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<p class="ltrs-br-ltr-br-title"><span class="bold">Metabolic Health of People Admitted to a Psychiatric Intensive Care Unit in Adelaide, South Australia</span></p>
<p class="ltrs-br-ltr-br-body-text"><span class="semibold">To the Editor:</span> People with psychiatric disorders have high rates of comorbid obesity, cardiovascular disease, metabolic syndrome, and diabetes. These disorders are associated with poor quality of life and premature mortality.<span class="htm-cite"><a href="#ref1">1</a></span></p>
<p class="ltrs-br-ltr-br-body-text">Lifestyle factors including poverty, poor diet, and lack of exercise contribute to physical comorbidity. In addition, many psychotropic drugs, including some of the atypical antipsychotics, mood stabilizers, and antidepressants, are associated with weight gain and increased risk of metabolic syndrome.</p>
<p class="ltrs-br-ltr-br-body-text">A recent voluntary screening program for public mental health patients in the United States<span class="htm-cite"><a href="#ref2">2</a></span> found high rates of obesity, hypertension, and elevated cholesterol, glucose, and triglycerides. John and colleagues<span class="htm-cite"><a href="#ref3">3</a></span> found that 54% of Australians attending community mental health clinics met International Diabetes Federation criteria for metabolic syndrome, compared to rates of 13.4%–30.7% in the general Australian population.<span class="htm-cite"><a href="#ref4">4</a></span> However, few data are available concerning the metabolic profiles of people admitted acutely to hospital with severe psychiatric disorders.</p>
<p class="ltrs-br-ltr-br-body-text">We assessed a range of metabolic parameters in patients admitted involuntarily to a 10-bed, closed psychiatric intensive care unit. This service managed the most severely behaviorally disturbed patients from a catchment population of approximately 750,000 people in Adelaide, South Australia. </p>
<p class="ltrs-br-ltr-br-body-text">&nbsp;</p>
<p class="ltrs-br-ltr-br-body-text"><span class="semibold-ital">Method.</span> One hundred nineteen consecutive patients were admitted during the study period. Fourteen patients refused measurement of body mass index (BMI) or venipuncture; data for the remaining 105 patients are included in the analysis. This study conformed to the ethical criteria of the Australian National Health and Medical Research Council (2003).<span class="htm-cite"><a href="#ref5">5</a></span></p>
<p class="ltrs-br-ltr-br-body-text"><span class="semibold-ital">Results.</span><span class="italic"> </span>The patients’ mean age was 35.21 years (SD<span class="thinspace"> </span>=<span class="thinspace"> </span>10.62), and 67% were male. Men were significantly younger, on average, than the women (<span class="italic">t</span><span class="thinspace"> </span>=<span class="thinspace"> </span>5.15, <span class="italic">df</span><span class="thinspace"> </span>=<span class="thinspace"> </span>103, <span class="italic">P</span><span class="thinspace"> </span>&lt;<span class="thinspace"> </span>.001). Thirteen subjects (12%) were Aboriginal. The most common clinical diagnosis (<span class="italic">DSM-IV</span> criteria) was nonaffective psychosis (67%, n<span class="thinspace"> </span>=<span class="thinspace"> </span>70), followed by bipolar disorder (21%, n<span class="thinspace"> </span>=<span class="thinspace"> </span>22).</p>
<p class="ltrs-br-ltr-br-body-text">The mean BMI was 27 (SD<span class="thinspace"> </span>=<span class="thinspace"> </span>6.14), with 4 subjects (3.8%) being underweight (BMI<span class="thinspace"> </span>&lt;<span class="thinspace"> </span>20), 31 (29.5%) overweight (BMI<span class="thinspace"> </span>=<span class="thinspace"> </span>25–30), and 32 (30.5%) obese (BMI<span class="thinspace"> </span>&gt;<span class="thinspace"> </span>30). The mean BMI did not significantly differ between men (mean<span class="thinspace"> </span>=<span class="thinspace"> </span>26.9, SD<span class="thinspace"> </span>=<span class="thinspace"> </span>6.25) and women (mean<span class="thinspace"> </span>=<span class="thinspace"> </span>27.3, SD<span class="thinspace"> </span>=<span class="thinspace"> </span>6.0). Standard laboratory criteria (Institute of Medical and Veterinary Science, Adelaide, South Australia<span class="htm-cite"><a href="#ref6">6</a></span>) were utilized to interpret the blood results. The mean fasting blood glucose level was 4.9 mg/dL, and 25 subjects (23.8%) had an elevated fasting glucose level (&gt;<span class="thinspace"> </span>5.5 mg/dL). The mean fasting cholesterol level was 4.43 mmol/L (SD<span class="thinspace"> </span>=<span class="thinspace"> </span>1.34), with 16 patients (15.2%) having borderline high cholesterol (5.18–6.18 mmol/L) and a further 9 (8.6%) classified as having high cholesterol (&gt;<span class="thinspace"> </span>6.19 mmol/L). The mean triglyceride level for the sample was 1.85 (SD<span class="thinspace"> </span>=<span class="thinspace"> </span>1.20), with 43 (43.9%) having elevated triglycerides (≥<span class="thinspace"> </span>1.6 mmol/L). The mean low-density lipoprotein cholesterol (LDL) level was 2.56 (SD<span class="thinspace"> </span>=<span class="thinspace"> 0</span>.91) mmol/L, and 17 patients (16.1%) had elevated LDL<span class="thinspace"> </span>≥<span class="thinspace"> </span>2.6 mmol/L. The mean high-density lipoprotein cholesterol (HDL) level was 1.19 (SD<span class="thinspace"> </span>=<span class="thinspace"> 0</span>.32) mmol/L. Men had significantly lower HDL (<span class="italic">t</span><span class="thinspace"> </span>=<span class="thinspace"> </span>2.49, <span class="italic">df</span><span class="thinspace"> </span>=<span class="thinspace"> </span>96, <span class="italic">P</span><span class="thinspace"> </span>=<span class="thinspace"> </span>.015). For each unit increase in HDL, BMI decreased by 4.49 (<span class="italic">P</span><span class="thinspace"> </span>=<span class="thinspace"> </span>.019).</p>
<p class="ltrs-br-ltr-br-body-text">There was a mean weight gain of 2.45 kg during hospitalization. The mean length of stay was 11.6 days, so patients gained a mean of 0.22 kg/d. Contributing factors include the lack of opportunity to exercise and a policy of allowing patients to purchase confectionery, chips, and soft drinks. Ninety percent of our sample (n<span class="thinspace"> </span>=<span class="thinspace"> </span>95) were treated with olanzapine, clozapine, and/or sodium valproate. The mean weight gain was greater for patients treated with these medications, although these differences did not reach significance. However, other medications with a more favorable metabolic profile are clearly preferable, even in the acute setting.</p>
<p class="ltrs-br-ltr-br-body-text">&nbsp;</p>
<p class="ltrs-br-ltr-br-body-text">Our study shows that about 60% of these acutely unwell patients are overweight or obese, almost half have elevated triglycerides, and a quarter have elevated fasting blood glucose and elevated cholesterol. These rates are very similar to rates in the healthy Australian population.<span class="htm-cite"><a href="#ref7">7</a>,<a href="#ref8">8</a></span></p>
<p class="ltrs-br-ltr-br-body-text">Compared to the US sample studied by Correll et al,<span class="htm-cite"><a href="#ref2">2</a></span> our patients had lower rates of obesity, and a smaller proportion had elevated fasting glucose and triglyceride levels. This finding may reflect population level differences between the United States<span class="htm-cite"><a href="#ref9">9</a></span> and Australia.<span class="htm-cite"><a href="#ref8">8</a></span></p>
<p class="ltrs-br-ltr-br-body-text">The participants in this study tend to be excluded from most research, as they are involuntary and behaviorally disturbed and often do not have capacity to give informed consent. It is essential that service level studies are undertaken to provide basic information about their rates of physical comorbidity. It does appear that these acutely admitted patients, many of whom were not receiving treatment prior to admission, have about the same level of cardiometabolic risk as the general population. From a metabolic perspective, they are healthier than people engaged in ongoing psychiatric treatment.<span class="htm-cite"><a href="#ref2">2</a>,<a href="#ref3">3</a></span> This is consistent with the findings of Foley and Morley,<span class="htm-cite"><a href="#ref10">10</a></span> who reported that, prior to treatment, first-episode psychosis patients had normal levels of cardiovascular risk, assessed using weight or metabolic indices, but their risk increased after first exposure to any antipsychotic drug.</p>
<p class="ltrs-br-ltr-br-body-text">Selecting medications that do not exacerbate cardiometabolic risk is important in this population. While in the short-term treatment of acute behavioral disturbance the sedative properties of a drug may outweigh the metabolic risks, consideration should be given to switching to a drug with a more favorable metabolic profile prior to discharge. It is also important that patients with metabolic measures requiring treatment receive the same level of general medical care as other members of the community.</p>
<p class="ltrs-br-ltr-br-references-head"><span class="smallcaps">References</span></p>
<p class="references-references-text-1-9"><a name="ref1"></a>1. Brown S, Kim M, Mitchell C, et al. Twenty-five year mortality of a community cohort with schizophrenia. <span class="italic">Br J Psychiatry</span>. 2010;196(2):116–121. <span class="pubmed-crossref"><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=20118455&dopt=Abstract">PubMed</a> <a href="http://dx.doi.org/10.1192/bjp.bp.109.067512">doi:10.1192/bjp.bp.109.067512</a></span></p>
<p class="references-references-text-1-9"><a name="ref2"></a>2. Correll CU, Druss BG, Lombardo I, et al. Findings of a US national cardiometabolic screening program among 10,084 psychiatric outpatients. <span class="italic">Psychiatr Serv</span>. 2010;61(9):892–898. <span class="pubmed-crossref"><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=20810587&dopt=Abstract">PubMed</a> <a href="http://dx.doi.org/10.1176/appi.ps.61.9.892">doi:10.1176/appi.ps.61.9.892</a></span></p>
<p class="references-references-text-1-9"><a name="ref3"></a>3. John AP, Koloth R, Dragovic M, et al. Prevalence of metabolic syndrome among Australians with severe mental illness. <span class="italic">Med J Aust</span>. 2009;190(4):176–179. <span class="pubmed-crossref"><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=19220180&dopt=Abstract">PubMed</a></span></p>
<p class="references-references-text-1-9"><a name="ref4"></a>4. Cameron AJ, Magliano DJ, Zimmet PZ, et al. The metabolic syndrome in Australia: prevalence using four definitions. <span class="italic">Diabetes Res Clin Pract</span>. 2007;77(3):471–478. <span class="pubmed-crossref"><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=17350710&dopt=Abstract">PubMed</a> <a href="http://dx.doi.org/10.1016/j.diabres.2007.02.002">doi:10.1016/j.diabres.2007.02.002</a></span></p>
<p class="references-references-text-1-9"><a name="ref5"></a>5. National Health and Medical Research Council (NHMRC). <span class="italic">When Does Quality Assurance in Health Care Require Independent Ethical Review? Advice to Institutions, Human Research Ethics Committees and Health Care Professionals</span>. Canberra, Australia: NHMRC; 2003.</p>
<p class="references-references-text-1-9"><a name="ref6"></a>6. Pathology Collection Guide. IMVS Pathology website. <span class="hyperlink"><a href="http://www.imvs.sa.gov.au/wps/wcm/connect/sa+pathology+internet+content/imvs/for+clinicians/pathology+collection+guide/pathology+collection+guide">http://www.imvs.sa.gov.au/wps/wcm/connect/sa+pathology+internet+content/imvs/for+clinicians/<br />pathology+collection+guide/pathology+collection+guide</a></span>. Accessed April 6, 2011.</p>
<p class="references-references-text-1-9"><a name="ref7"></a>7. Barr ELM, Magliano DJ, Zimmet PZ, et al. <span class="italic">AusDiab 2005: The Australian Diabetes, Obesity and Lifestyle Study -Tracking the Accelerating Epidemic: Its Cause and Outcomes</span>. Melbourne, Australia: International Diabetes Institute; 2006.</p>
<p class="references-references-text-1-9"><a name="ref8"></a>8. Dunstan D, Zimmet P, Welborn PT, et al. <span class="italic">Diabetes and Associated Disorders in Australia-2000: The Accelerating Epidemic. The Australian Diabetes, Obesity and Lifestyle Study (AusDiab)</span>. Melbourne, Australia: International Diabetes Institute; 2001.</p>
<p class="references-references-text-1-9"><a name="ref9"></a>9. US Obesity Trends. Centers for Disease Control and Prevention website. <span class="hyperlink"><a href="http://www.cdc.gov/obesity/data/trends.html">http://www.cdc.gov/obesity/data/trends.html</a></span>. Updated March 3, 2011. Accessed April 12, 2011.</p>
<p class="references-references-text-10-99"><a name="ref10"></a>10. Foley DL, Morley KI. Systematic review of early cardiometabolic outcomes of the first treated episode of psychosis. (published online ahead of print February 7, 2011) <span class="italic">Arch Gen Psychiatry</span>. 2011;68(6):609–616. <span class="pubmed-crossref"><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=21300937&dopt=Abstract">PubMed</a> <a href="http://dx.doi.org/10.1001/archgenpsychiatry.2011.2">doi:10.1001/archgenpsychiatry.2011.2</a></span></p>
<p class="ltrs-br-ltr-br-author"><span class="bold">David Ash, MBBS, DipPsychotherapy, FRANZCP</span></p>
<p class="ltrs-br-ltr-br-author"><span class="bold">Tushar Singh, MBBS, MD</span></p>
<p class="ltrs-br-ltr-br-author"><span class="bold">Tracy Air, MBiostatistics</span></p>
<p class="ltrs-br-ltr-br-author"><span class="bold">Cassandra Burton, BPsych (Hons)</span></p>
<p class="ltrs-br-ltr-br-author"><span class="bold">Cherrie Galletly, MBChB, DPM, FRANZCP, PhD</span></p>
<p class="ltrs-br-ltr-br-author"><a href="mailto:cherrie.galletly@adelaide.edu.au">cherrie.galletly@adelaide.edu.au</a></p>
<p class="ltrs-br-ltr-br-endmatter-fieldnotes"><span class="semibold-ital">Author affiliations:</span> Discipline of Psychiatry, <span class="apple-style-span">University of Adelaide (Drs Ash and Galletly and Ms Air); Ramsay Health Care (SA) Mental Health Services (Ms Burton and Dr Galletly); and Adelaide Metro Mental Health Directorate (Drs Ash, Singh, and Galletly), Adelaide, South Australia, Australia.</span></p>
<p class="ltrs-br-ltr-br-endmatter-fieldnotes"><span class="semibold-ital">Potential conflicts of interest:</span> None reported.</p>
<p class="ltrs-br-ltr-br-endmatter-fieldnotes"><span class="semibold-ital">Funding/support:</span> None reported.</p>
<p class="ltrs-br-ltr-br-endmatter-fieldnotes"><span class="semibold-ital">Previous presentation: </span>Presented at the <span class="apple-style-span">2nd Biennial Schizophrenia International Research Conference, April 10–14, 2010, Florence, Italy; and the Australian Society for Psychiatric Research Annual Conference, December 2–4, 2009, Canberra, Australia.</span></p>
<p class="ltrs-br-ltr-br-endmatter-fieldnotes"><span class="semibold-ital">Published online:</span> February 23, 2012.</p>
<p class="ltrs-br-ltr-br-copyright-doi"><span class="italic">Prim Care Companion CNS Disord 2012;14(1):</span><span class="doi">doi:10.4088/PCC.11l01207</span></p>
<p class="ltrs-br-ltr-br-copyright-doi"><span class="italic">© Copyright 2012 Physicians Postgraduate Press, Inc.</span></p>
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