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1 General aspects (0)   1.1 Epidemiology (6)   1.2 Population genetics (1)   1.3 Pathogenesis (0)   1.4 Quality of life (1)   1.5 Glaucomas as cause of blindness (4)   1.6 Prevention and screening (2) 2 Anatomical structures in glaucoma (0)   2.1 Conjunctiva (1)   2.2 Cornea (2)   2.3 Sclera (0)   2.4 Anterior chamber angle (2)   2.5 Meshwork (1)     2.5.1 Trabecular meshwork (16)     2.5.2 Schlemms canal (0)     2.5.3 Scleral outlet channels (0)   2.6 Aqueous humor dynamics (0)     2.6.1 Production (2)     2.6.2 Outflow (2)       2.6.2.1 Trabecular meshwork (2)       2.6.2.2 Uveoscleral (1)     2.6.3 Compostion (0)   2.7 Episcleral veins and venous pressure (0)   2.8 Iris (0)   2.9 Ciliary body (1)   2.10 Lens (0)   2.11 Vitreous body (0)   2.12 Choroid, peripapillary choroid, peripapillary atrophy (1)   2.13 Retina and retinal nerve fibre layer (8)   2.14 Optic disc (11)   2.15 Optic nerve (1)   2.16 Chiasma and retrochiasmal central nervous system (0)   2.17 Stem cells (0)   2.20 Other (1) 3 Laboratory methods (0)   3.1 Microscopy (0)   3.2 Electron microscopy (0)   3.3 Immunohistochemistry (11)   3.4 Molecular genetics (3)     3.4.1 Linkage studies (6)     3.4.2 Gene studies (7)   3.5 Molecular biology incl. 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Abstract #9920 Published in IGR 5-3

Intraocular pressure, safety, and quality of life in glaucoma patients switching to latanoprost from monotherapy treatments

Zimmerman TJ; Stewart WC
Journal of Ocular Pharmacology and Therapeutics 2003; 19: 405-415

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PURPOSE: To evaluate the efficacy, safety and quality of life in ocular hypertensive or open-angle glaucoma patients who required alteration in previous therapy and were changed to latanoprost. METHODS: A prospective, multicenter, active, historical controlled trial in which qualified patients had previous therapy substituted with latanoprost 0.005% and were followed for up to six months. RESULTS: Thirty-one hundred and seventy-nine patients were included in the intent-to-treat analysis. In all patients latanoprost reduced the intraocular pressure (IOP) from 20.1 ± 3.9 to 17.1 ± 3.5 mmHg (p < 0.0001) and when compared to previous monotherapies: beta-blockers (-3.0 ± 3.5, n = 1976), alpha-agonists (-3.6 ± 3.7, n = 581), miotics (-2.8 ± 3.0, n = 21), carbonic anhydrase inhibitors (-3.2 ± 3.5, n = 198), and other prostaglandin analogues (-1.6 ± 3.7, n = 402). The most common ocular adverse event with latanoprost was conjunctival hyperemia (n = 66, 2.0% incidence) and the most common systemic adverse event was headache (n = 9, 0.2%). Over the six-month treatment interval, 89.8% of patients were maintained on latanoprost. On the solicited symptom survey patients showed a preference for latanoprost compared to previous therapy for several reasons: (depending on the product) dryness, blurred vision, tearing, stinging on instillation, crusting, itching, fatigue, dizziness, despondency and dry mouth (p < 0.005). CONCLUSIONS: Latanoprost generally provides reduced IOP, limited side-effects, improvement in many quality of life measures and is maintained in patients who required a substitution from previous monotherapy.

Dr. W.C. Stewart, Pharmaceutical Research Network, L.L.C., 1639 Tatum Street, Charleston, SC 29412-2464, USA

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Classification:

11.4 Prostaglandins (Part of: 11 Medical treatment)

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