Chlorpromazine Induced Cataract In A Patient With Bipolar Syndrome.

Chlorpromazine, due to its low cost, is one of the commonly used antipsychotics.

In addition to neurological side effects, few cases of chlorpromazine-related lenticular and corneal abnormalities have been reported earlier.

However, there hasn't been much interest in the recent past, perhaps due to low usage.

It is important for clinicians to be aware of this side effect. We report a patient who developed a cataract due to prolonged intake of chlorpromazine for his bipolar syndrome.

A 43-year-old man, with no particular history apart from bipolar syndrome, followed for 11 years on Chlorpromazine: currently 200 mg/day (cumulative dose > 1000 g) who consults for a progressive and bilateral decline in his visual acuity since 5 months.

The ophthalmological examination finds:

A BCVA at 20/20 right eye and 20/40 left eye.

The slit-lamp examination revealed an incipient cortical cataract in the right eye, and a posterior subcapsular and cortical cataract in the left eye.

The rest of the examamination is unremarkable.

The patient benefited from a Phaco-emulsification of the left eye with intraocular implantation, the evolution is satisfactory 20/20 in both eyes.

An informative letter is addressed to the psychiatrist on the possible incrimination of chlorpromazine in the development of cataract for change of molecule.

Our case illustrates the importance of observing this rare side effect of chlorpromazine treatment. The patient had no other risk factors for cataract formation.

Previous reports have indicated that chronic chlorpromazine treatment is associated with the production of corneal and lenticular opacities (in half of patients who received a cumulative dose of more than 1000g in their lifetime). Animal models have also shown gradual deposition of chlorpromazine with continued treatment.

The mechanism of production of these opacities is not clearly known; chlorpromazine possibly alters the respiratory mechanisms of the lens by producing a metabolic block at a site preceding the succinate, which can lead to cataracts.

Alternatively, the cataract may represent foci of denatured protein resulting from the interaction of light with drug, a photosensitizing agent, and lens protein.

Antipsychotics differ in their propensity to cause cataract formation; Cataract formation has been reported with first-generation antipsychotics such as: chlorpromazine, thioridazine, thiothixene, and trifluperazine. Second-generation antipsychotics have not been associated with cataract formation, with the exception of quetiapine and olanzapine.

This case illustrates the importance of ophthalmological monitoring in patients on treatment with antipsychotics, particularly first-generation antipsychotics, given the possibility of resumption of use of these agents.

Also, ocular complaints in patients on antipsychotics should lead to early ophthalmologic evaluation to allow prompt treatment of potentially reversible conditions.