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To the Editor: A total of 15%–45% of all cases of priapism are caused by medications, and psychotropic drugs are the most common offenders (1).In addition to trazodone, chlorpromazine, and thioridazine, clozapine has also been cited as a causative agent. Central α1-adrenergic blockade is the mechanism thought to mediate this side effect. Most patients with priapism, as described in the literature, were not rechallenged with clozapine after experiencing an episode of priapism. However, clozapine is often the treatment of last resort for patients with extremely refractory psychosis; we found in the literature two reports of reexposure to clozapine after occurrence of priapism. One patient had two recurrences of priapism when he began taking lower doses of clozapine (2). The other patient remained free of psychosis and priapism for 2 weeks after clozapine was reinitiated. He then became noncompliant with CBC monitoring, and clozapine was discontinued (3). We report a case of successful, long-term continuation of clozapine for a treatment-resistant schizophrenic patient after an episode of clozapine-related priapism.
Mr. A was a 25-year-old Hispanic man who suffered from unrelenting paranoia, hallucinations, and negative symptoms. Trials of traditional neuroleptics, risperidone, and olanzapine were attempted. Risperidone was discontinued after one episode of priapism and poor response to treatment. Olanzapine was only minimally effective. When he was taking clozapine, 400 mg/day, Mr. A showed remarkable improvement and was able to seek and maintain employment.
Ten months into treatment, Mr. A had a painful, prolonged erection that lasted 33 hours. Nonsurgical methods were unsuccessful in relieving his discomfort. Placement of a cavernosal glandular shunt was required for detumescence. After Mr. A had recovered, various antipsychotic treatment options were offered to him. Both he and his family felt that the benefits of clozapine outweighed the risk of priapism. Given the refractory nature of his illness as well as the severity of his symptoms at decompensation, he continued to take clozapine at one-half the original dose. Except for one episode of noncompliance and subsequent decompensation, Mr. A has continued to do well and has had only residual negative symptoms. The previous episode of priapism resolved, and Mr. A has reported no recurrence of priapism in over a year.
While discontinuation of the causative drug is the usual recommendation for serious side effects such as priapism, patients taking clozapine frequently have severe symptoms not ameliorated by use of other medications. In such cases, a careful risk-benefit assessment involving the patient and significant others may indicate that continuation of the causative agent is the best choice. To our knowledge, this is the first report of successful, sustained clozapine continuation with no recurrence of priapism in a patient with a history of clozapine-associated priapism.
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