Australian and New Zealand Journal of Psychiatry http://anp.sagepub.com/
Interpretation of recurrent isolated creatine kinase elevation Titus Mohan, Anna Kennedy, Tarun Bastiampillai and Simon Hayward Aust N Z J Psychiatry 2014 48: 962 originally published online 14 May 2014 DOI: 10.1177/0004867414535672 The online version of this article can be found at: http://anp.sagepub.com/content/48/10/962.2
Published by: http://www.sagepublications.com
On behalf of:
The Royal Australian and New Zealand College of Psychiatrists
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962
A case of priapism associated with paliperidone Deborah Wearne Maia House, Midland, Perth, Australia Corresponding author: Deborah Wearne, Maia House, 152 Morrison Road, Midland, Perth, WA 6056, Australia. Email: [email protected] DOI: 10.1177/0004867414532551
To the Editor This is a case of priapism occurring in a patient on paliperidone. Priapism occurs as a rare side effect described with most antipsychotic medications, although there have been no case reports with paliperidone to date (Paklet et al., 2013). Priapism is a painful, prolonged erection, which can have serious consequences such as impotency. Priapism is thought to be mediated via the alpha-1 adrenergic antagonist effects of medications. Ziprasidone and risperidone have the highest affinity for the adrenergic receptors followed by clozapine and quetiapine. Paliperidone, like risperidone, has a relatively high affinity for adrenergic receptors (Sood et al., 2008). The absence of case reports associated with paliperidone is likely to relate to
Interpretation of recurrent isolated creatine kinase elevation Titus Mohan, Anna Kennedy, Tarun Bastiampillai and Simon Hayward Department of Psychiatry, Flinders Medical Centre, Bedford Park, Australia Corresponding author: Titus Mohan, Flinders Medical Centre Margaret Tobin Centre, Adelaide, SA 5042, Australia. Email: [email protected] DOI: 10.1177/0004867414535672
ANZJP Correspondence the fact that it is a relatively new drug and priapism is a rare side effect. Mr A is a 38-year-old man with a diagnosis of schizophrenia from 20 years previously. He was assessed in 2012 because of an increase in auditory hallucinations and paranoid ideation. He described clear episodes of intense badgering by multiple external voices that left him disorientated and confused. His family also reported that paranoid ideation regarding neighbours had resulted in multiple house moves. He had been on trifluoperazine 5 mg for many years. The hallucinations and paranoid ideation were both highly distressing to Mr A and his family. His antipsychotic was changed to paliperidone 6 mg and increased to 9 mg after 1 month, resulting in excellent resolution of symptoms with no significant side effects. Mr A had 12 months of significantly improved function. In January 2014, Mr A experienced one episode of painless, prolonged erection that spontaneously resolved. This episode was followed 3 weeks later with an episode of priapism that was intensely painful and distressing. Mr A had no other risk factors for priapism. He presented to the emergency department of the local hospital. Conservative management failed and he underwent a Winter shunt followed
by an Al-Ghorab shunt. He has been left with impotency. He was commenced on olanzapine 10 mg due to its relative low affinity for adrenergic receptors, although case reports of priapism have been reported with this medication. Both aripiprazole and amisulpiride would be reasonable choices for treatment (Paklet et al., 2013). Although priapism is a rare side effect it can be devastating for patients. Clinically it can be very difficult to consider rare side effects and how to approach discussion with our patients.
To the Editor
remained haemodynamically stable with a temperature of 35.4°C. There was no rigidity, diaphoresis, or tremor. Mr K also had a negative urine drug screen, rheumatology, and myositis immunoglobulin screen. Due to his high CK, atypical neuroleptic malignant syndrome (NMS) was considered and quetiapine was ceased. A review of Mr K’s treatments since 2003 showed multiple trials of antipsychotics including aripiprazole, amisulpride, and olanzapine. These were ceased after similar presentations of altered mental state and isolated CK rise. Peak CK levels and time
We present a case of isolated creatine kinase (CK) rise secondary to multiple antipsychotics. Mr K is a 48 year old male with a diagnosis of schizophrenia, treated effectively with quetiapine. He was hospitalized with insomnia, urinary incontinence, social withdrawal, fixed staring, mutism, and pacing. These symptoms were unlike his usual acute presentation with persecutory delusions. His CK on admission was 1344 U/l, with electrolytes, white cell count, creatinine, and troponin within normal limits. He
Funding This research received no specific grant from any funding agency in the public, commercial or not-for-profit sectors.
Declaration of interest The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.
References Paklet L, Abe M and Olanjide D (2013) Priapism associated with risperidone: A case report, literature review and review of the South London and Maudsley hospital patients’ database. Therapeutic Advances in Psychopharmacology 3: 3–13. Sood S, James W and Bailon M (2008) Priapism associated with atypical antipsychotic medications: A review. International Clinical Psychopharmacology 23: 9–17.
Australian & New Zealand Journal of Downloaded Psychiatry, 48(10) from anp.sagepub.com at Bobst Library, New York University on October 15, 2014
963
ANZJP Correspondence to develop this adverse effect were as follows: aripiprazole after 10 days with a CK of 1263 U/l, amisulpride after 5 years to 25810 U/l, and olanzapine after 5 years to 9728 U/l. During this admission the patient’s CK values normalized after ceasing antipsychotics but his delusions intensified. Given CK rise to multiple antipsychotics, clozapine was considered. Patient’s CK levels were normal on clozapine and he attained remission. In our patient the initial diagnosis for the elevated CK was a subsyndromal NMS implying central mechanisms like sympathetic dysregulation or hypothalamic dopamine antagonism (Gurrera, 1999). However a recent review of antipsychotic medication and
rhabdomyolysis by Packard (2014), discusses local mechanisms, wherein antipsychotics with high 5-HT2a antagonism elevate CK by increasing sarcolemmal permeability (Packard et al., 2014). This implies that antipsychotics with greater 5HT2a binding (paliperidone, ziprasidone, asenapine, etc) would have a higher incidence of rhabdomyolysis. Whilst antipsychotic medication may elevate CK there is evidence that this can also occur intrinsically within the acute and maintenance phases of schizophrenia after controlling for nonspecific factors such as stress, trauma, or hyperactivity (Meltzer, 1976). In our patient, after ruling out other medical causes of rhabdomyolysis (cocaine use, heat
stroke, Legionella infection, etc.) the recurrent CK rise most likely appears to be a local effect of antipsychotics rather than centrally mediated. Clinicians should consider CK elevation within a broader context when the classical syndrome of NMS is absent. References Gurrera RJ (1999). Sympathoadrenal hyperactivity and the etiology of neuroleptic malignant syndrome. American Journal of Psychiatry 156: 169–180. Meltzer HY (1976). Serum creatine phosphokinase in schizophrenia. American Journal of Psychiatry 133: 192–197. Packard K, Hanson A and Price P (2014). Antipsychotic use and risk of rhabdomyolysis. Journal of Pharmacy Practice [Epub ahead of print].
Australian & New Zealand Journal of Psychiatry, 48(10)
Downloaded from anp.sagepub.com at Bobst Library, New York University on October 15, 2014
Interpretation of recurrent isolated creatine kinase elevation Titus Mohan, Anna Kennedy, Tarun Bastiampillai and Simon Hayward Aust N Z J Psychiatry 2014 48: 962 originally published online 14 May 2014 DOI: 10.1177/0004867414535672 The online version of this article can be found at: http://anp.sagepub.com/content/48/10/962.2
Published by: http://www.sagepublications.com
On behalf of:
The Royal Australian and New Zealand College of Psychiatrists
Additional services and information for Australian and New Zealand Journal of Psychiatry can be found at: Email Alerts: http://anp.sagepub.com/cgi/alerts Subscriptions: http://anp.sagepub.com/subscriptions Reprints: http://www.sagepub.com/journalsReprints.nav Permissions: http://www.sagepub.com/journalsPermissions.nav
>> Version of Record - Sep 25, 2014 OnlineFirst Version of Record - May 14, 2014 What is This?
Downloaded from anp.sagepub.com at Bobst Library, New York University on October 15, 2014
962
A case of priapism associated with paliperidone Deborah Wearne Maia House, Midland, Perth, Australia Corresponding author: Deborah Wearne, Maia House, 152 Morrison Road, Midland, Perth, WA 6056, Australia. Email: [email protected] DOI: 10.1177/0004867414532551
To the Editor This is a case of priapism occurring in a patient on paliperidone. Priapism occurs as a rare side effect described with most antipsychotic medications, although there have been no case reports with paliperidone to date (Paklet et al., 2013). Priapism is a painful, prolonged erection, which can have serious consequences such as impotency. Priapism is thought to be mediated via the alpha-1 adrenergic antagonist effects of medications. Ziprasidone and risperidone have the highest affinity for the adrenergic receptors followed by clozapine and quetiapine. Paliperidone, like risperidone, has a relatively high affinity for adrenergic receptors (Sood et al., 2008). The absence of case reports associated with paliperidone is likely to relate to
Interpretation of recurrent isolated creatine kinase elevation Titus Mohan, Anna Kennedy, Tarun Bastiampillai and Simon Hayward Department of Psychiatry, Flinders Medical Centre, Bedford Park, Australia Corresponding author: Titus Mohan, Flinders Medical Centre Margaret Tobin Centre, Adelaide, SA 5042, Australia. Email: [email protected] DOI: 10.1177/0004867414535672
ANZJP Correspondence the fact that it is a relatively new drug and priapism is a rare side effect. Mr A is a 38-year-old man with a diagnosis of schizophrenia from 20 years previously. He was assessed in 2012 because of an increase in auditory hallucinations and paranoid ideation. He described clear episodes of intense badgering by multiple external voices that left him disorientated and confused. His family also reported that paranoid ideation regarding neighbours had resulted in multiple house moves. He had been on trifluoperazine 5 mg for many years. The hallucinations and paranoid ideation were both highly distressing to Mr A and his family. His antipsychotic was changed to paliperidone 6 mg and increased to 9 mg after 1 month, resulting in excellent resolution of symptoms with no significant side effects. Mr A had 12 months of significantly improved function. In January 2014, Mr A experienced one episode of painless, prolonged erection that spontaneously resolved. This episode was followed 3 weeks later with an episode of priapism that was intensely painful and distressing. Mr A had no other risk factors for priapism. He presented to the emergency department of the local hospital. Conservative management failed and he underwent a Winter shunt followed
by an Al-Ghorab shunt. He has been left with impotency. He was commenced on olanzapine 10 mg due to its relative low affinity for adrenergic receptors, although case reports of priapism have been reported with this medication. Both aripiprazole and amisulpiride would be reasonable choices for treatment (Paklet et al., 2013). Although priapism is a rare side effect it can be devastating for patients. Clinically it can be very difficult to consider rare side effects and how to approach discussion with our patients.
To the Editor
remained haemodynamically stable with a temperature of 35.4°C. There was no rigidity, diaphoresis, or tremor. Mr K also had a negative urine drug screen, rheumatology, and myositis immunoglobulin screen. Due to his high CK, atypical neuroleptic malignant syndrome (NMS) was considered and quetiapine was ceased. A review of Mr K’s treatments since 2003 showed multiple trials of antipsychotics including aripiprazole, amisulpride, and olanzapine. These were ceased after similar presentations of altered mental state and isolated CK rise. Peak CK levels and time
We present a case of isolated creatine kinase (CK) rise secondary to multiple antipsychotics. Mr K is a 48 year old male with a diagnosis of schizophrenia, treated effectively with quetiapine. He was hospitalized with insomnia, urinary incontinence, social withdrawal, fixed staring, mutism, and pacing. These symptoms were unlike his usual acute presentation with persecutory delusions. His CK on admission was 1344 U/l, with electrolytes, white cell count, creatinine, and troponin within normal limits. He
Funding This research received no specific grant from any funding agency in the public, commercial or not-for-profit sectors.
Declaration of interest The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.
References Paklet L, Abe M and Olanjide D (2013) Priapism associated with risperidone: A case report, literature review and review of the South London and Maudsley hospital patients’ database. Therapeutic Advances in Psychopharmacology 3: 3–13. Sood S, James W and Bailon M (2008) Priapism associated with atypical antipsychotic medications: A review. International Clinical Psychopharmacology 23: 9–17.
Australian & New Zealand Journal of Downloaded Psychiatry, 48(10) from anp.sagepub.com at Bobst Library, New York University on October 15, 2014
963
ANZJP Correspondence to develop this adverse effect were as follows: aripiprazole after 10 days with a CK of 1263 U/l, amisulpride after 5 years to 25810 U/l, and olanzapine after 5 years to 9728 U/l. During this admission the patient’s CK values normalized after ceasing antipsychotics but his delusions intensified. Given CK rise to multiple antipsychotics, clozapine was considered. Patient’s CK levels were normal on clozapine and he attained remission. In our patient the initial diagnosis for the elevated CK was a subsyndromal NMS implying central mechanisms like sympathetic dysregulation or hypothalamic dopamine antagonism (Gurrera, 1999). However a recent review of antipsychotic medication and
rhabdomyolysis by Packard (2014), discusses local mechanisms, wherein antipsychotics with high 5-HT2a antagonism elevate CK by increasing sarcolemmal permeability (Packard et al., 2014). This implies that antipsychotics with greater 5HT2a binding (paliperidone, ziprasidone, asenapine, etc) would have a higher incidence of rhabdomyolysis. Whilst antipsychotic medication may elevate CK there is evidence that this can also occur intrinsically within the acute and maintenance phases of schizophrenia after controlling for nonspecific factors such as stress, trauma, or hyperactivity (Meltzer, 1976). In our patient, after ruling out other medical causes of rhabdomyolysis (cocaine use, heat
stroke, Legionella infection, etc.) the recurrent CK rise most likely appears to be a local effect of antipsychotics rather than centrally mediated. Clinicians should consider CK elevation within a broader context when the classical syndrome of NMS is absent. References Gurrera RJ (1999). Sympathoadrenal hyperactivity and the etiology of neuroleptic malignant syndrome. American Journal of Psychiatry 156: 169–180. Meltzer HY (1976). Serum creatine phosphokinase in schizophrenia. American Journal of Psychiatry 133: 192–197. Packard K, Hanson A and Price P (2014). Antipsychotic use and risk of rhabdomyolysis. Journal of Pharmacy Practice [Epub ahead of print].
Australian & New Zealand Journal of Psychiatry, 48(10)
Downloaded from anp.sagepub.com at Bobst Library, New York University on October 15, 2014
