and identification of its defective gene [26].
• Due to opticin's protein profile in the eye, we have also screened OPTC for mutations in individuals with primary open-angle glaucoma (POAG), normal-tension glaucoma (NTG) or AMD [27].
• PURPOSE: It has been shown that mutations in the optineurin (OPTN) gene are involved in the etiology of adult-onset primary open-angle glaucoma (POAG) [28].
• These results indicate that unlike NTG, the OPA1 genotype IVS8+4 C/T,+32T/C is not significantly associated with high-tension primary open angle glaucoma, and suggest genetic heterogeneity between the conditions [29].

Analytical, diagnostic and therapeutic context of Glaucoma, Open-Angle

• In a prospective randomized single-masked study lasting 6 months, 39 eyes with primary open-angle glaucoma showing a long-term drift with 0.5% timolol were put on a "timolol holiday" lasting 30 or 60 days [30].
• Antinuclear antibodies (ANA) were examined in the sera of 28 patients with chronic open angle glaucoma (COAG) and 24 normal volunteers by an immunoperoxidase technique [31].
• Immunohistochemistry was also used to assess the NOS-2 level in the ONH from primary open-angle glaucoma (POAG) and nonglaucomatous human eyes [32].
• METHODS: Patients with phakic, uncontrolled, open-angle glaucoma who were undergoing initial trabeculectomy were prospectively assigned to the 5-FU group on the first postoperative day [33].
• A 12-month, randomized, double-masked study comparing latanoprost with timolol in pigmentary glaucoma [34].

References