Sumatriptan-induced angle-closure glaucoma

Hsu, Cherng-Ru; Chen, Yi-Hao; Tai, Ming‐Cheng; Lu, Da‐Wen

doi:10.1097/md.0000000000006953

Cited by 12 publications

(11 citation statements)

References 8 publications

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“… 5 Several medications have been reported to cause this type of drug-induced angle closure, most of which are sulfonamide derivatives such as topiramate, acetazolamide, methazolamide, indapamide and hydrochlorothiazide. 6 Other compounds such as venlafaxine, 7 escitalopram, 8 isotretetoin, 9 zolmitriptan 10 and sumatriptan 11 have also been described in the literature.…”

Section: Discussionmentioning

confidence: 99%

Acute bilateral angle closure induced by monoclonal antibody (Daratumumab) infusion

Saengsirinavin

Wutthayakorn

Chansangpetch

et al. 2021

American Journal of Ophthalmology Case Reports

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Purpose To report a case of daratumumab-induced bilateral angle closure glaucoma and myopia that showed no recurrence after repeated drug administration with prophylactic cycloplegia. Observations A 63-year-old man with relapsing multiple myeloma presented with acute bilateral eye pain and blurred vision 14 hours after first daratumumab infusion. Eye examination revealed raised intraocular pressure and shallow anterior chamber. Anterior segment ocular coherence tomography and ultrasound biomicroscopy showed ciliochoroidal effusions in both eyes. The diagnosis of bilateral acute angle closure glaucoma and induced myopia was made. Cycloplegia- and intraocular-pressure-lowering medications were given, which gradually deepened the anterior chambers and normalized intraocular pressure and refraction. The ciliochoroidal effusions completely resolved on day 14. The cycloplegic was given as a premedication for subsequent infusions. There was no recurrence of effusion throughout his 6-month daratumumab treatment course. Conclusions and importance Daratumumab can induce ciliochoroidal effusion, which results in acute secondary angle closure and myopia. The potential prophylactic effect of the cycloplegic drug may enable continuation of daratumumab infusion under close monitoring.

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Section: Discussionmentioning

confidence: 99%

Acute bilateral angle closure induced by monoclonal antibody (Daratumumab) infusion

Saengsirinavin

Wutthayakorn

Chansangpetch

et al. 2021

American Journal of Ophthalmology Case Reports

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“…Convincing evidence demonstrates that serotonin also exists in the mammalian retina (Osborne et al, 1981; Chanut et al, 2002) and has many functions, including altering retinal amacrine cell processing; additionally, serotonin is expressed in the aqueous humor of the eyes, while 5-HT1A receptor agonist can reduce intraocular pressure (IOP) in rabbits, but not in monkeys (George et al, 2005; Sharif, 2010). In contrast, it has been found that activation of 5-HT7 receptors can increase the generation of aqueous humor, thus inducing the increase of IOP (Costagliola et al, 2008; Hsu et al, 2017). Serotonin can act on different receptors and regulate different functions, and according to its structure and function, it can be classified into seven families (5-HT1R to 5-HT7R), which are further subdivided into 14 subtypes.…”

Section: Introductionmentioning

confidence: 94%

5-HT1A Receptor Agonist Promotes Retinal Ganglion Cell Function by Inhibiting OFF-Type Presynaptic Glutamatergic Activity in a Chronic Glaucoma Model

Zhou

Zhang

et al. 2019

Front. Cell. Neurosci.

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Serotonin receptors are potential neuroprotective agents in degenerative diseases of the central nervous system. The protective effects of serotonin receptor (5-HT1A) agonists on the survival and function of retinal ganglion cells (RGCs) by regulating the release of the presynaptic neurotransmitter γ-aminobutyric acid (GABA) were confirmed in our previous study of a chronic glaucoma rat model. However, the roles of excitatory amino acids and their interactions with the 5-HT1A receptor in glaucoma remain unknown. Here, we found that ocular hypertension increased glutamine synthetase (GS) and excitatory amino acid transporter 2 (EAAT2) expression in rat retinas. In addition, the high expression of GS and EAAT2 induced by glaucoma was downregulated by the 5-HT1A receptor agonist 8-OH-DPAT and the 5-HT1A receptor antagonist WAY-100635, respectively. Patch-clamp techniques were used to record glutamate receptor-mediated spontaneous and miniature glutamatergic excitatory post-synaptic currents (sEPSCs and mEPSCs) as well as L -glutamate-induced current in OFF-type and ON-type RGCs in rat retinal slices. Although there were no significant differences in the frequency and amplitude of sEPSC and mEPSC release between normal and glaucoma OFF- and ON-type RGCs, exogenous 8-OH-DPAT administration specifically reduced the frequency, but not the amplitude, of sEPSC and mEPSC release in glaucoma OFF-type rather than ON-type RGCs; these effects were completely blocked by WAY-100635. In summary, 8-OH-DPAT decreases and increases GS and EAAT2 expression of glaucomatous retina, respectively, while decreasing sEPSC and mEPSC frequency. In contrast, WAY-100635 increases and decreases GS and EAAT2 expression of glaucomatous retina, respectively, while increasing sEPSC and mEPSC frequency. The reduction of glutamatergic presynaptic transmission by 8-OH-DPAT deactivates RGCs at the neural network level and reduces the excitotoxic damage in the pathological process of chronic glaucoma.

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“…There exist case reports of duloxetine and venlafaxine causing ACG (20). Sumatriptan has also been reported to influence ACG [21,22]. The proposed mechanism is drug-induced malignant glaucoma, forward rotation of the lens-iris diaphragm, zonular relaxation and increased curvature of the lens.…”

Section: Serotonergic Agentsmentioning

confidence: 99%

“…The proposed mechanism is drug-induced malignant glaucoma, forward rotation of the lens-iris diaphragm, zonular relaxation and increased curvature of the lens. These factors contribute to a predisposition for ACG [22]. A proposed mechanism for ACG induced by Aripripazole is also activity at the 5H-T receptors or supraciliary effusion induction that displaces the lens-iris diaphragm anteriorly [23].…”

Section: Serotonergic Agentsmentioning

confidence: 99%

Drug-Induced Acute Angle-Closure Glaucoma: Raising your Index of Suspicion

An¹,

Bahajjaj

Lateef

et al. 2021

BJSTR

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Aim: To highlight polypharmacy as a risk factor for acute angle-closure glaucoma (AACG) in the emergency department (ED) with a brief literature review and propose an approach to early identification of AACG in the critically ill patients.Background: Acute angle-closure glaucoma (AACG) is an ophthalmological emergency that can lead to rapid, irreversible vision loss as a result of ischemia and atrophy of the optic nerve. Various drugs have been known to precipitate an acute angleclosure attack including adrenergics, anticholinergics, antihistamines, cholinergics, sulfonamides and serotonergic agents. Drug-induced AACG is usually observed in patients with predisposing risk factors. Anatomical risk factors include shallow chamber depth, small anterior segment and plateau iris configuration. Demographic risk factors include advanced age, family history, female gender and Asian ethnicity. Increasing rates of polypharmacy in the population, especially amongst the elderly, result in many patients with these predisposing risk factors also being on drugs that may precipitate AACG. More importantly, many drugs routinely prescribed acutely in the ED tend to overlap with the drugs reported to trigger AACG. Lastly, when an unresponsive patient presented to the ED, a diagnosis of AACG might be missed if the patient is unable to relay the classical symptoms. These three factors necessitate a high index of suspicion to ensure that a sight-threatening cause is not missed out in our patients.

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Sumatriptan-induced angle-closure glaucoma

Cited by 12 publications

References 8 publications

Acute bilateral angle closure induced by monoclonal antibody (Daratumumab) infusion

Acute bilateral angle closure induced by monoclonal antibody (Daratumumab) infusion

5-HT1A Receptor Agonist Promotes Retinal Ganglion Cell Function by Inhibiting OFF-Type Presynaptic Glutamatergic Activity in a Chronic Glaucoma Model

Drug-Induced Acute Angle-Closure Glaucoma: Raising your Index of Suspicion

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