Literature DB >> 22174540

Switching to quetiapine for risperidone-induced amenorrhea: Report of two cases.

P K Pardal1, Raaj Konwar, Jyoti Prakash.   

Abstract

Almost all the antipsychotics can cause hyperprolactinemia-related side-effects like amenorrhea. Quetiapine has been reported to have minimal propensity to cause hyperprolactinemia. We report here two cases of risperidone-induced amenorrhea, who resumed their normal cycle on switching over the medication to quetiapine.

Entities:  

Keywords:  Amenorrhea; prolactin; quetiapine; risperidone

Year:  2010        PMID: 22174540      PMCID: PMC3237133          DOI: 10.4103/0972-6748.90348

Source DB:  PubMed          Journal:  Ind Psychiatry J        ISSN: 0972-6748


Conventional antipsychotics like haloperidol can cause hyperprolactinemia due to D2 receptor blockade in the brain.[1] Recent reports have indicated that risperidone, an atypical antipsychotic, can also cause hyperprolactinemia.[23] Hyperprolactinemia can result in a variety of sexual adverse effects. In men, there may be decreased libido.[4] In women, there may be decreased libido, galactorrhea and amenorrhea.[5] Quetiapine has been reported to have a minimal effect on serum prolactin levels and hence can be expected to have least chances of causing amenorrhea and other sexual side-effects.[36] We report here two cases of risperidone-induced amenorrhea who resumed their normal menstrual cycle after switching to quetiapine.

CASE REPORT

Case 1

A 23-year-old unmarried girl was on risperidone since the last 3 years as a case of schizophrenia. Since the last 1 year she had been stabilized on 4 mg/day of risperidone. She reported amenorrhea for the last 6 months. Her serum prolactin was found to be elevated (94.2 ng/ml; normal range 2.80–29.20 ng/ml). Her amenorrhea was diagnosed to be risperidone induced. It was decided to switch her to quetiapine. She was started on quetiapine 100 mg/day, which was gradually increased to 300 mg/day over the next 10 days. Risperidone was tapered off and stopped in the next 10 days. She showed no worsening of her psychotic symptoms. She resumed normal menstruation after 2 months and her serum prolactin level returned to normal (20.6 ng/ml). She has subsequently been on regular follow-up for a further 6 months till now. She continues to have normal menstrual cycles. Her mental state has remained stable on quetiapine 300 mg/day.

Case 2

A 37-year-old married female, a case of schizophrenia, was on risperidone 6 mg/day since several years. Efforts to reduce the dose in the past had resulted in worsening of her psychotic symptoms. She had been having amenorrhea since the last 6 months, for which she had consulted a gynaecologist who opined the amenorrhea to be risperidone induced. Her serum prolactin was found to be elevated (110.02 ng/ml). She was started on quetiapine 50 mg/day, which was gradually increased to 400 mg/day over the next 2 months. Simultaneously, risperidone was tapered off and stopped in 2 weeks. Her mental status remained stable. She started resumed her normal menstrual cycle after 3 months and her prolactin returned to normal (19.8 ng/ml). She has till now been on follow-up for more than 1 year and is having normal menstrual cycles. She continues to take quetiapine 400 mg/day.

DISCUSSION

Both the above patients, who had risperidone-induced amenorrhea, started normal menstruation after switching over to quetiapine. Their prolactin levels returned to normal. Quetiapine is “very atypical,” in that it virtually causes no extrapyramidal symptoms (EPS) or prolactin elevation, perhaps due to its particularly rapid dissociation from D2 receptors. A positron emission tomography study has shown that quetiapine shows a transient and high D2 occupancy 2–3 h after one final dose, with a rapid decline during the next 9 h.[7] The transient and high D2 occupancy may be sufficient to induce antipsychotic response, and rapid release of quetiapine from D2 receptors does not lead to drug accumulation, thereby preventing sustained prolactin elevation.[8] The above two cases suggest that switching to quetiapine may be an appropriate strategy for patients having amenorrhea induced by conventional antipsychotics or risperidone. Further long-term studies with a control group are required to see the return of menses in patients who remained on risperidone to substantiate the benefit of this switching strategy.
  8 in total

Review 1.  Does fast dissociation from the dopamine d(2) receptor explain the action of atypical antipsychotics?: A new hypothesis.

Authors:  S Kapur; P Seeman
Journal:  Am J Psychiatry       Date:  2001-03       Impact factor: 18.112

2.  A positron emission tomography study of quetiapine in schizophrenia: a preliminary finding of an antipsychotic effect with only transiently high dopamine D2 receptor occupancy.

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Journal:  Arch Gen Psychiatry       Date:  2000-06

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Authors:  A L Nordström; L Farde
Journal:  J Clin Psychopharmacol       Date:  1998-08       Impact factor: 3.153

4.  Plasma prolactin in schizophrenia subjects treated with Seroquel (ICI 204,636).

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Journal:  Psychopharmacol Bull       Date:  1996

Review 5.  Prolactin elevation with antipsychotic medications: mechanisms of action and clinical consequences.

Authors:  Gerald A Maguire
Journal:  J Clin Psychiatry       Date:  2002       Impact factor: 4.384

6.  The effects of olanzapine, risperidone, and haloperidol on plasma prolactin levels in patients with schizophrenia.

Authors:  S R David; C C Taylor; B J Kinon; A Breier
Journal:  Clin Ther       Date:  2000-09       Impact factor: 3.393

7.  Effect of risperidone and olanzapine on reproductive hormones, psychopathology and sexual functioning in male patients with schizophrenia.

Authors:  Beata Konarzewska; Sławomir Wołczyński; Agata Szulc; Beata Galińska; Regina Popławska; Napoleon Waszkiewicz
Journal:  Psychoneuroendocrinology       Date:  2008-10-05       Impact factor: 4.905

8.  Effectiveness of switching to quetiapine for neuroleptic-induced amenorrhea.

Authors:  Hitoshi Takahashi; Hisashi Higuchi; Mitsuhiro Kamata; Shingo Naitoh; Keizo Yoshida; Tetsuo Shimizu; Takio Sugita
Journal:  J Neuropsychiatry Clin Neurosci       Date:  2003       Impact factor: 2.198

  8 in total

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