Uveal Effusion as a Mechanism of Bilateral Angle-Closure Glaucoma Induced by Chlorthalidone

Singer, James R.; Pearce, Zachary D.; Westhouse, Scott J.; Siebert, Karl J.

doi:10.1097/ijg.0000000000000037

Cited by 13 publications

(8 citation statements)

References 4 publications

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“…Sulfa-based medications implicated in AACG include topiramate and less commonly acetazolamide, trimethoprim-sulfamethoxazole, zonisamide, chlorthalidone, and hydrochlorothiazide. [36][37][38][39] Topiramate, commonly prescribed for seizures and migraines, is classically associated with AACG 32 (Table 1). Angle closure typically occurs within 2 weeks of starting topiramate, but reports have ranged between 1 days and 262 days.…”

Section: Sulfonamides (Topiramate)mentioning

confidence: 99%

Drug-induced Acute Angle-closure Glaucoma: A Review

Yang

Lin

2019

Journal of Current Glaucoma Practice

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Aim: Our goal is to review current literature regarding drug-induced acute angle-closure glaucoma (AACG) and provide ophthalmologists and general practitioners with a thorough understanding of inciting medications and treatment pitfalls to be avoided. Background: Drug-induced AACG is an ophthalmological emergency that ophthalmologists and general practitioners should be familiar with, given its potentially blinding consequences. Common anatomical risk factors for AACG include a shallow anterior chamber depth, short axial length, plateau iris configuration, thick lens, anteriorly positioned lens, and rarely, intraocular tumor. Demographic risk factors include female sex, Asian ethnicity, family history, and advanced age. In patients with predisposing factors, acute angle closure can be triggered by various classes of medications including adrenergic agonists, anticholinergics, cholinergics, sulfonamides, supplements, and serotonergic medications. Physicians prescribing such inciting medications should be aware of their potentially sight-threatening adverse effects and to inform patients of the warning symptoms. Patients typically present with elevated intraocular pressure (IOP), headache, nausea, blurry vision, and halos around lights. Review results: There are two main mechanisms of drug-induced AACG, both with different treatment strategies. The first mechanism of druginduced AACG is pupillary block and iridocorneal angle closure secondary to thickening of iris base with mydriasis. The second mechanism of drug-induced AACG is anterior displacement of the lens-iris diaphragm due to mass effect (e.g., blood, misdirected aqueous humor, and tumors), uveal effusion, or weakened zonules. Conclusion:This paper reviews drug-induced AACG, high-risk anatomical features, underlying mechanisms, inciting medications, and options for treatment and prevention. Clinical significance: With proper understanding of the underlying mechanism of drug-induced AACG, physicians can respond promptly to save their patients' vision by employing the correct treatment strategy.

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Section: Sulfonamides (Topiramate)mentioning

confidence: 99%

Drug-induced Acute Angle-closure Glaucoma: A Review

Yang

Lin

2019

Journal of Current Glaucoma Practice

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“…The following publications associate this idiosyncratic hypersensitivity reaction that translates into progressive narrowing of a previous normal anterior chamber (and, sometimes, acute angle closure) with the intake of drugs containing sulfonamide derivatives, that is, acetazolamide,17–19 chlorthalidone,4 20 21 furosemide,9 hydrochlorothiazide,22–24 indapamide,15 25 26 methazolamide,27 28 sulfasalazine,29 30 triplixam31 and topiramate,32 33 or some combinations5 34–36 (please see table 1).…”

Section: Discussionmentioning

confidence: 99%

Application of pharmacovigilance tools in a case of subacute anterior angle narrowing while under furosemide exposure

et al. 2022

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Sulfonamides have been related to drug-induced acute angle closure of the eye, but scarce reports exist concerning furosemide. We describe the second case of acute chamber narrowing (ACN) during furosemide exposure. A 65-year-old man with a renal transplant presented with ACN, after 3 months of furosemide intake. Finally, the patient required a bilateral iridotomy and right lens replacement. ACN has been associated with drugs containing sulfonamide derivatives, but an evaluation with pharmacovigilance scales for adverse drug reaction (ADR)-standardised causality assessment has not been provided. We use this case to illustrate how medicines and an ADR should be evaluated and reported. The spreading of pharmacovigilance information on what should be a rare and unexpected condition related to a drug could mean that other reports emerge about ADR with this drug and regulatory agencies perform consequently, as happened with topiramate.

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“…Several pharmacologic agents are known to induce bilateral angle closure via uveal effusions, including topiramate, flucloxacillin, carbamazepine, venlafaxine, trimethoprim/sulfamethoxazole, hydrochlorothiazide, chlorthalidone, buproprion, indapamide, and escitalopram [2][3][4][5][6][7][8][9][10][11][12][13] ; nevertheless, the pathophysiology of druginduced bilateral angle closure via uveal effusions is unclear. Many of the medications implicated in bilateral uveal effusions have sulfa moieties, although this has not yet been postulated as a definitive cause in the pathophysiology of uveal effusions.…”

Section: Diagnosis and Discussionmentioning

confidence: 99%

Bilateral uveal effusions in a 23-year-old man

Jeng-Miller

Gaier

Turalba³

2018

Digit J Ophthalmol

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A 23-year-old white man with a past medical history of seasonal allergies and no prior ocular history presented emergently to the Massachusetts Eye and Ear Emergency Ward with acute, bilateral blurry vision of one day's duration that had worsened overnight. He reported epiphora in both eyes and head pressure without headache. He described intermittent scintillations in both eyes of white and blue color. The patient reported taking a single dose of a "muscle relaxer" 10 days prior; he was unsure of the name of the drug. He denied any other new medications. He also reported an isolated episode of diarrhea on the day his blurry vision started. He denied eye pain, floaters, trauma, diplopia, fevers, rashes, recent travel, insect bites, myalgias, joint pain, dysuria, hematuria, melena, hematochezia, or shortness of breath. He cited occasional marijuana usage but no other recreational drug use. Figure 1. B-scan ultrasound of the left eye showing uveal effusion and no evidence of an intraocular mass. The same findings were present in the right eye.

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Uveal Effusion as a Mechanism of Bilateral Angle-Closure Glaucoma Induced by Chlorthalidone

Abstract: The antihypertensive medication chlorthalidone may cause bilateral uveal effusions inducing acute angle-closure glaucoma and acute myopia.

Cited by 13 publications

References 4 publications

Drug-induced Acute Angle-closure Glaucoma: A Review

Drug-induced Acute Angle-closure Glaucoma: A Review

Application of pharmacovigilance tools in a case of subacute anterior angle narrowing while under furosemide exposure

Bilateral uveal effusions in a 23-year-old man

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