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1 General aspects (0)   1.1 Epidemiology (10)   1.2 Population genetics (0)   1.3 Pathogenesis (2)   1.4 Quality of life (3)   1.5 Glaucomas as cause of blindness (2)   1.6 Prevention and screening (7) 2 Anatomical structures in glaucoma (0)   2.1 Conjunctiva (9)   2.2 Cornea (20)   2.3 Sclera (6)   2.4 Anterior chamber angle (4)   2.5 Meshwork (0)     2.5.1 Trabecular meshwork (11)     2.5.2 Schlemms canal (1)     2.5.3 Scleral outlet channels (0)   2.6 Aqueous humor dynamics (0)     2.6.1 Production (1)     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 (9)   2.9 Ciliary body (0)   2.10 Lens (2)   2.11 Vitreous body (0)   2.12 Choroid, peripapillary choroid, peripapillary atrophy (3)   2.13 Retina and retinal nerve fibre layer (20)   2.14 Optic disc (23)   2.15 Optic nerve (5)   2.16 Chiasma and retrochiasmal central nervous system (18)   2.17 Stem cells (3)   2.20 Other (0) 3 Laboratory methods (0)   3.1 Microscopy (2)   3.2 Electron microscopy (0)   3.3 Immunohistochemistry (0)   3.4 Molecular genetics (0)     3.4.1 Linkage studies (0)     3.4.2 Gene studies (22)   3.5 Molecular biology incl. 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associated with intraocular tumors (6)     9.4.9 Glaucomas associated with elevated episcleral venous pressure (1)       9.4.10 Glaucomas associated with hemorrhage (1)     9.4.11 Glaucomas following intraocular surgery (0)       9.4.11.1 Ciliary block (malignant) glaucoma (3)       9.4.11.2 Glaucomas in aphakia and pseudophakia (12)       9.4.11.3 Epithelial, fibrous, and endothelial proliferation (0)       9.4.11.4 Glaucomas associated with corneal surgery (8)       9.4.11.5 Glaucomas associated with vitreoretinal surgery (5)     9.4.15 Glaucoma in relation to systemic disease (27)     9.4.20 Other (4) 10 Differential diagnosis e.g. anterior and posterior ischemic optic neuropathy (4) 11 Medical treatment (0)   11.1 General management, indication (2)   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 (3)     11.3.4 Betablocker (3)     11.3.5 Other (0)   11.4 Prostaglandins 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Miscellaneous (18)

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Abstract #53540 Published in IGR 15-2

Oseltamivir (Tamiflu)-induced bilateral acute angle closure glaucoma and transient myopia

Lee JW; Lee JE; Choi HY; Lee JS
Indian Journal of Ophthalmology 2014; 62: 1165-1167

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A 27-year-old woman developed bilateral acute angle closure glaucoma (AACG) and transient myopia after taking oseltamivir for four days. On the fourth day, she received systemic and topical intraocular pressure (IOP)-lowering agents, and IOP decreased in both eyes. However, her visual acuity was unchanged. A myopic shift of -5.25 D OD and -5.0 D OS was estimated to have occurred in the acute phase. A-scan ultrasonography and Pentacam showed markedly shallow anterior chambers and increased lens thickness. Ultrasound biomicroscopy revealed an annular ciliochoroidal effusion with forward displacement of the lens-iris diaphragm. Ciliochoroidal effusion and transient myopia were resolved after discontinuation of oseltamivir.

Department of Ophthalmology, Pusan National University School of Medicine, Busan, Korea.

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Classification:

9.4.5.5 Other (Part of: 9 Clinical forms of glaucomas > 9.4 Glaucomas associated with other ocular and systemic disorders > 9.4.5 Glaucomas associated with disorders of the retina, choroid and vitreous)
9.4.20 Other (Part of: 9 Clinical forms of glaucomas > 9.4 Glaucomas associated with other ocular and systemic disorders)

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