Abstract
To the Editor
In a comprehensive review of antipsychotic induced hyperprolactinaemia by Inder and Castle in October 2011, it was discussed that hyperprolactinaemia can occur in up to 70% of patients with schizophrenia due to prescribed antipsychotic agents.
Prolactin elevation is predominantly associated with first generation antipsychotics. Amongst the second-generation agents, amisulpride and risperidone are associated with higher rates of hyperprolactinaemia. Aripiprazole is associated with the lowest rates around 5% or less (Inder and Castle, 2011).
The management of clinically relevant hyperprolactinaemia is usually limited to switching to a prolactin-sparing antipsychotic. The decision to switch could potentially be problematic in the setting of compliance difficulties in patients stable on a depot antipsychotic. We present a case of a woman with schizophrenia who had her hyperprolactinaemia successfully treated while she remained on depot risperidone for a period of time.
Mrs RU is a 27 year old female of an African background who was diagnosed 15 months earlier with schizophrenia. Her psychosis consisted of auditory hallucinations, persecutory delusions, and somatic passivity. She was stabilised on oral risperidone 3 mg/day which was switched later to risperidone consta because of her poor insight and past compliance problems. With risperidone consta, Mrs RU started complaining of breast tenderness and galactorrhoea. Her serum prolactin levels were raised to 4098 IU. All investigations including an MRI of her head were normal. The hyperprolactinaemia was attributed to risperidone.
Mrs RU agreed to commence aripiprazole 15 mg to treat her hyperprolactinaemia as she did not want a change in her antipsychotic regime fearing other potential side effects. Oral antipsychotic agents were not considered at this stage because of the anticipated risk of non compliance in the community. Her breast tenderness and galactorrhoea resolved rapidly after the commencement of aripiprazole. A repeat serum prolactin level done after 2 weeks was 156 IU. Although her insight remained limited, Mrs RU agreed to continue aripiprazole as she did not want her symptoms of breast tenderness and galactorrhoea to recur.
Aripiprazole due to its unique mechanism of action has been of reported benefit to treat antipsychotic induced hyperprolactinaemia (Hoffer et al., 2009; Inder and Castle, 2011; Lu et al., 2008; Shim et al., 2007). Aripiprazole is a potent partial agonist, exerting both agonistic and antagonistic effects on D2 and 5-HT1A receptors and potent antagonistic activity on 5-HT2A receptors. The partial agonist properties of aripiprazole allows it to function as a dopamine agonist in the milieu of dopamine hypoactivity caused by risperidone with intrinsic activity at the postsynaptic receptors, thus restoring tonic inhibition to the anterior pituitary lactotrophs, and lowering prolactin levels (Inder and Castle, 2011; Shim et al., 2007)
The utilization of aripiprazole to resolve hyperprolactinaemia can be utilized to avoid switching antipsychotic agents and compromising clinical stability especially in the setting of depot use. The strategy of successfully treating hyperprolactinaemia with aripiprazole while maintaining depot risperidone can offer clinicians some flexibility in their decision making when encountering a similar complication. Whether this proposed strategy will work with other depot agents (haloperidol, fluphenazine, flupenthixol, zuclopenthixol, paliperidone) warrants further investigation. As noted in this case, the rapid resolution of hyperprolactinaemia with aripiprazole might warrant further investigation to clarify if the rate of prolactin reduction was dose dependant. Based on a review of literature, we recommend in the future commencing with a dose of aripiprazole greater than 6mg/day, before increasing the dose gradually if needed while closely monitoring prolactin levels to better understand this interesting relationship (Inder and Castle, 2011; Shores, 2005; Yasui-Furukori et al., 2010).