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Letter to the Editor
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Objective: Unrecognized bipolar disorder in patients presenting with a major depressive episode may lead to delayed diagnosis, inappropriate treatment, and excessive costs. This study models the cost effectiveness of screening for bipolar disorder among adults presenting for the first time with symptoms of major depressive disorder.
Method: A decision-analysis model was used to evaluate the outcomes and cost over 5 years of screening versus not screening for bipolar disorder. Screening was defined as a 1-time administration of the Mood Disorder Questionnaire at the initial visit followed by referral to a psychiatrist for patients screening positive for bipolar disorder. Health states included correctly diagnosed bipolar disorder, unrecognized bipolar disorder, and correctly diagnosed major depressive episodes. Model outcomes included rates of correct diagnosis of bipolar disorder and discounted costs (2006 US dollars) of screening and treating major depressive episodes. Literature was the primary source of data and was collected from September 2007 through March 2009.
Results: According to the model, 1,000 adults in a health plan with 1 million adult members annually present with symptoms of major depressive disorder. An additional 38 patients were correctly diagnosed with depression (unipolar or a major depressive episode) or bipolar disorder (440 with screening vs 402 without screening) through a 1-time screening for bipolar disorder. Estimated 5-year discounted costs per patient were $36,044 without screening and $34,107 with screening (savings of $1,937). Accordingly, total 5-year budgetary savings were estimated at $1.94 million. Results were most sensitive to difference in treatment costs for patients with recognized versus unrecognized bipolar disorder.
Conclusion: A 1-time screening program for bipolar disorder, when patients first present with a major depressive episode, can reduce health care costs to managed-care plans.
Submitted: December 11, 2008; accepted April 21, 2009.
Online ahead of print: August 11, 2009.
Corresponding author: Joseph Menzin, PhD, Boston Health Economics, Inc, 20 Fox Rd, Waltham, MA 02451 (jmenzin@bhei.com).
Because this piece does not have an abstract, we have provided for your benefit the first 3 sentences of the full text.
Patients with severe mental disorders have increased mortality rates compared with the general population. The leading cause of death for individuals with psychotic illnesses or bipolar disorder is cardiovascular disease (CVD), which is often the result of patients' health problems associated with their psychiatric disorders, including, but not limited to, obesity, metabolic syndrome, and diabetes. Such problems occur more often and have worse outcomes in patients with serious mental illness than the general population because of a combination of factors such as inadequate access to quality care, poor lifestyle choices, and the association between some antipsychotic medications and weight gain. Coordinated somatic and psychiatric treatment, weight-neutral or weight-reducing pharmaceuticals, and behavioral weight management programs may help lessen the burden of CVD in the mental health population.
Objective: Pegylated interferon (PegIFN) and ribavirin (RBV) treatment for the hepatitis C virus (HCV) infection can induce depressive episodes. Personality traits have been associated with mood disorders. The aim of this study was to evaluate the personality profile as a risk factor for induced depression by PegIFN and RBV treatment in patients with HCV.
Method: In a prospective cohort study, 204 consecutive HCV outpatients who received PegIFN and RBV were assessed using the Structured Clinical Interview for DSM-IV Axis I Disorders and the Temperament and Character Inventory-Revised (TCI-R). Moreover, the Patient Health Questionnaire and the Hospital Anxiety and Depression Scale were administered at baseline and at 4, 12, 24, and/or 48 weeks of treatment. Patients were recruited between September 2003 and December 2006.
Results: One hundred eighteen patients (57.8%) were men. The mean (SD) age was 44.39 (10.4) years. The incidence of induced depression during the 48 weeks of antiviral treatment was 73 (42%). Low self-directedness dimension (HR = 0.63, 95% CI = 0.446 to 0.890, p =.009), baseline subclinical depression levels (HR = 1.113, 95% CI = 1.023 to 1.22, p =.013), and history of mood disorders (HR = 0.372, 95% CI = 0.220 to 0.629, p
Conclusion: Low self-directedness, depressive symptoms at baseline, and history of previous mood disorders may predict induced depression by PegIFN and RBV in euthymic HCV patients.
Objective: To review extant literature implicating inflammation in the pathophysiology of bipolar disorder. Furthermore, we review evidence regarding the anti-inflammatory actions of mood-stabilizing medication, the putative reciprocal association of inflammation with behavioral parameters and medical burden in bipolar disorder, and the potential role of anti-inflammatory agents in the treatment of bipolar disorder.
Data Sources: MEDLINE and PubMed searches were conducted of English-language articles published from 1950 to April 2008 using the search terms bipolar disorder, manic, or mania, cross-referenced with inflammation, inflammatory, interleukin, cytokine, C-reactive protein, or tumor necrosis factor. The search, which was conducted most recently on August 20, 2008, was supplemented by manually reviewing reference lists from the identified publications.
Study Selection: Articles selected for review were based on adequacy of sample size, the use of standardized experimental procedures, validated assessment measures, and overall manuscript quality.
Data Extraction: Studies were reviewed for statistical comparisons of cytokines among persons with and without bipolar disorder, during symptomatic and non-symptomatic intervals and before and after pharmacologic treatment. Significant and nonsignificant findings were tabulated.
Data Synthesis: Available evidence indicates that bipolar disorder and inflammation are linked through shared genetic polymorphisms and gene expression as well as altered cytokine levels during symptomatic (i.e., mania and depression) and asymptomatic intervals. However, results are inconsistent. Several conventional mood stabilizers have anti-inflammatory properties. The cyclooxygenase-2-selective anti-inflammatory celecoxib may offer antidepressant effects. Inflammation is closely linked with behavioral parameters such as exercise, sleep, alcohol abuse, and smoking, as well as with medical comorbidities including coronary artery disease, obesity and insulin resistance, osteoporosis, and pain. Methodological limitations precluding definitive conclusions are heterogeneity in sample composition, cytokine assessment procedures, and treatment regimens. The inclusion of multiple ethnic groups introduces another source of variability but also increases the generalizability of study findings.
Conclusion:Inflammation appears relevant to bipolar disorder across several important domains. Further research is warranted to parse the reciprocal associations between inflammation and symptoms, comorbidities, and treatments in bipolar disorder. Studies of this topic among youth are needed and may best serve this purpose.
Received June 29, 2008; accepted Aug. 22, 2008. From the Western Psychiatric Institute and Clinic, University of Pittsburgh School of Medicine, Pa. (Dr. Goldstein); the Department of Psychiatry, Case Western Reserve University School of Medicine, Cleveland, Ohio (Dr. Kemp); the Mood Disorders Psychopharmacology Unit, University Health Network, and the Institute of Medical Science, University of Toronto, Ontario, Canada (Dr. McIntyre and Ms. Soczynska); and the Departments of Psychiatry and Pharmacology, University of Toronto, Ontario, Canada (Dr. McIntyre).
Dr. Kemp has received grant/research support from the National Institutes of Health and Takeda; has received honoraria from Servier; has been a consultant for Abbott, Bristol-Myers Squibb, and Wyeth; and has received other financial or material support from Organon. Dr. McIntyre has received grant/research support from the Stanley Medical Research Institute, NARSAD, and Eli Lilly; has been a member of the speakers/advisory boards for AstraZeneca, Bristol-Myers Squibb, the France Foundation, GlaxoSmithKline, Janssen-Ortho, Solvay/Wyeth, Eli Lilly, Organon, Lundbeck, Biovail, Pfizer, and Shire; and has received other financial or material support from AstraZeneca, Bristol-Myers Squibb, the France Foundation, 13CME, Solvay/Wyeth, and Physicians Postgraduate Press. Dr. Goldstein and Ms. Soczynska report no financial or other relationship relevant to the subject of this article.
Corresponding author and reprints: Benjamin I. Goldstein, M.D., Ph.D., Western Psychiatric Institute and Clinic, University of Pittsburgh School of Medicine, 3811 O' Hara Street, Pittsburgh, PA 16213 (e-mail: goldsteinbi@upmc.edu).
Because this piece has no abstract, we have provided for your benefit the first 3 sentences of the full text.