The Annals of pharmacotherapy · 2003
Resolution of risperidone-induced hyperprolactinemia with substitution of quetiapine.
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Kunwar Arun Raj, Megna James L
Аннотация
OBJECTIVE: To report a case of risperidone-induced hyperprolactinemia that was successfully managed with quetiapine.
CASE SUMMARY: A 30-year-old white woman with schizoaffective disorder, depressive type, and comorbid alcohol and cocaine abuse was treated successfully for her psychotic symptoms with risperidone until she developed adverse effects consistent with hyperprolactinemia. This was confirmed by laboratory blood tests, as her prolactin level was 186.9 ng/mL (normal for nonpregnant women 2.8-29.2). The woman had experienced similar effects in the past, which had led to noncompliance and subsequent psychotic relapse. Normalization of prolactin levels and associated adverse effects were achieved upon switching to quetiapine. No psychotic symptoms reoccurred.
DISCUSSION: Dopamine type 2 (D(2)) receptor blockade in the mesolimbic tract is thought to mediate the therapeutic effects of antipsychotics. This action in the tuberoinfundibular system produces prolactin level elevation. Risperidone has a relatively higher affinity for the D(2) receptor in comparison with other atypical antipsychotics, which may explain why it is associated with a higher incidence of hyperprolactinemia. Quetiapine, which has one of the lowest D(2) receptor affinities, is not known to increase prolactin levels to any significant degree. This pharmacologic property allows quetiapine to be a reasonable treatment option for patients who develop risperidone-induced hyperprolactinemia.
CONCLUSIONS: Quetiapine may be a suitable substitute when a patient taking risperidone develops hyperprolactinemia.
CASE SUMMARY: A 30-year-old white woman with schizoaffective disorder, depressive type, and comorbid alcohol and cocaine abuse was treated successfully for her psychotic symptoms with risperidone until she developed adverse effects consistent with hyperprolactinemia. This was confirmed by laboratory blood tests, as her prolactin level was 186.9 ng/mL (normal for nonpregnant women 2.8-29.2). The woman had experienced similar effects in the past, which had led to noncompliance and subsequent psychotic relapse. Normalization of prolactin levels and associated adverse effects were achieved upon switching to quetiapine. No psychotic symptoms reoccurred.
DISCUSSION: Dopamine type 2 (D(2)) receptor blockade in the mesolimbic tract is thought to mediate the therapeutic effects of antipsychotics. This action in the tuberoinfundibular system produces prolactin level elevation. Risperidone has a relatively higher affinity for the D(2) receptor in comparison with other atypical antipsychotics, which may explain why it is associated with a higher incidence of hyperprolactinemia. Quetiapine, which has one of the lowest D(2) receptor affinities, is not known to increase prolactin levels to any significant degree. This pharmacologic property allows quetiapine to be a reasonable treatment option for patients who develop risperidone-induced hyperprolactinemia.
CONCLUSIONS: Quetiapine may be a suitable substitute when a patient taking risperidone develops hyperprolactinemia.