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Letters   |    
Successful Treatment With Blonanserin for Drug-Induced Hyperprolactinemia in Chronic Schizophrenia Patients: A Six-Month Follow-Up of Two Cases
Shinsuke Kito, M.D., Ph.D.; Takashi Hasegawa, M.D., Ph.D.; Toru Nakajima, M.D., Ph.D.; Yoshihiko Koga, M.D., Ph.D.; Shintaro Hibi, M.D.; Yukiko Tobe, M.D.; Masahiko Mochida, M.D., Ph.D.
The Journal of Neuropsychiatry and Clinical Neurosciences 2013;25:E29-E30. doi:10.1176/appi.neuropsych.12060161
View Author and Article Information

Dept. of Neuropsychiatry Kyorin University School of Medicine Tokyo, Japan
Tokyokaido Hospital Tokyo, Japan
Tama Hospital Tokyo, Japan

Correspondence: Shinsuke Kito, M.D., Ph.D.; e-mail: kito@ks.kyorin-u.ac.jp

Copyright © 2013 American Psychiatric Association

To the Editor: Some antipsychotics cause elevations in serum prolactin (PRL) levels, which can lead to galactorrhea, infertility, menstrual disorders, sexual dysfunction, and reduction in bone mineral density,1 although recent atypical antipsychotics do so less often than conventional ones. We present two cases of chronic schizophrenia with risperidone-induced hyperprolactinemia, of whom one, especially, had sexual dysfunction. Their elevated PRL levels were normalized after switching to blonanserin.

“Ms. I,” A 53-year-old woman with schizophrenia (DSM-IV-TR) had been hospitalized several times. Her first psychotic episode, including disorganized speech, auditory hallucinations, and delusions, occurred at the age of 17. Because she had menstrual irregularities, her blood sample was taken, disclosing serum PRL levels of 114.8 ng/ml. As she was taking risperidone 5 mg per day, risperidone-induced hyperprolactinemia was suspected. Subsequently, risperidone was tapered and ceased while, instead, blonanserin was cross-titrated up to 24 mg per day for 4 weeks. The characteristics and changes in serum PRL levels are shown in Table 1.

 
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TABLE 1.Clinical Characteristics and Changes in Serum PRL Levels in Two Schizophrenia Patients With a Six-Month Follow-Up
Table Footer Note

BW indicates body weight (kg); PRL, prolactin (ng/ml); BPRS, Brief Psychiatric Rating Scale score.

“Mr. M,” A 41-year-old man with schizophrenia (DSM-IV-TR) presented with his first psychotic episode, characterized by auditory hallucinations, delusions, irritability, and aggression, at the age of 21. He complained of ejaculation disorder and took a blood test, revealing that serum PRL levels were 51.5 ng/ml. Risperidone 6 mg was then tapered and ceased while blonanserin started to be cross-titrated up to 24 mg per day for 4 weeks. His sexual dysfunction was improved, but he presented with irritability and aggression. Sodium valproate increased to 800 mg relieved these symptoms. The characteristics and changes in serum PRL levels are shown in Table 1.

PRL is released from lactotrophic cells in the anterior pituitary, and its secretion is regulated by PRL-releasing factor (PRF) and PRL-inhibiting factor (PIF).1 The regulation of PRL secretion is mainly affected by dopamine, one of the PIFs.1 Blonanserin has a high affinity for dopamine D2,3 and serotonin 5-HT2A receptor subtypes, whose affinity is higher for D2 receptors than for 5-HT2A receptors, compared with that of risperidone, while blonanserin has low or very low affinity for all other neurotransmitter receptors.2 Several studies in rats and humans have shown a correlation between the serum PRL levels and the penetrability of antipsychotics across the blood–brain barrier.3,4 Antipsychotics need to pass across the blood–brain barrier to ameliorate the psychotic symptoms, whereas the anterior pituitary is outside the blood–brain barrier and is accessible to antipsychotics.1,3 Therefore, antipsychotics such as risperidone, with a lower penetrability across the blood–brain barrier may cause higher plasma PRL levels.3,4 Blonanserin has been shown to have a high affinity for D2 receptors2 as well as a potentially high penetrability of the blood–brain barrier.5 The two schizophrenic patients with risperidone-induced hyperprolactinemia presented herein were improved by switching to blonanserin. The findings in these case reports suggest that blonanserin, with a potentially high penetrability of the blood–brain barrier, might be one of the treatment options for drug-induced hyperprolactinemia. To test the efficacy, it would need a well-designed study in a larger sample size.

Haddad  PM;  Wieck  A:  Antipsychotic-induced hyperprolactinaemia: mechanisms, clinical features and management.  Drugs 2004; 64:2291–2314
[CrossRef] | [PubMed]
 
Deeks  ED;  Keating  GM:  Blonanserin: a review of its use in the management of schizophrenia.  CNS Drugs 2010; 24:65–84
[CrossRef] | [PubMed]
 
Kapur  S;  Langlois  X;  Vinken  P  et al:  The differential effects of atypical antipsychotics on prolactin elevation are explained by their differential blood–brain disposition: a pharmacological analysis in rats.  J Pharmacol Exp Ther 2002; 302:1129–1134
[CrossRef] | [PubMed]
 
Arakawa  R;  Okumura  M;  Ito  H  et al:  Positron emission tomography measurement of dopamine D₂ receptor occupancy in the pituitary and cerebral cortex: relation to antipsychotic-induced hyperprolactinemia.  J Clin Psychiatry 2010; 71:1131–1137
[CrossRef] | [PubMed]
 
Inoue  T;  Osada  K;  Tagawa  M  et al:  Blonanserin, a novel atypical antipsychotic agent not actively transported as substrate by P-glycoprotein.  Prog Neuropsychopharmacol Biol Psychiatry 2012; 39:156–162[E-pub ahead of print]
[CrossRef] | [PubMed]
 
References Container
Anchor for Jump
TABLE 1.Clinical Characteristics and Changes in Serum PRL Levels in Two Schizophrenia Patients With a Six-Month Follow-Up
Table Footer Note

BW indicates body weight (kg); PRL, prolactin (ng/ml); BPRS, Brief Psychiatric Rating Scale score.

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References

Haddad  PM;  Wieck  A:  Antipsychotic-induced hyperprolactinaemia: mechanisms, clinical features and management.  Drugs 2004; 64:2291–2314
[CrossRef] | [PubMed]
 
Deeks  ED;  Keating  GM:  Blonanserin: a review of its use in the management of schizophrenia.  CNS Drugs 2010; 24:65–84
[CrossRef] | [PubMed]
 
Kapur  S;  Langlois  X;  Vinken  P  et al:  The differential effects of atypical antipsychotics on prolactin elevation are explained by their differential blood–brain disposition: a pharmacological analysis in rats.  J Pharmacol Exp Ther 2002; 302:1129–1134
[CrossRef] | [PubMed]
 
Arakawa  R;  Okumura  M;  Ito  H  et al:  Positron emission tomography measurement of dopamine D₂ receptor occupancy in the pituitary and cerebral cortex: relation to antipsychotic-induced hyperprolactinemia.  J Clin Psychiatry 2010; 71:1131–1137
[CrossRef] | [PubMed]
 
Inoue  T;  Osada  K;  Tagawa  M  et al:  Blonanserin, a novel atypical antipsychotic agent not actively transported as substrate by P-glycoprotein.  Prog Neuropsychopharmacol Biol Psychiatry 2012; 39:156–162[E-pub ahead of print]
[CrossRef] | [PubMed]
 
References Container
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