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Development of a registry for monitoring psychotropic drug prescriptions: aims, methods and implications for ordinary practice and research.
In psychiatry, individual-based registries have provided key information on risks and benefits associated with the use of psychotropic drugs but they have rarely been employed for monitoring and evaluating the everyday prescribing of psychopharmacological treatments. This article describes the cultural background that gave impetus to the idea of registering all prescriptions of psychotropic drugs dispensed by physicians working in the South Verona community mental health service, and presents the methodology employed to develop such a registry in a community psychiatric service where a psychiatric case register (PCR) has been operating since 1978. We developed a registry including every patient receiving psychotropic medications in ordinary practice. This registry is linked to the PCR in order to obtain data on social and demographic characteristics, clinical symptoms, diagnosis, use of services, and outcomes. No exclusion criteria are allowed--anyone receiving treatment is automatically included. This system, which can link drug and service-use data with hard outcome indicators, can generate information on the proportion of subjects discontinuing treatment, switching medication because of side-effects, recovery or inefficacy, as well as on the proportion of subjects failing to return to the physician, and the proportion of patients who improve. The innovative aspect of this approach is that this registry is developed, organized and used by physicians interested in monitoring their clinical practice and in providing patients, relatives and the public with accurate information on drug use in their specific context of care.
Meta-Review: Network Meta-Analyses in Child and Adolescent Psychiatry.
OBJECTIVE: Network meta-analyses (NMAs) are gaining traction as the preferred method for evidence synthesis of intervention studies. This review aimed to summarize the basics of NMAs and conduct a meta-review of available NMAs on the treatment of child and adolescent psychiatric disorders by appraising their quality. METHOD: PubMed (Medline), PsycInfo, Embase, Ovid Medline, and Web of Knowledge were systematically searched (last update January 9, 2018). The quality of each included NMA was appraised using the AMSTAR-2 tool and the PRISMA-NMA checklist, which includes specific items for NMAs. RESULTS: Eighteen NMAs (6 on attention-deficit/hyperactivity disorder; 4 on psychotic disorders; 2 on depression; 2 on anxiety disorders; 1 on obsessive-compulsive disorder; 1 on disruptive behavior disorder, 1 on bipolar disorder, and 1 on antipsychotics across disorders) were retrieved. Results from the AMSTAR-2 assessment showed that only 27% of appraised NMAs were rated as moderate quality; most were rated as low (33%) or critically low (40%) quality. Only 3 of the appraised NMAs reported on all PRISMA-NMA items specific for NMAs; the network structure was graphically presented in most NMAs (80%), and inconsistency was described in only 47%. CONCLUSION: Given the paucity of head-to-head trials in child and adolescent psychiatry, NMAs have the potential to contribute to the field, because they provide evidence-based hierarchies for treatment decision making, even in the absence of trials directly comparing at least 2 treatments. However, because of important limitations in the included NMAs, additional methodologically sound NMAs are needed to inform future guidelines and clinical practice in child and adolescent psychiatry.
Antidepressants versus placebo for panic disorder in adults
© 2013 The Cochrane Collaboration. This is the protocol for a review and there is no abstract. The objectives are as follows: To assess the effects of antidepressants for panic disorder in adults, specifically: To determine the efficacy of antidepressants in alleviating symptoms of panic disorder, with or without agoraphobia, in comparison to placebo; To review the acceptability of antidepressants in panic disorder, with or without agoraphobia, in comparison with placebo; and To investigate the adverse effects of antidepressants in panic disorder, with or without agoraphobia, including the general prevalence of adverse effects, compared to placebo.
Benzodiazepines versus placebo for panic disorder in adults
© 2013 The Cochrane Collaboration. This is the protocol for a review and there is no abstract. The objectives are as follows: To assess the effects of benzodiazepines (BDZs) for panic disorder in adults, specifically: To determine the efficacy of BDZs in alleviating symptoms of panic disorder with or without agoraphobia in comparison to placebo; To review the acceptability of BDZs in panic disorder with or without agoraphobia in comparison with placebo; and To investigate the adverse effects of BDZs in panic disorder with or without agoraphobia, including the general prevalence of adverse effects, compared to placebo.
Benzodiazepines versus placebo for panic disorder in adults.
BACKGROUND: Panic disorder is characterised by recurrent unexpected panic attacks consisting of a wave of intense fear that reaches a peak within a few minutes. Panic disorder is a common disorder, with an estimated lifetime prevalence of 1% to 5% in the general population and a 7% to 10% prevalence in primary care settings. Its aetiology is not fully understood and is probably heterogeneous.Panic disorder is treated with psychological and pharmacological interventions, often used in combination. Although benzodiazepines are frequently used in the treatment of panic disorder, guidelines recommend antidepressants, mainly selective serotonin reuptake inhibitors (SSRIs), as first-line treatment for panic disorder, particularly due to their lower incidence of dependence and withdrawal reaction when compared to benzodiazepines. Despite these recommendations, benzodiazepines are widely used in the treatment of panic disorder, probably because of their rapid onset of action. OBJECTIVES: To assess the efficacy and acceptability of benzodiazepines versus placebo in the treatment of panic disorder with or without agoraphobia in adults. SEARCH METHODS: We searched the Cochrane Common Mental Disorders Controlled Trials Register (CCMDCTR Studies and References), the Cochrane Central Register of Controlled Trials (CENTRAL), MEDLINE (1950-), Embase (1974-), and PsycINFO (1967-) up to 29 May 2018. We handsearched reference lists of relevant papers and previous systematic reviews. We contacted experts in the field for supplemental data. SELECTION CRITERIA: All double-blind (blinding of patients and personnel) controlled trials randomising adults with panic disorder with or without agoraphobia to benzodiazepine or placebo. DATA COLLECTION AND ANALYSIS: Two review authors independently checked the eligibility of studies and extracted data using a standardised form. Data were then entered data into Review Manager 5 using a double-check procedure. Information extracted included study characteristics, participant characteristics, intervention details, settings, and outcome measures in terms of efficacy, acceptability, and tolerability. MAIN RESULTS: We included 24 studies in the review with a total of 4233 participants, of which 2124 were randomised to benzodiazepines and 1475 to placebo. The remaining 634 participants were randomised to other active treatments in three-arm trials. We assessed the overall methodological quality of the included studies as poor. We rated all studies as at unclear risk of bias in at least three domains. In addition, we judged 20 of the 24 included studies as having a high risk of bias in at least one domain.Two primary outcomes of efficacy and acceptability showed a possible advantage of benzodiazepines over placebo. The estimated risk ratio (RR) for a response to treatment was 1.65 (95% confidence interval (CI) 1.39 to 1.96) in favour of benzodiazepines, which corresponds to an estimated number needed to treat for an additional beneficial outcome (NNTB) of 4 (95% CI 3 to 7). The dropout rate was lower among participants treated with benzodiazepines (RR 0.50, 95% CI 0.39 to 0.64); the estimated NNTB was 6 (95% CI 5 to 9). We rated the quality of the evidence as low for both primary outcomes. The possible advantage of benzodiazepine was also seen for remission (RR 1.61, 95% CI 1.38 to 1.88) and the endpoint data for social functioning (standardised mean difference (SMD) -0.53, 95% CI -0.65 to -0.42), both with low-quality evidence. We assessed the evidence for the other secondary outcomes as of very low quality. With the exception of the analyses of the change score data for depression (SMD -0.22, 95% CI -0.48 to 0.04) and social functioning (SMD -0.32, 95% CI -0.88 to 0.24), all secondary outcome analyses showed an effect in favour of benzodiazepines compared to placebo. However, the number of dropouts due to adverse effects was higher with benzodiazepines than with placebo (RR 1.58, 95% CI 1.16 to 2.15; low-quality evidence). Furthermore, our analyses of adverse events showed that a higher proportion of participants experienced at least one adverse effect when treated with benzodiazepines (RR 1.18, 95% CI 1.02 to 1.37; low-quality evidence). AUTHORS' CONCLUSIONS: Low-quality evidence shows a possible superiority of benzodiazepine over placebo in the short-term treatment of panic disorders. The validity of the included studies is questionable due to possible unmasking of allocated treatments, high dropout rates, and probable publication bias. Moreover, the included studies were only short-term studies and did not examine the long-term efficacy nor the risks of dependency and withdrawal symptoms. Due to these limitations, our results regarding the efficacy of benzodiazepines versus placebo provide only limited guidance for clinical practice. Furthermore, the clinician's choice is not between benzodiazepines and placebo, but between benzodiazepines and other agents, notably SSRIs, both in terms of efficacy and adverse effects. The choice of treatment should therefore be guided by the patient's preference and should balance benefits and harms from treatment in a long-term perspective.
Association of Cannabis Use in Adolescence and Risk of Depression, Anxiety, and Suicidality in Young Adulthood: A Systematic Review and Meta-analysis.
Importance: Cannabis is the most commonly used drug of abuse by adolescents in the world. While the impact of adolescent cannabis use on the development of psychosis has been investigated in depth, little is known about the impact of cannabis use on mood and suicidality in young adulthood. Objective: To provide a summary estimate of the extent to which cannabis use during adolescence is associated with the risk of developing subsequent major depression, anxiety, and suicidal behavior. Data Sources: Medline, Embase, CINAHL, PsycInfo, and Proquest Dissertations and Theses were searched from inception to January 2017. Study Selection: Longitudinal and prospective studies, assessing cannabis use in adolescents younger than 18 years (at least 1 assessment point) and then ascertaining development of depression in young adulthood (age 18 to 32 years) were selected, and odds ratios (OR) adjusted for the presence of baseline depression and/or anxiety and/or suicidality were extracted. Data Extraction and Synthesis: Study quality was assessed using the Research Triangle Institute item bank on risk of bias and precision of observational studies. Two reviewers conducted all review stages independently. Selected data were pooled using random-effects meta-analysis. Main Outcomes and Measures: The studies assessing cannabis use and depression at different points from adolescence to young adulthood and reporting the corresponding OR were included. In the studies selected, depression was diagnosed according to the third or fourth editions of Diagnostic and Statistical Manual of Mental Disorders or by using scales with predetermined cutoff points. Results: After screening 3142 articles, 269 articles were selected for full-text review, 35 were selected for further review, and 11 studies comprising 23 317 individuals were included in the quantitative analysis. The OR of developing depression for cannabis users in young adulthood compared with nonusers was 1.37 (95% CI, 1.16-1.62; I2 = 0%). The pooled OR for anxiety was not statistically significant: 1.18 (95% CI, 0.84-1.67; I2 = 42%). The pooled OR for suicidal ideation was 1.50 (95% CI, 1.11-2.03; I2 = 0%), and for suicidal attempt was 3.46 (95% CI, 1.53-7.84, I2 = 61.3%). Conclusions and Relevance: Although individual-level risk remains moderate to low and results from this study should be confirmed in future adequately powered prospective studies, the high prevalence of adolescents consuming cannabis generates a large number of young people who could develop depression and suicidality attributable to cannabis. This is an important public health problem and concern, which should be properly addressed by health care policy.
Psychotropic drug epidemiology and systematic reviews of randomised clinical trials: The roads travelled, the roads ahead
© 2013 by John Wiley & Sons, Ltd. All rights reserved. This chapter describes the epidemiology of psychotropic drug prescription in the mental health services. Physicians should combine their own clinical expertise and training with high-quality systematic reviews of scientific evidence in order to make optimal decisions about therapeutic interventions. It is possible to describe how drugs are prescribed and used, investigate reasons underlying prescriptions and monitor outcomes and the variables which may affect them. The study designs developed to summarise scientific evidence in the format of systematic reviews, and pharmaco-epidemiological approaches developed to study the use and the effects of drugs in large numbers of individuals, are reviewed. This chapter therefore aims to assess whether and how these two disciplines can constitute a permanent link between the experimental world of clinical trials and the real world of everyday prescribing and their possible impact on improving global mental health.
Ketamine: stimulating antidepressant treatment?
SUMMARY: The appeal of ketamine - in promptly ameliorating depressive symptoms even in those with non-response - has led to a dramatic increase in its off-label use. Initial promising results await robust corroboration and key questions remain, particularly concerning its long-term administration. It is, therefore, timely to review the opinions of mood disorder experts worldwide pertaining to ketamine's potential as an option for treating depression and provide a synthesis of perspectives - derived from evidence and clinical experience - and to consider strategies for future investigations. DECLARATION OF INTERESTS: G.S.M. Grant/research support: National Health Medical Research Council, NSW Health, Ramsay Health, American Foundation for Suicide Prevention, AstraZeneca, Eli Lilly & Co, Organon, Pfizer, Servier, and Wyeth; has been a speaker for Abbott, AstraZeneca, Eli Lilly & Co, Janssen Cilag, Lundbeck, Pfizer, Ranbaxy, Servier, and Wyeth; consultant: AstraZeneca, Eli Lilly & Co, Janssen Cilag, Lundbeck, and Servier. M.A.F. Grant support: AssureRx, Janssen Research & Development, Mayo Foundation, Myriad, National Institute of Alcohol Abuse and Alcoholism (NIAAA), National Institute of Mental Health (NIMH), Pfizer. Consultant (Mayo): Janssen Research & Development, LLC, Mitsubishi Tanabe Pharma Corporation, Myriad Genetics, Neuralstem Inc., Sunovion, Supernus Pharmaceuticals, Teva Pharmaceuticals. CME/travel support: American Physician Institute, CME Outfitters. Financial interest/Mayo Clinic 2016: AssureRx. S.H.K. Grant/research support: Brain Canada, Bristol Meyer Squibb, CIHR, Janssen, Johnson & Johnson, Lundbeck, Ontario Brain Institute, Pfizer, Servier, St. Jude Medical, Sunovion. T.A.K. Grant/research support (through Stanford University): Sunovion Pharmaceuticals and Merck & Co., Inc.; consultant/advisory board bember: Allergan, Inc., Janssen Pharmaceuticals, Myriad Genetic Laboratories, Inc., and Sunovion Pharmaceuticals; lecture honoraria (not Speaker's Bureau payments): GlaxoSmithKline, and Sunovion Pharmaceuticals; royalties from American Psychiatric Publishing, Inc. Also, AstraZeneca Pharmaceuticals LP provided publication support to Parexel for preparation of a manuscript. Spouse employee and stockholder of Janssen Pharmaceuticals. R.W.L. Honoraria for speaking/advising/consulting, and/or received research funds: AstraZeneca, Brain Canada, Bristol Myers Squibb, Canadian Institutes of Health Research, Canadian Depression Research and Intervention Network, Canadian Network for Mood and Anxiety Treatments, Canadian Psychiatric Association, Coast Capital Savings, Johnson and Johnson, Lundbeck, Lundbeck Institute, Pfizer, Servier, St. Jude Medical, Takeda University, Health Network Foundation, and Vancouver Coastal Health Research Institute. R.M. Investigator Janssen trials of esketamine; 'paid-for' ketamine clinic operated by Oxford Health NHS Foundation Trust - fees used to support the Trust. M.J.O. Consultant: Sunovion and Acadia Pharmaceuticals. Full-time employee of U.S. Department of Veterans Affairs. M.E.T. Advisory/Consultant: Alkermes, Allergan, AstraZeneca, Bristol-Myers Squibb Company, Cerecor inc., Eli Lilly & Co., Forest Laboratories, Gerson Lehrman Group, Fabre-Kramer Pharmaceuticals, Inc., GlaxoSmithKline, Guidepoint Global, H. Lundbeck A/S, MedAvante Inc., Merck and Co. Inc. (formerly Schering Plough and Organon), Moksha8, Naurex Inc., Neuronetics Inc., Novartis, Ortho-McNeil Pharmaceuticals (Johnson & Johnson; Janssen), Otsuka, Pamlab, L.L.C. (Nestle), Pfizer (formerly Wyeth Ayerst Pharmaceuticals), Shire US Inc., Sunovion Pharmaceuticals Inc., Trius Therapeutical Inc. and Takeda. Grant support: Agency for Healthcare Research and Quality, Alkermes, AssureRx, Avanir, Forest Pharmaceuticals, Janssen, National Institute of Mental Health, and Otsuka Pharmaceuticals. Speakers Bureau: None since June, 2010. Equity Holdings: MedAvante, Inc. Royalties: American Psychiatric Foundation, Guilford Publications, Herald House, W.W. Norton & Company, Inc. Spouse's employment: Peloton Advantage, which does business with Pfizer. M.T. Full-time employee at Lilly 1997 to 2008. Honoraria/consulted: Abbott, AstraZeneca, Bristol Myers Squibb, GlaxoSmithKline, Lilly, Johnson & Johnson, Allergan, Otsuka, Merck, Sunovion, Forest, Geodon Richter Plc, Roche, Elan, Alkermes, Lundbeck, Teva, Pamlab, Minerva, Wyeth and Wiley Publishing. Spouse was full time-employee at Lilly 1998-2013. COPYRIGHT AND USAGE: © The Royal College of Psychiatrists 2016. This is an open access article distributed under the terms of the Creative Commons Non-Commercial, No Derivatives (CC BY-NC-ND) licence.
Chronic Fatigue & Fibromyalgia Syndromes
With four newly authored chapters and extensive revisions made to the remaining chapters, this third edition of The American Psychiatric Publishing Textbook of Psychosomatic Medicine and Consultation-Liaison Therapy has been thoroughly ...
Prebiotic reduction of brain histone deacetylase (HDAC) activity and olanzapine-mediated weight gain in rats, are acetate independent.
The intestinal microbiome is emerging as a novel therapeutic target owing to the wide range of potential health benefits that could result by manipulating the microbiota composition through relatively simple interventions. Ingestion of the prebiotic Bimuno™ galacto-oligosaccharide (B-GOS®) is one such intervention that has been shown to attenuate olanzapine-induced weight gain and improve cognitive flexibility in rats, potentially through mechanisms involving acetate, the major short-chain fatty acid (SCFA) that is produced by B-GOS® fermentation. The present study investigated the individual influences of B-GOS® and sodium acetate intake on brain histone acetyltransferase (HAT) and histone deacetylase (HDAC) activities, cortical and hippocampal expression of HDAC1-4 and N-methyl-d-aspartate receptor subunits in saline or olanzapine injected female rats. The effect of sodium acetate on olanzapine-induced weight gain was also investigated. Daily ingestion of B-GOS® for 21 days, reduced HDAC activity and hippocampal HDAC-4, and elevated levels of cortical HDAC-1 and HDAC-3 mRNAs. Sodium acetate supplementation significantly decreased HAT, but not HDAC, activity and increased hippocampal HDAC-3 and HDAC-4 mRNAs. Olanzapine-induced weight gain and fourteen genera of intestinal bacteria, were not influenced by sodium acetate intake. Together these data suggests the effects of B-GOS® in rats cannot be replicated by acetate ingestion, and that mechanisms beyond the production of this SCFA are likely to underlie the psychotropic and metabolic actions of this prebiotic.