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A 53-year-old woman with a severe headache, bilateral eye pain, blurred vision, and photophobia
Digital Journal of Ophthalmology 2011
Volume 17, Number 3
August 28, 2011
DOI: 10.5693/djo.03.2011.05.002
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Pedro Barros, MD | Department of Ophthalmology, Hospital Pedro Hispano, Porto, Portugal Liliana Paris, MD | Department of Ophthalmology, Hospital Pedro Hispano, Porto, Portugal Joana Martins, MD | Department of Ophthalmology, Hospital Pedro Hispano, Porto, Portugal Paula Tenedorio, MD | Department of Ophthalmology, Hospital Pedro Hispano, Porto, Portugal
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| Diagnosis and Discussion | In this case, ultrasound biomicroscopy and B-mode echography as well as the patient’s history made the diagnosis of secondary angle closure glaucoma without pupillary block due to intake oral topiramate (Figures 1-4).
Topiramate, a widely used anti-epileptic sulfamate-derived drug, has recently gained widespread use for migraine prophylaxis. It is also used to manage depression and neuropathic pain; off-label use as a weight-reduction and bipolar disorder agent has also become more widespread. Uveal effusion and secondary angle-closure glaucoma associated with topiramate use was first reported in July 2001 by Banta et al.(1) Since then several case reports have shown evidence of ciliary process inflammation and forward displacement of the lens-iris diaphragm with secondary angle-closure and myopia related to topiramate therapy.(2,3) Almost always bilateral, angle-closure glaucoma has been reported in patients with ages varying from 3 to 70 years and with doses from 50 mg or less to 100 mg or more.(4) Onset may occur within hours; the majority of cases present in the first two weeks of therapy.(4) Other reported ocular effects include scleritis, blepharospasm, myokymia, oculogyric crisis, nystagmus, and diplopia associated with dosages of at least 200 to 400 mg per day.(4,5)Topiramate is quickly absorbed after oral use, has a half-life of 24 hours and is rapidly excreted in urine. The exact mechanism of action is unknown, but research has shown that the drug blocks sodium channels, hyperpolarizes potassium currents, activates some subtypes of the GABA-A receptors and weakly inhibits carbonic anhydrase.(6) Utrasound technology has shown that angle-closure glaucoma can be induced when edema of the ciliary body leads to relaxation of the lens zonules, allowing the lens to thicken.(7,8) Suprachoroidal effusion, frequently present, and simultaneous anterolateral rotation of the ciliary body leads to anterior displacement of the iris-lens diaphragm, resulting in induced myopia and secondary anterior chamber shallowing with consequent angle-closure.
Uveal effusions as well as acute myopia have been reported in association with several sulfa-derived drugs, including acetazolamide, indapamide, chlorothiazide, promethazine, spironolactone and antibacterial sulfa preparations.(7,9-13)
Treatment of this condition requires IOP-lowering drugs and discontinuation of the sulfa-derived drug. Topical atropine 1% may lower IOP by causing retraction of the ciliary process thereby reducing lens thickness.(14) Methylprednisolone, possibly because of its stabilizing effect of the blood-retina barrier, may accelerate the resolution of the choroidal effusion.(8) Miotics are contraindicated in these cases since they induce contraction, mainly of the longitudinal portion of the ciliary muscle, which in turn can lead to further anterior displacement of the lens-iris diaphragm and increased angle narrowing.(7,10,15) Peripheral iridotomies are also ineffective because this entity occurs without pupillary block.(2,16) In our case, topiramate was discontinued and hypotensive medication and topical prednisone 1% were administered; we did not administer an oral corticosteroid since the patient had a history of corticosteroid allergy. Her condition resolved rapidly, probably because she had had a single, low dose (25 mg) of topiramate.
Her allergy to corticosteroid shows some idiosyncrasy for adverse reactions to drugs. Although there have been reports of bilateral angle-closure glaucoma after oral acetazolamide apparently by the same mechanism, we chose to administer the hypotensive agent to our patient since these cases have not been reported after a single dose of acetazolamide but only after a sensitizing dose in the past or repeated dosing. | |
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