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      Acetazolamide-induced cilio-choroidal effusion after cataract surgery: unusual posterior involvement

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          Abstract

          Idiosyncratic reactions to a large number of drugs have been reported to cause choroidal detachment and secondary angle-closure glaucoma (ACG). We report a case of bilateral acute ACG and peculiar choroidal effusion following administration of oral acetazolamide immediately after cataract surgery. Few cases of acute secondary ACG with choroidal effusion and anterior shift of the lens-iris diaphragm have been associated with acetazolamide compared with other sulfonamides. As far as we are aware, posterior involvement with retinal folds and papillary edema due to acetazolamide has not been described before.

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          Most cited references 19

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          Topiramate-associated acute, bilateral, secondary angle-closure glaucoma.

          To evaluate spontaneous reports of ocular side effects associated with topiramate use. Retrospective case series. One hundred fifteen case reports, primarily of a specific ocular syndrome (acute secondary angle-closure glaucoma), were collected from spontaneous reporting systems: the Drug Safety section of Ortho-McNeil Pharmaceuticals, Inc. (Raritan, NJ), the Food and Drug Administration (Rockville, MD), the World Health Organization (Uppsala, Sweden), the National Registry of Drug-Induced Side Effects (Casey Eye Institute, Oregon Health & Science University, Portland, Oregon), and the world literature. The data were evaluated using the World Health Organization Causality Assessment Guide to the certainty of a suspected adverse drug reaction. Eighty-six cases of acute-onset glaucoma (83 bilateral and 3 unilateral), 17 cases of acute bilateral myopia (up to 8.75 diopters), 9 cases of suprachoroidal effusions, 3 cases of periorbital edema, and 4 cases of scleritis were reported. In those cases for which management was reported, 38% had laser or surgical peripheral iridectomy (21 cases). In the "certain" category of the World Health Organization classification system, the following are caused by topiramate therapy: abnormal vision, acute secondary angle-closure glaucoma, acute myopia, and suprachoroidal effusions. All findings are reversible if recognized early and if the drug is discontinued. The first presenting symptom of acute secondary angle-closure glaucoma in many patients was blurring of vision. Peripheral iridectomy is ineffective for this type of angle-closure glaucoma.
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            Sulfonamides: a patent review (2008 - 2012).

            The primary sulfonamide moiety is present in many clinically used drugs, such as diuretics (furosemide, indapamide, chlorthalidone, thiazides); carbonic anhydrase (CA) inhibitors (CAIs) (including acetazolamide, dichlorophenamide, dorzolamide and brinzolamide); antiepileptics (zonisamide and sulthiame); the antipsychotic sulpiride and the cycloxygenase 2 (COX2) inhibitors celecoxib and valdecoxib. Recently, novel drugs have been launched, such as apricoxib and pazopanib, which also incorporate this group. The article presents the main classes of sulfonamides investigated between 2008 and 2012. Specifically, the authors review the scientific and patent literature on CAIs, COX2 inhibitors, pazopanib and its congeners, which are multi-targeted receptor tyrosine kinase inhibitor of VEGFR-1, VEGFR-2, VEGFR-3, PDGFR-a/β, and c-kit. Most patents deal with sulfonamide CAIs incorporating NO-donating moieties as antiglaucoma agents, or with compounds targeting the tumor-associated isoforms CA IX/XII. The antidandruff actions of sulphonamides, which inhibit yeast CAs, were also claimed. Apricoxib (a COX2 inhibitor) and pazopanib, a tyrosine kinase inhibitor, show significant antitumor activity and several patents deal with these drugs. There is a constant need of novel sulfonamides to act as selective antiglaucoma drugs (targeting CA II), as antitumor agents/diagnostic tools (targeting CA IX/XII), and to treat and diagnose other disease. This privileged structural motif is likely to be present in other drugs in the future.
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              Drug-induced acute angle closure glaucoma.

              Acute angle closure glaucoma is a potentially blinding side effect of a number of local and systemic drugs, including adrenergic, both anticholinergic and cholinergic, antidepressant and antianxiety, sulfa-based, and anticoagulant agents. The purpose of this article is to bring this condition to the attention of clinicians using these compounds as well as ophthalmologists called to see the patient. Acute angle closure glaucoma due to pupillary block, treatable by peripheral iridotomy, can be caused by adrenergic agents, either locally (phenylephrine drops, nasal ephedrine, or nebulized salbutamol) or systemically (epinephrine for anaphylactic shock), drugs with anticholinergic effects including tropicamide and atropine drops, tri and tetracyclic antidepressants, and cholinergic agents like pilocarpine. A novel anticholinergic form is the use of periocular botulinum toxin diffusing back to the ciliary ganglion inhibiting the pupillary sphincter. Sulfa-based drugs (acetazolamide, hydrochlorothiazide, cotrimoxazole, and topiramate) can cause acute angle closure glaucoma by ciliary body edema with anterior rotation of the iris-lens diaphragm. Iridotomy is not effective. Most attacks of acute angle closure glaucoma involving pupillary block occur in individuals that are unaware that they have narrow iridocorneal angles. Practitioners using any of the above drugs should be aware of their potential to cause acute angle closure.
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                Author and article information

                Journal
                Drug Des Devel Ther
                Drug Des Devel Ther
                Drug Design, Development and Therapy
                Dove Medical Press
                1177-8881
                2013
                23 January 2013
                : 7
                : 33-36
                Affiliations
                Department of Ophthalmology, University of Rome “La Sapienza,” Rome, Italy
                Author notes
                Correspondence: Loredana Arrico, Department of Ophthalmology, University of Rome “Sapienza,” Viale del Policlinico 155m, 00161 Rome, Italy, Tel +39 335 690 0888, Email loredana.arrico@ 123456uniroma1.it
                Article
                dddt-7-033
                10.2147/DDDT.S38324
                3556858
                23378740
                © 2013 Malagola et al, publisher and licensee Dove Medical Press Ltd.

                This is an Open Access article which permits unrestricted noncommercial use, provided the original work is properly cited.

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