Drug-induced glaucomas: mechanism and management.

作者: Ramesh C Tripathi , Brenda J Tripathi , Chris Haggerty

DOI: 10.2165/00002018-200326110-00002

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摘要: Glaucoma comprises a heterogeneous group of diseases that have in common characteristic optic neuropathy and visual field defects, for which elevated intraocular pressure is the major risk factor. The level within eye depends on steady state formation drainage clear watery fluid, called aqueous humour, anterior chamber eye. An obstruction circulatory pathway humour causes an elevation pressure. Because most modifiable parameter, therapeutic measures (medical surgical) are aimed at reducing to protect against nerve damage. Glaucomatous results from degeneration axonal fibres death their cell bodies, retinal ganglion cells. Clinical examination head or disc peripapillary fibre layer retina reveals specific changes, resulting defects can be documented by perimetry. classified into four main groups: primary open-angle glaucoma; angle-closure secondary developmental glaucoma. Drug-induced glaucoma should considered as form because it brought about systemic topical medications. Although there high prevalence worldwide, incidence drug-induced uncertain. Drugs cause exacerbate mostly glucocorticoids. Several classes drugs, including adrenergic agonists, cholinergics, anticholinergics, sulpha-based selective serotonin reuptake inhibitors, tricyclic tetracyclic antidepressants, anticoagulants histamine H1 H2 receptor antagonists, been reported induce precipitate acute glaucoma, especially individuals predisposed with narrow angles chamber. In some instances, bilateral involvement even blindness occurred. this article, mechanism management glaucomatous disease emphasised. product package insert may mention contraindication adverse effect, type usually not specified. Clinicians mindful possibility whether listed and, if doubt, consult ophthalmologist.

参考文章(71)
J R Polansky, J A Alvarado, A J Yun, D A Newsome, C G Murphy, Proteins secreted by human trabecular cells. Glucocorticoid and other effects. Investigative Ophthalmology & Visual Science. ,vol. 30, pp. 2012- 2022 ,(1989)
R R Allingham, K Wilson, A F Clark, M D McCartney, A W de Kater, Dexamethasone-induced ocular hypertension in perfusion-cultured human eyes. Investigative Ophthalmology & Visual Science. ,vol. 36, pp. 478- 489 ,(1995)
W Katowitz, M Gorla, E B Dreyer, D Zurakowski, P Simon, C K Vorwerk, L A Levin, Pilocarpine toxicity in retinal ganglion cells. Investigative Ophthalmology & Visual Science. ,vol. 40, pp. 813- 816 ,(1999)
K Wilson, S T Miggans, D Lane, A F Clark, M D McCartney, Inhibition of dexamethasone-induced cytoskeletal changes in cultured human trabecular meshwork cells by tetrahydrocortisol. Investigative Ophthalmology & Visual Science. ,vol. 37, pp. 805- 813 ,(1996)
W Howe, K Wilson, S T Miggans, M Kunkle, A F Clark, M D McCartney, Glucocorticoid-induced formation of cross-linked actin networks in cultured human trabecular meshwork cells Investigative Ophthalmology & Visual Science. ,vol. 35, pp. 281- 294 ,(1994)
J F Howes, Loteprednol etabonate: a review of ophthalmic clinical studies. Die Pharmazie. ,vol. 55, pp. 178- 183 ,(2000)
Luanna K. Putney, James D Brandt, Martha E O'Donnell, Effects of dexamethasone on sodium-potassium-chloride cotransport in trabecular meshwork cells Investigative Ophthalmology & Visual Science. ,vol. 38, pp. 1229- 1240 ,(1997)
S L Browder, K L Wilson, S T Miggans, M B Julian, A F Clark, H T Steely, The effects of dexamethasone on fibronectin expression in cultured human trabecular meshwork cells. Investigative Ophthalmology & Visual Science. ,vol. 33, pp. 2242- 2250 ,(1992)
Karanjit S. Kooner, Mordechai Sharir, Thom J. Zimmerman, Textbook of ocular pharmacology Lippincott-Raven. ,(1997)
Frederick T. Fraunfelder, Drug-Induced Ocular Side Effects ,(1996)