ABSTRACT
Hyperprolactinemia is a well-known consequence of conventional antipsychotic therapy. The atypical antipsychotic clozapine is reported to lack this effect. We describe a case of attenuated serum prolactin levels after conversion to clozapine therapy in an adolescent. A 13-year-old female patient developed hyperprolactinemia with galactorrhea and amenorrhea while receiving thioridazine 300 mg daily. These symptoms continued throughout 3 years of treatment with haloperidol 10 mg daily and then fluphenazine 10 mg daily. Subsequently, after an incomplete improvement in her psychiatric symptoms and hyperprolactinemia on thioridazine 150 mg and bromocriptine 15 mg daily, the patient was changed to clozapine at age 16. Clozapine 150 mg twice daily improved her psychiatric status and corrected her serum prolactin concentrations after 2 weeks; bromocriptine was able to be discontinued. We recommend systematic evaluation of atypical neuroleptics as alternative treatments for refractory hyperprolactinemia induced by conventional antipsychotics.
Subject(s)
Antipsychotic Agents/adverse effects , Clozapine/therapeutic use , Hyperprolactinemia/chemically induced , Thioridazine/adverse effects , Adolescent , Amenorrhea/chemically induced , Bromocriptine/adverse effects , Female , Fluphenazine/adverse effects , Galactorrhea/chemically induced , Haloperidol/adverse effects , Humans , Hyperprolactinemia/drug therapy , Prolactin/blood , Psychotic Disorders/drug therapyABSTRACT
As part of a prospective efficacy and safety monitoring system, patients receiving clozapine are assessed monthly for dyskinetic events (DE), using the Abnormal involuntary Movement Scale (AIMS). Longitudinal analysis of 45 patients revealed 20 with baseline DE, 7 who developed emergent DE after a negative baseline assessment, and 18 patients with no DE symptoms throughout treatment with clozapine. Eight of the 20 patients with baseline DE were assessed to resolution of symptoms, with an average time of 261 +/- 188 days; 5 were evaluated until complete resolution of symptoms (AIMS = 0), with an average time of 691 +/- 462 days. The average time to onset of DE in emergent DE patients was 238 +/- 179 days, and the average time to resolution was 347 +/- 179 days after diagnosis. Four patients attained complete resolution with an average time of 629 +/- 293 days after diagnosis. It appears this emergent type of dyskinesia is different from other currently described dyskinesias. Overall, of the 27 patients having DE at any point in treatment, 15 of 27 (56%) had resolution of symptoms and 10 of 27 (37%) had complete resolution of DE. Clinicians should be aware of the utility of clozapine in dyskinesia and the extended time frame of response.
