Bilateral Angle-Closure Glaucoma in a Young Female Receiving Cabergoline: A Case Report

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Abstract

Purpose

To report a case of bilateral acute angle-closure glaucoma after oral administration of cabergoline for the treatment of galactorrhea.

Methods

A diagnosis of secondary drug-induced angle-closure glaucoma was made in a patient with elevated intraocular pressure (IOP) and myopic refractive shift, which was confirmed by ultrasound biomicroscopy (UBM) of the ciliary body and anterior segment, sonography, and optical coherence tomography. The treatment included the discontinuation of the culprit drug and the administration of topical anti-glaucoma drops. The treatment course was followed with serial measurements of the IOP and refraction, and with performing UBM.

Results

Five hours after he received a single 0.5-mg oral cabergoline tablet, the patient suffered from acute secondary angle-closure glaucoma and myopic refractive error. UBM demonstrated both effusion of the ciliary body and an anterior rotation of the iris-ciliary body. IOP was reduced 8 h after cessation of the causative agent and administration of anti-glaucoma drops. Refractive errors returned to normal levels after 8 days.

Conclusion

Secondary acute angle-closure glaucoma has been reported to occur after the administration of some drugs. In this report, an attempt has been made to describe this adverse reaction after oral cabergoline intake.

Related collections

Most cited references 20

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Presumed topiramate-induced bilateral acute angle-closure glaucoma.

James Banta, Kara Hoffman, Donald L. Budenz … (2001)

We describe a case of bilateral angle-closure glaucoma associated with oral topiramate therapy. Interventional case report. Case report with echographic illustration. A 51-year-old man developed bilateral acute angle-closure glaucoma 2 weeks after beginning topiramate therapy for bipolar affective disorder. Laser peripheral iridotomy was performed in the right eye without resolution of the acute attack. Echography revealed lens thickening and ciliochoroidal detachments in both eyes. Visual acuity, intraocular pressure, and anterior and posterior segment anatomy normalized 2 weeks after cessation of topiramate therapy. Topiramate, a new sulfa-derivative antiepileptic medication, may cause idiosyncratic ciliochoroidal detachments and ciliary body edema leading to anterior displacement of the lens-iris diaphragm, lens thickening, and acute angle-closure glaucoma.

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Mechanism of topiramate-induced acute-onset myopia and angle closure glaucoma.

O. E. Craig, Giang T. Ong, L. Louis … (2003)

Interventional case report. In an institutional practice setting, two women, aged 25 and 45, developed acute myopia after starting topiramate for epilepsy. One patient also developed bilateral angle closure glaucoma. Topiramate was discontinued. Anterior chamber shallowing was noted in both patients at presentation. Ultrasonography showed ciliochoroidal effusion. Baseline measurements of anterior chamber depth and lens thickness were obtained. Topiramate may be associated with ciliochoroidal effusion with forward displacement of the lens-iris diaphragm and anterior chamber shallowing, resulting in acute myopia and angle-closure glaucoma. Increased lens thickness contributes only minimally (9%-16%) to anterior chamber shallowing.

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Drug-induced glaucomas: mechanism and management.

C. Tripathi, Brenda J Tripathi, G C Haggerty (2002)

Glaucoma comprises a heterogeneous group of diseases that have in common a characteristic optic neuropathy and visual field defects, for which elevated intraocular pressure is the major risk factor. The level of intraocular pressure within the eye depends on the steady state of formation and drainage of the clear watery fluid, called the aqueous humour, in the anterior chamber of the eye. An obstruction in the circulatory pathway of aqueous humour causes an elevation in intraocular pressure. Because intraocular pressure is the most modifiable parameter, therapeutic measures (medical and surgical) are aimed at reducing the pressure to protect against optic nerve damage. Glaucomatous optic neuropathy results from degeneration of the axonal nerve fibres in the optic nerve and death of their cell bodies, the retinal ganglion cells. Clinical examination of the optic nerve head or disc and the peripapillary nerve fibre layer of the retina reveals specific changes, and the resulting visual field defects can be documented by perimetry. Glaucoma can be classified into four main groups: primary open-angle glaucoma; angle-closure glaucoma; secondary glaucoma; and developmental glaucoma. Drug-induced glaucoma should be considered as a form of secondary glaucoma because it is brought about by specific systemic or topical medications. Although there is a high prevalence of glaucoma worldwide, the incidence of drug-induced glaucoma is uncertain. Drugs that cause or exacerbate open-angle glaucoma are mostly glucocorticoids. Several classes of drugs, including adrenergic agonists, cholinergics, anticholinergics, sulpha-based drugs, selective serotonin reuptake inhibitors, tricyclic and tetracyclic antidepressants, anticoagulants and histamine H(1) and H(2) receptor antagonists, have been reported to induce or precipitate acute angle-closure glaucoma, especially in individuals predisposed with narrow angles of the anterior chamber. In some instances, bilateral involvement and even blindness have occurred. In this article, the mechanism and management of drug-induced glaucomatous disease of the eye are emphasised. Although the product package insert may mention glaucoma as a contraindication or as an adverse effect, the type of glaucoma is usually not specified. Clinicians should be mindful of the possibility of drug-induced glaucoma, whether or not it is listed as a contraindication and, if in doubt, consult an ophthalmologist.

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Author and article information

Journal

Journal ID (nlm-ta): Case Report Ophthalmol

Journal ID (publisher-id): COP

Title: Case Reports in Ophthalmology

Publisher: S. Karger AG (Allschwilerstrasse 10, P.O. Box · Postfach · Case postale, CH–4009, Basel, Switzerland · Schweiz · Suisse, Phone: +41 61 306 11 11, Fax: +41 61 306 12 34, karger@karger.ch )

ISSN (Electronic): 1663-2699

Publication date Collection: Jan-Apr 2011

Publication date (Electronic): 21 January 2011

Publication date PMC-release: 21 January 2011

Volume: 2

Issue: 1

Pages: 30-33

Affiliations

Isfahan University of Medical Sciences and Health Services, Isfahan, Iran

Author notes

*Leila Rezaei, Isfahan University of Medical Sciences and Health Services, Isfahan 8138791985 (Iran), Tel. +98 311 445 2031, E-Mail leyla_rezaei60@ 123456yahoo.com

Article

Publisher ID: cop0002-0030

DOI: 10.1159/000324099

PMC ID: 3042015

PubMed ID: 21347189

SO-VID: 3765e16d-76bf-485d-a7b7-5aa9886d02ab

License:

This is an Open Access article distributed under the terms of the Creative Commons Attribution-Noncommercial-No-Derivative-Works License ( http://creativecommons.org/licenses/by-nc-nd/3.0/). Users may download, print and share this work on the Internet for noncommercial purposes only, provided the original work is properly cited, and a link to the original work on http://www.karger.com and the terms of this license are included in any shared versions.

History

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Figures: 1, References: 20, Pages: 4

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