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      Steroid-Induced Iatrogenic Glaucoma

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          Abstract

          Steroids in susceptible individuals can cause a clinical condition similar to primary open-angle glaucoma. Five percent of the population are high steroid responders and develop an intraocular pressure (IOP) elevation of more than 15 mm Hg above baseline. IOP elevation may occur as early as 1 day to as late as 12 weeks after intravitreal triamcinolone in 20–65% of patients. On average, 75% of eyes with steroid implants require IOP-lowering therapy at some point within 3 years of follow-up. The exact mechanism of steroid-induced glaucoma is not totally understood, but decreased trabecular meshwork outflow is regarded as the main cause of IOP elevation. High-risk patients who receive steroids should be monitored closely and if they develop elevated IOP, steroids with lower potency or steroid-sparing agents should be used. The IOP usually returns to normal within 2–4 weeks after stopping the steroid. About 1–5% of patients do not respond to medical therapy and need surgery. Trabeculectomy, trabeculotomy, shunt surgery, and cyclodestructive procedures are among the methods employed. Removal of residual sub-Tenon or intravitreal steroids may help hasten the resolution of the steroid response. Early results with anecortave acetate, an analog of cortisol acetate with antiangiogenic activity, in controlling IOP have been promising.

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          Most cited references90

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          The Tight Junction Protein ZO-1 Establishes a Link between the Transmembrane Protein Occludin and the Actin Cytoskeleton

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            Corticosteroid-induced glaucoma: a review of the literature.

            The intraocular pressure rise that can complicate the use of topical or systemic corticosteroid has been recognised for 50 years. More recently, following isolation of the myocilin gene (previously known as the trabecular meshwork inducible glucocorticoid response or TIGR gene), there has been renewed interest in this steroid-responsive phenomenon. Furthermore, the currently fashionable use of injectable intraocular steroids in the management of clinically significant subretinal fluid and macular oedema has resulted in an increased incidence. Animal studies, cell biology, molecular biology, and an improved knowledge of genetics have provided a better understanding of the mechanisms behind the response. The purpose of this review is to describe the risk factors for developing corticosteroid-induced glaucoma, to discuss the underlying mechanisms and genetics of the condition and to present management options.
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              Analysis of myocilin mutations in 1703 glaucoma patients from five different populations.

              A glaucoma locus, GLC1A, was identified previously on chromosome 1q. A gene within this locus (encoding the protein myocilin) subsequently was shown to harbor mutations in 2-4% of primary open angle glaucoma patients. A total of 1703 patients was screened from five different populations representing three racial groups. There were 1284 patients from primarily Caucasian populations in Iowa (727), Australia (390) and Canada (167). A group of 312 African American patients was from New York City and 107 Asian patients from Japan. Overall, 61 different myocilin sequence variations were identified. Of the 61 variations, 21 were judged to be probable disease-causing mutations. The number of probands found to harbor such mutations in each population was: Iowa 31/727 (4.3%), African Americans from New York City 8/312 (2.6%), Japan 3/107 (2.8%), Canada 5/167 (3.0%), Australia 11/390 (2.8%) and overall 58/1703 (3. 4%). Overall, 16 (76%) of 21 mutations were found in only one population. The most common mutation observed, Gln368Stop, was found in 27/1703 (1.6%) glaucoma probands and was found at least once in all groups except the Japanese. Studies of genetic markers flanking the myocilin gene suggest that most cases of the Gln368Stop mutations are descended from a common founder. Although the specific mutations found in each of the five populations were different, the overall frequency of myocilin mutations was similar ( approximately 2-4%) in all populations, suggesting that the increased rate of glaucoma in African Americans is not due to a higher prevalence of myocilin mutations.
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                Author and article information

                Journal
                ORE
                Ophthalmic Res
                10.1159/issn.0030-3747
                Ophthalmic Research
                S. Karger AG
                0030-3747
                1423-0259
                2012
                January 2012
                13 July 2011
                : 47
                : 2
                : 66-80
                Affiliations
                aDepartment of Ophthalmology, Shiraz University of Medical Sciences, Shiraz, Iran; bWills Eye Institute, Philadelphia, Pa., USA
                Author notes
                *L. Jay Katz, MD, Glaucoma Service at Wills Eye Institute, 840 Walnut Street, Suite 1130, Philadelphia, PA 19107 (USA), Tel. +1 215 928 0166, E-Mail LJKwayne@aol.com
                Article
                328630 Ophthalmic Res 2012;47:66–80
                10.1159/000328630
                21757964
                14e8175f-d6ee-4e6b-8308-bda1fa3898c8
                © 2011 S. Karger AG, Basel

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                History
                : 01 September 2010
                : 08 April 2011
                Page count
                Tables: 3, Pages: 15
                Categories
                Review

                Vision sciences,Ophthalmology & Optometry,Pathology
                Steroid-induced ocular hypertension,Glaucoma,Intravitreal drug delivery

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