Transient Myopia Induced by Sulfonamides

Hook, Stephen R.; Holladay, Jack T.; Prager, Thomas C.; Goosey, John D.

doi:10.1016/0002-9394(86)90660-4

Cited by 44 publications

(10 citation statements)

References 4 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…These episodes do not involve the pupil and are not responding to cycloplegic agents. This observation has been confirmed by A-scan measurements of the eye during such an attack 16 . …”

Section: Sulfa Drugssupporting

confidence: 57%

Drug-Induced Glaucoma (Glaucoma Secondary to Systemic Medications)

Rath¹

2011

Glaucoma - Basic and Clinical Concepts

View full text Add to dashboard Cite

“…These episodes do not involve the pupil and are not responding to cycloplegic agents. This observation has been confirmed by A-scan measurements of the eye during such an attack 16 . …”

Section: Sulfa Drugssupporting

confidence: 57%

Drug-Induced Glaucoma (Glaucoma Secondary to Systemic Medications)

Rath¹

2011

Glaucoma - Basic and Clinical Concepts

View full text Add to dashboard Cite

“…Sulfonamide-derived medications, such as topiramate, are well known to induce transient myopia through ciliary body edema, causing relaxation of the zonules, lens thickening, and forward movement of the lens-iris diaphragm. [2][3][4] Although the…”

Section: Discussionmentioning

confidence: 98%

Delayed Topiramate-induced Bilateral Angle-Closure Glaucoma

Czyz

Clark

Justice

et al. 2014

Journal of Glaucoma

View full text Add to dashboard Cite

show abstract

“…Ciliary body oedema resulting in either anterior displacement or thickening of the crystalline lens has been suggested as the probable cause (Bovino & Marcus 1982;Hook et al 1986). …”

Section: Sulphonamidesmentioning

confidence: 98%

Clinically Important Ocular Reactions to Systemic Drug Therapy

Rennie

1993

Drug Safety

View full text Add to dashboard Cite

Many systemically administered drugs produce ocular adverse effects. Fortunately, relatively few are capable of causing significant, irreversible visual impairment. It is the responsibility of every clinician when prescribing systemic therapeutic agents to be aware of potential adverse ocular reactions, to appreciate their significance, and to inform the patient of the potential risks of treatment. In instances where serious adverse reactions relate to the cumulative effects of prolonged treatment, it is the responsibility of the prescribing physician to institute appropriate methods of visual screening. In this respect, it is most important to obtain the necessary individual baseline measurements before treatment is commenced. Chloroquine retinopathy is probably the most feared of all adverse ocular reactions to systemic drug therapy. However, it occurs only rarely if the daily dosage of chloroquine does not exceed 250mg. Regular screening using automated perimetry is mandatory if prolonged therapy is contemplated. Amiodarone almost inevitably produces corneal deposits. These rarely produce symptoms, and resolve upon withdrawal of the drug. Optic neuropathy has recently been described with amiodarone. Systemic anticoagulant therapy may be associated with intraocular hemorrhage in patients with pre-existing disciform macular degeneration, and such agents should be used with caution in affected individuals. Systemic corticosteroids produce posterior subcapsular cataracts in susceptible individuals which may profoundly affect visual acuity. Although elevated intraocular pressure may also result from systemic therapy, the relationship between the pressure rise and development of glaucomatous changes remains unclear. Ethambutol may produce optic neuropathy if the daily dosage exceeds 15 mg/kg. The changes are usually reversible within a few weeks of stopping treatment. High doses of tamoxifen may produce a maculopathy with loss of visual acuity, if given for prolonged periods. The risk must be weighed against the benefits of treatment. Patients receiving more than 800 mg/day of thioridazine have developed retinopathy, which is usually reversible if detected early enough. Tricyclic antidepressants and other agents with anticholinergic properties may cause disturbances of accommodation and pupillary dilatation. The latter may rarely precipitate acute angle closure glaucoma in susceptible individuals.

show abstract

Transient Myopia Induced by Sulfonamides

Cited by 44 publications

References 4 publications

Drug-Induced Glaucoma (Glaucoma Secondary to Systemic Medications)

Drug-Induced Glaucoma (Glaucoma Secondary to Systemic Medications)

Delayed Topiramate-induced Bilateral Angle-Closure Glaucoma

Clinically Important Ocular Reactions to Systemic Drug Therapy

Contact Info

Product

Resources

About