960
ANZJP Correspondence
Figure 1. MRI brain showing bilateral T1 hyperintensities in the caudate, putamen, and globus pallidus (A) with a normal T2 signal (B). Improvement in the T1 basal ganglia hyperintensity was seen at 3 months (C) and 9 months (D).
and intravenous use of manganesecontaminated drugs such as methcathinone (Fernández-Rodriguez et al., 2010; Ferrara and Jankovic, 2009). If left untreated the course is progressive, but symptoms, serum manganese levels and MRI changes all improve when hepatic function is restored (Ferrara and Jankovic, 2009). AHD is therefore an important differential diagnosis when seeking reversible causes of cognitive impairment in patients with alcoholic liver disease. 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
The clinical and radiological features of AHD are associated with elevated manganese levels in the serum, CSF and globus pallidus on autopsy. Potential causes include impaired
biliary excretion and portosystemic shunting (Ferrara and Jankovic, 2009). A similar pattern is seen in manganese toxicity from occupational exposure, long-term total parenteral nutrition
Value of real world economic evaluations of crisis accommodation programmes for patients with severe mental illness Dan Siskind1,2,3, Meredith Harris1 and Harvey Whiteford1
To the Editor
1School
of Population Health, The University of Queensland, Brisbane St Lucia, Australia 2School of Medicine, The University of Queensland, Brisbane St Lucia, Australia 3Metro South Addiction and Mental Health Services, Woolloongabba, Australia Corresponding author: Dan Siskind, Queensland Centre for Mental Health Research, Level 3 Dawson House, The Park, Wacol, QLD 4076, Australia Email: [email protected] DOI: 10.1177/0004867414529478
We appreciate the comments provided by Dr Amos (Amos, 2014) regarding our evaluation of a crisis house for people with severe and persistent mental illness (Siskind et al., 2013). The core of Dr Amos’s comments relate to the difficulties in selecting appropriate controls from administrative data extracts for use in retrospective quasi-experimental evaluations of existing mental health services. While we agree that a limitation of this study was that there were differences between the intervention and control groups, we disagree with the view that no valid conclusions can be drawn from the study. In consultation with our statistical advisor, we believe that the statistical techniques used to
Fernández-Rodriguez R, Contreras A, de Villoria JG, et al. (2010) Acquired hepatocerebral degeneration: clinical characteristics and MRI findings. European Journal of Neurology 17: 1463–1470. Ferrara J and Jankovic J (2009) Acquired hepatocerebral degeneration. Journal of Neurology 256: 320–332. Stracciari A, Mattarozzi K, D’Alessandro R, et al. (2008) Cognitive functioning in chronic acquired hepatocerebral degeneration. Metabolic Brain Disease 23: 155–160.
adjust for differences between the intervention and control groups permit us to make meaningful economic interpretations of our results. There are inherent limitations when using retrospective administrative data. As variables cannot be prospectively selected, researchers must make interpretations form available data. Missing data can make certain variables unusable, as was the case for our data related to community clinical contacts. However retrospective administrative datasets allow for the evaluation of real world interventions. Insights into the efficacy of programmes targeted to actual public mental health service patients are inherently valuable as the results of randomised controlled trials with
Australian & New Zealand Journal of Psychiatry, 48(10) Downloaded from anp.sagepub.com at University of Manitoba Libraries on June 18, 2015
961
ANZJP Correspondence strict inclusion criteria can be difficult to translate to the real world. We thank Dr Amos for his comments, but believe that the economic evaluation of real world programmes such as ours provides useful information for service planners regarding programmes that can have an immediate benefit for mental health patients in need.
Funding
References
This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.
Amos A (2014) Selection bias in the economic evaluation of crisis accommodation for patients with severe mental illness. Australian and New Zealand Journal of Psychiatry 48: 200–201. Siskind D, Harris M, Kisely S, et al. (2013) A retrospective quasi-experimental study of a community crisis house for patients with severe and persistent mental illness. Australian and New Zealand Journal of Psychiatry 47: 667–675.
QTc prolongation with asenapine Felix Kotasek1, Prashant Tibrewal2 and Rohan Dhillon2
not have a clinically relevant effect on the QT interval. We present a case of asenapine-induced QTc prolongation. Mr C is a 54-year-old man with a long history of clozapine-resistant schizophrenia who presented to hospital in late 2013 following a psychotic relapse. Over the last decade, antipsychotics including aripiprazole, amisupride, ziprasidone and paliperidone have been used to augment his clozapine. At the time of his recent admission, a routine ECG was conducted revealing a prolonged QTc of 496 ms on the combination of clozapine and quetiapine. Quetiapine, a drug associated with moderate increases in QTc, was immediately ceased and his QTc reduced to 470 ms. After receiving advice from cardiology, asenapine was selected to replace quetiapine for its purportedly low effect on QTc. However, within 24 hours of commencing asenapine, an ECG revealed Mr C’s QT had risen 30 ms to 500 ms. Asenapine was immediately ceased, and his QTc fell once again, and remained within acceptable limits for the remainder of his admission. The QTc prolongation seen after Mr C was commenced on asenapine is consistent with a Naranjo score of 7, indicating probable causation (Naranjo et al., 1981). Subsequently, olanzapine was used to augment his clozapine with no marked effect on QTc. Independently of each other, clozapine and asenapine are two drugs
1University
of Adelaide, Adelaide, Australia Queen Elizabeth Hospital, Woodville, South Adelaide, Australia
2The
Corresponding author: Prashant Tibrewal, Queen Elizabeth Hospital, c/- Cramond Clinic, The Queen Elizabeth Hospital, Woodville, SA 5011, Australia. Email: [email protected] DOI: 10.1177/0004867414531832
To the Editor Prolongation of QTc is a relatively common adverse effect of antipsychotic medication. QTc prolongation has been associated with development of potentially fatal cardiac arrhythmias, most notably torsades de pointes. The primary mechanism whereby antipsychotics induce QTc prolongation is through their blockage of the hERG rapid-delayed rectifier potassium channels in cardiomyocytes (Menkes and Knight, 2002). Asenapine is a recently introduced atypical antipsychotic that, in Australia, is indicated in the treatment of schizophrenia and bipolar I disorder. Presently, there is limited information available regarding asenapine’s effect on QTc, aside from manufacturer information. In a study of asenapine’s effect on QTc, Chapel et al. (2009) concluded that asenapine did
Declaration of interest The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.
that have ostensibly minor effects on QTc. However, when used in conjunction with one another in this case, these drugs led to significant QTc prolongation. Whilst no firm conclusions can be drawn from a single case, it highlights the need for further research into asenapine’s effects on QTc, especially in the context of combination therapy with other antipsychotics. Additionally, this case highlights the importance of ECG monitoring of patients on multiple antipsychotic therapy, given its common clinical practice in treatment resistant schizophrenia. 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 Chapel S, Hutmacher MM, Haig G, et al. (2009) Exposure-response analysis in patients with schizophrenia to assess the effect of asenapine on QTc prolongation. The Journal of Clinical Pharmacology 30: 1297–1308. Menkes DB and Knight JC (2002) Cardiotoxicity and prescription of thioridazine in New Zealand. Australian and New Zealand Journal of Psychiatry 36: 492–498. Naranjo CA, Busto U, Sellers EM, et al. (1981) A method for estimating the probability of adverse drug reactions. Clinical Pharmacology and Therapeutics 30: 239–245.
Australian & New Zealand Journal of Psychiatry, 48(10)
Downloaded from anp.sagepub.com at University of Manitoba Libraries on June 18, 2015
ANZJP Correspondence
Figure 1. MRI brain showing bilateral T1 hyperintensities in the caudate, putamen, and globus pallidus (A) with a normal T2 signal (B). Improvement in the T1 basal ganglia hyperintensity was seen at 3 months (C) and 9 months (D).
and intravenous use of manganesecontaminated drugs such as methcathinone (Fernández-Rodriguez et al., 2010; Ferrara and Jankovic, 2009). If left untreated the course is progressive, but symptoms, serum manganese levels and MRI changes all improve when hepatic function is restored (Ferrara and Jankovic, 2009). AHD is therefore an important differential diagnosis when seeking reversible causes of cognitive impairment in patients with alcoholic liver disease. 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
The clinical and radiological features of AHD are associated with elevated manganese levels in the serum, CSF and globus pallidus on autopsy. Potential causes include impaired
biliary excretion and portosystemic shunting (Ferrara and Jankovic, 2009). A similar pattern is seen in manganese toxicity from occupational exposure, long-term total parenteral nutrition
Value of real world economic evaluations of crisis accommodation programmes for patients with severe mental illness Dan Siskind1,2,3, Meredith Harris1 and Harvey Whiteford1
To the Editor
1School
of Population Health, The University of Queensland, Brisbane St Lucia, Australia 2School of Medicine, The University of Queensland, Brisbane St Lucia, Australia 3Metro South Addiction and Mental Health Services, Woolloongabba, Australia Corresponding author: Dan Siskind, Queensland Centre for Mental Health Research, Level 3 Dawson House, The Park, Wacol, QLD 4076, Australia Email: [email protected] DOI: 10.1177/0004867414529478
We appreciate the comments provided by Dr Amos (Amos, 2014) regarding our evaluation of a crisis house for people with severe and persistent mental illness (Siskind et al., 2013). The core of Dr Amos’s comments relate to the difficulties in selecting appropriate controls from administrative data extracts for use in retrospective quasi-experimental evaluations of existing mental health services. While we agree that a limitation of this study was that there were differences between the intervention and control groups, we disagree with the view that no valid conclusions can be drawn from the study. In consultation with our statistical advisor, we believe that the statistical techniques used to
Fernández-Rodriguez R, Contreras A, de Villoria JG, et al. (2010) Acquired hepatocerebral degeneration: clinical characteristics and MRI findings. European Journal of Neurology 17: 1463–1470. Ferrara J and Jankovic J (2009) Acquired hepatocerebral degeneration. Journal of Neurology 256: 320–332. Stracciari A, Mattarozzi K, D’Alessandro R, et al. (2008) Cognitive functioning in chronic acquired hepatocerebral degeneration. Metabolic Brain Disease 23: 155–160.
adjust for differences between the intervention and control groups permit us to make meaningful economic interpretations of our results. There are inherent limitations when using retrospective administrative data. As variables cannot be prospectively selected, researchers must make interpretations form available data. Missing data can make certain variables unusable, as was the case for our data related to community clinical contacts. However retrospective administrative datasets allow for the evaluation of real world interventions. Insights into the efficacy of programmes targeted to actual public mental health service patients are inherently valuable as the results of randomised controlled trials with
Australian & New Zealand Journal of Psychiatry, 48(10) Downloaded from anp.sagepub.com at University of Manitoba Libraries on June 18, 2015
961
ANZJP Correspondence strict inclusion criteria can be difficult to translate to the real world. We thank Dr Amos for his comments, but believe that the economic evaluation of real world programmes such as ours provides useful information for service planners regarding programmes that can have an immediate benefit for mental health patients in need.
Funding
References
This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.
Amos A (2014) Selection bias in the economic evaluation of crisis accommodation for patients with severe mental illness. Australian and New Zealand Journal of Psychiatry 48: 200–201. Siskind D, Harris M, Kisely S, et al. (2013) A retrospective quasi-experimental study of a community crisis house for patients with severe and persistent mental illness. Australian and New Zealand Journal of Psychiatry 47: 667–675.
QTc prolongation with asenapine Felix Kotasek1, Prashant Tibrewal2 and Rohan Dhillon2
not have a clinically relevant effect on the QT interval. We present a case of asenapine-induced QTc prolongation. Mr C is a 54-year-old man with a long history of clozapine-resistant schizophrenia who presented to hospital in late 2013 following a psychotic relapse. Over the last decade, antipsychotics including aripiprazole, amisupride, ziprasidone and paliperidone have been used to augment his clozapine. At the time of his recent admission, a routine ECG was conducted revealing a prolonged QTc of 496 ms on the combination of clozapine and quetiapine. Quetiapine, a drug associated with moderate increases in QTc, was immediately ceased and his QTc reduced to 470 ms. After receiving advice from cardiology, asenapine was selected to replace quetiapine for its purportedly low effect on QTc. However, within 24 hours of commencing asenapine, an ECG revealed Mr C’s QT had risen 30 ms to 500 ms. Asenapine was immediately ceased, and his QTc fell once again, and remained within acceptable limits for the remainder of his admission. The QTc prolongation seen after Mr C was commenced on asenapine is consistent with a Naranjo score of 7, indicating probable causation (Naranjo et al., 1981). Subsequently, olanzapine was used to augment his clozapine with no marked effect on QTc. Independently of each other, clozapine and asenapine are two drugs
1University
of Adelaide, Adelaide, Australia Queen Elizabeth Hospital, Woodville, South Adelaide, Australia
2The
Corresponding author: Prashant Tibrewal, Queen Elizabeth Hospital, c/- Cramond Clinic, The Queen Elizabeth Hospital, Woodville, SA 5011, Australia. Email: [email protected] DOI: 10.1177/0004867414531832
To the Editor Prolongation of QTc is a relatively common adverse effect of antipsychotic medication. QTc prolongation has been associated with development of potentially fatal cardiac arrhythmias, most notably torsades de pointes. The primary mechanism whereby antipsychotics induce QTc prolongation is through their blockage of the hERG rapid-delayed rectifier potassium channels in cardiomyocytes (Menkes and Knight, 2002). Asenapine is a recently introduced atypical antipsychotic that, in Australia, is indicated in the treatment of schizophrenia and bipolar I disorder. Presently, there is limited information available regarding asenapine’s effect on QTc, aside from manufacturer information. In a study of asenapine’s effect on QTc, Chapel et al. (2009) concluded that asenapine did
Declaration of interest The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.
that have ostensibly minor effects on QTc. However, when used in conjunction with one another in this case, these drugs led to significant QTc prolongation. Whilst no firm conclusions can be drawn from a single case, it highlights the need for further research into asenapine’s effects on QTc, especially in the context of combination therapy with other antipsychotics. Additionally, this case highlights the importance of ECG monitoring of patients on multiple antipsychotic therapy, given its common clinical practice in treatment resistant schizophrenia. 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 Chapel S, Hutmacher MM, Haig G, et al. (2009) Exposure-response analysis in patients with schizophrenia to assess the effect of asenapine on QTc prolongation. The Journal of Clinical Pharmacology 30: 1297–1308. Menkes DB and Knight JC (2002) Cardiotoxicity and prescription of thioridazine in New Zealand. Australian and New Zealand Journal of Psychiatry 36: 492–498. Naranjo CA, Busto U, Sellers EM, et al. (1981) A method for estimating the probability of adverse drug reactions. Clinical Pharmacology and Therapeutics 30: 239–245.
Australian & New Zealand Journal of Psychiatry, 48(10)
Downloaded from anp.sagepub.com at University of Manitoba Libraries on June 18, 2015
