Chlorpromazine Epithelial Keratopathy

Johnson, Albin W.; Buffaloe, William J.

doi:10.1001/archopht.1966.03850010666007

Cited by 31 publications

(9 citation statements)

References 6 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: 70%

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: 70%

Amiodarone in the treatment of refractory supraventricular and ventricular arrhythmias

Wheeler

Ingram

Puritz

et al. 1979

Postgraduate Medical Journal

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“…This condition seems to be secondary to large dosages (>2 g/day) of the drug, and consists of swirling lines or fine streaks in the corneal epithelium. [6][7][8] It is not a serious condition because it does not cause visual impairment and tends to disappear, or at least diminish, after cessation of the drug.…”

Section: Phenothiazinesmentioning

confidence: 99%

Ocular Adverse Effects of Common Psychotropic Agents

Richa¹,

Yazbek²

2010

CNS Drugs

174

143

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All psychotropic medications have the potential to induce numerous and diverse unwanted ocular effects. Visual adverse effects can be divided into seven major categories: eyelid and keratoconjunctival disorders; uveal tract disorders; accommodation interference; angle-closure glaucoma; cataract/pigmentary deposits in the lens and cornea; retinopathy; and other disorders. The disorders of the eyelid and of the keratoconjunctiva are mainly related to phenothiazines and lithium. Chlorpromazine, at high dosages, can commonly cause abnormal pigmentation of the eyelids, interpalpebral conjunctiva and cornea. It can also cause a more worrisome but rarer visual impairment, namely corneal oedema. Lithium can rarely lead to a bothersome eye irritation by affecting sodium transport. Uveal tract problems are mainly associated with tricyclic antidepressants (TCAs), typical antipsychotics, topiramate and selective serotonin reuptake inhibitors (SSRIs). TCAs, typical antipsychotics and SSRIs can all cause mydriasis that is often transient and with no major consequences, but that can promote closure of angles in susceptible patients. Topiramate has been frequently associated with a number of significant ocular symptoms including acquired myopia and angle-closure glaucoma. Problems with accommodation are related to TCAs and to low-potency antipsychotics. TCAs cause transient blurred vision in up to one-third of patients. Angle-closure glaucoma is a serious condition that has been mainly associated with TCAs, low-potency antipsychotics, topiramate and, to a lesser extent, SSRIs. When patients with narrow angles are given TCAs, they all appear to experience induction of glaucomatous attacks. Antipsychotics and SSRIs may lead to an added risk of developing angle-closure glaucoma, but only in predisposed eyes. Topiramate can lead to an allergic-type reaction whereby structures of the lens and ciliary body are displaced, which results in angle-closure glaucoma. Cataractous changes can result from antipsychotics, mainly from high dosages of chlorpromazine or thioridazine. These two drugs, when used at high dosages and for prolonged periods, frequently cause lenticular opacifications. Retinopathy has been shown to be related to high dosages of typical antipsychotics, mainly chlorpromazine and thioridazine. The frequency of occurrence of retinal effects seems to be proportional to the total amount of drug used over a long period of time. Other visual problems of special concern are the ocular dystonias, other eye movement disorders, and decreased ability to perceive colours and to discriminate contrast. Ocular dystonias can occur with antipsychotics (especially high-potency ones), carbamazepine (especially in polytherapy), topiramate and, rarely, with SSRIs. Disturbance in various eye movements is frequently seen with benzodiazepines, antiepileptic drugs and lithium. Impairment in the perception of colours and the discrimination of contrasts has been shown to occur not uncommonly with carbamazepine and lorazepam. Thus, typical antipsycho...

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“…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: 99%