Corneal changes in patients treated with clofazimine.

Wålinder, Per-Erik; L, Gip; Stempa, M.

doi:10.1136/bjo.60.7.526

Cited by 28 publications

(12 citation statements)

References 5 publications

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“…In the patients in whom it has been tested, colour vision remains unimpaired but no electro-diagnostic or angiographic studies have been undertaken. The changes resemble those seen in chloroquine keratopathy (Hobbs and Calnan, 1958), chlorpromazine toxicity (Johnson and Buffaloe, 1966) and the recently described keratopathy in some patients treated with clofazimine (a phenazine derivative) (Walinder, Gip and Stempa, 1976). Therapy has not been discontinued in any patient because of this effect although all remain under regular ophthalmological supervision.…”

Section: Toxicitysupporting

confidence: 69%

Amiodarone in the treatment of refractory supraventricular and ventricular arrhythmias

Wheeler

Ingram

Puritz

et al. 1979

Postgraduate Medical Journal

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Summary Amiodarone is an antiarrhythmic agent unrelated to other drugs in current use. It has been little used in Britain, and no formal clinical trials have been possible because the drug has not been licensed by the Committee on Safety of Medicines. Nevertheless it has unique properties which can be valuable in the treatment of a wide spectrum of arrhythmias, particularly supraventricular tachycardias. Amiodarone has a slow onset of action and is cumulative. A sustained action is therefore achieved without the need for frequent maintenance dosage. Fifty patients have been treated with amiodarone in maintenance doses ranging from 200 mg on alternate days to 200 mg twice daily either alone, or in combination with conventional therapy. All were resistant to conventional therapy alone or could not be treated with usual agents because of unwanted drug effects. Of 27 patients with supraventricular arrhythmias, 18 were completely controlled and the other 9 were markedly improved. Six of 8 patients with recurrent life-threatening ventricular arrhythmias were well controlled symptomatically. Results were predictably less satisfactory in 15 high risk post-infarction patients with malignant arrhythmias and severe myocardial damage, but 6 were probably improved as a result of amiodarone. All patients on maintenance therapy for 3 months or more developed corneal microdeposits. None has any visual symptoms or other ocular defect, and treatment has not been curtailed as a result of this well recognized effect which is believed to be reversible and benign. Amiodarone can control patients with otherwise refractory arrhythmias including some which are life-threatening. Formal clinical trials are needed to define accurately its future role in the prevention and treatment of serious rhythm disorders of the heart.

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Section: Toxicitysupporting

confidence: 69%

Amiodarone in the treatment of refractory supraventricular and ventricular arrhythmias

Wheeler

Ingram

Puritz

et al. 1979

Postgraduate Medical Journal

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“…79 Clofazimine is a riminophenazine antibiotic that is no longer available in the United States, but is still used in other countries as a component of multidrug therapy for leprosy. Corneal changes due to clofazimine are typically described as a fine granular line or lines in the inferior cornea that can be brown 80 to reddish brown and can occur in a little over half of all treated patients, frequently in conjunction with conjunctival pigmentation. 25 These changes do not result in decreased visual acuity.…”

Section: Antibioticsmentioning

confidence: 99%

Drug-induced corneal epithelial changes

Raizman

Hamrah

Holland

et al. 2017

Survey of Ophthalmology

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Drugs across many pharmacologic classes induce corneal epithelial changes. Many of these drugs have cationic amphiphilic structures, with a hydrophobic ring and hydrophilic cationic amine side chain that allow them to cross cell membranes. These drugs lead to intracellular phospholipid accumulation, often manifested in the cornea by vortex keratopathy, with no effect on visual acuity and few ocular symptoms. Other drugs, notably antineoplastic agents, produce a fine diffuse corneal haze, sometimes accompanied by decreased vision that can be dose limiting. Still other medications cause crystalline epithelial precipitation that might require debridement for resolution. An understanding of the variety of drugs involved, the multiple mechanisms responsible, and the systemic diseases that produce similar changes can lead to improved management strategies for patients with corneal epithelial deposits. In most cases, drug therapy need not be modified or discontinued, but if visual acuity is affected, close collaboration with the prescribing physician can result in determining an optimized dose that treats systemic disease and minimizes these deposits. Additionally, close monitoring might be required if the drug is also associated with other ocular findings, such as optic neuropathy or retinopathy.

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“…Subepithelial deposits were described in 10 of 26 (38.5%) patients on 100 to 300 mg/d, which resolved upon drug cessation [66]. Pigmented superficial lines in a whorl-like pattern were observed in 2 of 19 (10.5%) patients on 100 to 400 mg/d [41]. Crystalline deposition in the cornea (anterior stroma) and conjunctiva has been reported, which resolved with discontinuation and reaccumulated upon reinstitution of clofazimine [67].…”

Section: Pigmentary Depositionmentioning

confidence: 94%

“…Atovaquone, an antiparasitic agent used in the treatment of Pneumocystis carinii pneumonia in patients intolerant to sulfa compounds, may also lead to a vortex keratopathy [39]. In addition to corneal stromal deposition (See "Stromal manifestations" below), phenothiazines [40] and clofazimine [41] may also produce cornea verticillata. Tilorone hydrochloride, an antineoplastic agent, may produce a vortex keratopathy as well as a retinopathy [42].…”

Section: Epithelial Manifestations Vortex Keratopathymentioning

confidence: 97%