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1 General aspects (0)   1.1 Epidemiology (13)   1.2 Population genetics (0)   1.3 Pathogenesis (6)   1.4 Quality of life (7)   1.5 Glaucomas as cause of blindness (5)   1.6 Prevention and screening (6) 2 Anatomical structures in glaucoma (0)   2.1 Conjunctiva (6)   2.2 Cornea (17)   2.3 Sclera (14)   2.4 Anterior chamber angle (6)   2.5 Meshwork (0)     2.5.1 Trabecular meshwork (16)     2.5.2 Schlemms canal (4)     2.5.3 Scleral outlet channels (2)   2.6 Aqueous humor dynamics (0)     2.6.1 Production (0)     2.6.2 Outflow (0)       2.6.2.1 Trabecular meshwork (1)       2.6.2.2 Uveoscleral (0)     2.6.3 Compostion (1)   2.7 Episcleral veins and venous pressure (0)   2.8 Iris (6)   2.9 Ciliary body (1)   2.10 Lens (1)   2.11 Vitreous body (0)   2.12 Choroid, peripapillary choroid, peripapillary atrophy (18)   2.13 Retina and retinal nerve fibre layer (33)   2.14 Optic disc (34)   2.15 Optic nerve (2)   2.16 Chiasma and retrochiasmal central nervous system (4)   2.17 Stem cells (5)   2.20 Other (0) 3 Laboratory methods (0)   3.1 Microscopy (5)   3.2 Electron microscopy (0)   3.3 Immunohistochemistry (4)   3.4 Molecular genetics (0)     3.4.1 Linkage studies (2)     3.4.2 Gene studies (29)   3.5 Molecular biology incl. 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Refractive errors in relation to glaucoma (0)   8.1 Myopia (10)   8.2 Hypermetropia (1)   8.3 Contact lenses (1)   8.4 Refractive surgical procedures (0)   8.5 Other (0) 9 Clinical forms of glaucomas (0)   9.1 Developmental glaucomas (0)     9.1.1 Congenital glaucoma, Buphthalmos (17)     9.1.2 Juvenile glaucoma (21)     9.1.3 Syndromes of Axenfeld, Rieger, Peters, aniridia (3)     9.1.4 Other (0)   9.2 Primary open angle glaucomas (0)     9.2.1 Ocular hypertension (11)     9.2.2 Other risk factors for glaucoma (5)     9.2.3 Open angle glaucoma with elevated IOP (1)     9.2.4 Normal pressure glaucoma (15)   9.3 Primary angle closure glaucomas (0)     9.3.1 Acute primary angle closure glaucoma (pupillary block) (9)     9.3.2 Chronic primary angle closure glaucoma (pupillary block) (7)     9.3.3 Plateau iris syndrome (2)     9.3.4 Primary angle closure suspect (0)     9.3.5 Primary angle closure (3)     9.3.10 Other (0)   9.4 Glaucomas associated with other ocular and systemic disorders (0)     9.4.1 Steroid-induced glaucoma (7)     9.4.2 Glaucomas associated with disorders of the cornea, conjunctiva, sclera (1)       9.4.2.1 Iridocorneal endothelial syndrome (ICE, incl. irisatrophy) (1)       9.4.2.2 Posterior polymorphous dystrophy (0)       9.4.2.3 Fuchs' endothelial dystrophy (0)       9.4.2.5 Other (1)     9.4.3 Glaucomas associated with disorders of the iris and ciliary body (0)       9.4.3.1 Pigmentary glaucoma (1)       9.4.3.5 Other (0)     9.4.4 Glaucomas associated with disorders of the lens (0)       9.4.4.1 Exfoliation syndrome (14)       9.4.4.2 Glaucomas associated with cataracts (0)       9.4.4.3 Glaucomas associated with lens dislocation (0)       9.4.4.5 Other (1)     9.4.5 Glaucomas associated with disorders of the retina, choroid and vitreous (0)       9.4.5.1 Neovascular glaucoma (6)       9.4.5.5 Other (9)     9.4.6 Glaucomas associated with inflammation, uveitis (14)     9.4.7 Glaucomas associated with ocular trauma (1)     9.4.8 Glaucomas associated with intraocular tumors (3)     9.4.9 Glaucomas associated with elevated episcleral venous pressure (2)       9.4.10 Glaucomas associated with hemorrhage (1)     9.4.11 Glaucomas following intraocular surgery (0)       9.4.11.1 Ciliary block (malignant) glaucoma (1)       9.4.11.2 Glaucomas in aphakia and pseudophakia (7)       9.4.11.3 Epithelial, fibrous, and endothelial proliferation (0)       9.4.11.4 Glaucomas associated with corneal surgery (3)       9.4.11.5 Glaucomas associated with vitreoretinal surgery (3)     9.4.15 Glaucoma in relation to systemic disease (42)     9.4.20 Other (2) 10 Differential diagnosis e.g. anterior and posterior ischemic optic neuropathy (4) 11 Medical treatment (0)   11.1 General management, indication (6)   11.2 Cholinergic drugs (0)   11.3 Adrenergic drugs (0)     11.3.1 Epinephrine (0)     11.3.2 Thymoxamine, dapiprazole (0)     11.3.3 Apraclonidine, brimonidine (5)     11.3.4 Betablocker (4)     11.3.5 Other (0)   11.4 Prostaglandins 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    12.8.1 Without tube implant (13)     12.8.2 With tube implant or other drainage devices (29)     12.8.3 Non-perforating (2)     12.8.4 Using laser (0)     12.8.5 Other (2)     12.8.10 Woundhealing antifibrosis (13)     12.8.11 Complications, endophthalmitis (10)   12.9 Trabeculotomy, goniotomy (10)   12.10 Cyclodestruction (3)   12.11 Cyclodialysis (1)   12.12 Cataract extraction (1)     12.12.1 Intracapsular (0)     12.12.2 Extracapsular (0)     12.12.3 Phacoemulsification (4)   12.14 Combined cataract extraction and glaucoma surgery (0)     12.14.1 Intracapsular (0)     12.14.2 Extracapsular (0)     12.14.3 Phacoemulsification (7)   12.15 Capsulotomy (0)   12.16 Vitrectomy (2)   12.17 Anesthesia (5)   12.20 Other (1) 13 Therapeutic prognosis and outcome (0)   13.1 Prognostic factors (2)   13.2 Outcome (0)     13.2.1 IOP (2)     13.2.2 Visual field (0)       13.2.2.1 Progression (0)       13.2.2.2 Improvement (0)     13.2.3 Other (0) 14 Costing studies; pharmacoeconomics (4) 15 Miscellaneous (23)

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Abstract #69257 Published in IGR 18-1

Ocular hypotensive effect of fixed-combination brinzolamide/brimonidine adjunctive to a prostaglandin analog: a randomized clinical trial

Fechtner RD; Myers JS; Hubatsch DA; Budenz DL; Dubiner HB
Eye 2016; 30: 1343-1350

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PURPOSE: To determine whether intraocular pressure (IOP) lowering with fixed-combination brinzolamide/brimonidine (BBFC) adjunctive to a prostaglandin analog (PGA) was superior to that of vehicle+PGA in patients with open-angle glaucoma or ocular hypertension who were inadequately controlled with PGA monotherapy METHODS: This 6-week, multicenter, randomized, double-masked, parallel-group trial was conducted at 30 clinical sites in the United States between October 2013 and May 2014. Eligible patients were adults with open-angle glaucoma or ocular hypertension and with mean IOP ≥21 and <32 mm Hg, whereas receiving an open-label PGA (latanoprost, bimatoprost, or travoprost). Patients instilled a PGA once-daily in a run-in phase before randomization to masked BBFC or vehicle adjunctive treatment. Masked treatments were instilled 3 times daily for 6 weeks, and patients continued once-daily use of their PGA. The primary efficacy end point was the between-group difference in mean diurnal IOP (average of 0800, 1000, 1500, and 1700 hours time points) at week 6. RESULTS: At week 6, mean diurnal IOP with BBFC+PGA was lower than with vehicle+PGA (17.1±0.4 mm Hg vs 20.5±0.4 mm Hg; between-group difference, -3.4±0.5 mm Hg; P<0.0001; 95% confidence interval, -4.5 to -2.4 mm Hg). BBFC+PGA reduced mean diurnal IOP by 5.7 mm Hg (25%) from the baseline IOP achieved with PGA monotherapy. CONCLUSIONS: Therapy with BBFC produced an additive IOP-lowering effect compared with a PGA alone or in conjunction with vehicle. BBFC may provide an effective treatment option for patients receiving PGA monotherapy who require additional IOP reduction.

Department of Ophthalmology, SUNY Upstate Medical University, Syracuse, NY, USA.

Full article

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Classification:

11.13.5 Other (Part of: 11 Medical treatment > 11.13 Combination therapy)
11.4 Prostaglandins (Part of: 11 Medical treatment)

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