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Biomedical subjects

R S McIntyre

Publications and source records attributed to R S McIntyre.

6 recordsLinked to original sources
PubMed2001

Antipsychotic metabolic effects: weight gain, diabetes mellitus, and lipid abnormalities.

OBJECTIVE: To review published and nonpublished literature describing changes in weight, glucose homeostasis, and lipid milieu with antipsychotics. METHODS: A Medline search was completed using the words weight gain, diabetes mellitus, cholesterol, triglycerides, risperidone, clozapine, olanzapine, quetiapine, ziprasidone, predictors, prolactin, obesity, and conventional antipsychotics. Publications, including original articles, review articles, letters to the editor, abstracts or posters presented at professional meetings in the last 4 years, and references from published articles, were collected. Manufacturers, including Eli Lilly Canada Inc, JanssenOrtho Inc, Pfizer Canada Inc, AstraZeneca Inc, and Novartis Pharmaceuticals, were contacted to retrieve additional medical information. RESULTS: The topic of antipsychotic-induced weight gain is understudied, and there are relatively few well-controlled studies. Weight gain as a side effect has been described with both conventional and atypical antipsychotics. Moreover, some atypical antipsychotics are associated with de novo diabetes mellitus and increased serum triglyceride levels. Predictors of weight gain may be age, baseline body mass index, appetite stimulation, previous antipsychotic exposure, and antipsychotic treatment duration. CONCLUSION: Significant weight gain is reported with the existing atypical antipsychotics. The weight gain described is highly distressing to patients, may reduce treatment adherence, and may increase the relative risk for diabetes mellitus and hypertriglyceridemia. Physicians employing these agents should routinely monitor weight, fasting blood glucose, and lipid profiles.

Adult↗
PubMed2001

Lithium revisited.

OBJECTIVE: To review lithium's utility in the treatment of mood disorders. METHOD: We reviewed the safety, tolerability, teratogenicity, optimal dosing regimens, and mortality-lowering effects of lithium. Clinical relevance and scientific rigour determined which articles we selected for review. RESULTS: Lithium is the paradigmatic treatment for bipolar disorder (BD). In treating BD, optimal maintenance plasma levels may be approximately 0.75 to 0.85 mEq/L. Although nephrogenic diabetes insipidus is not uncommon, irreversible renal failure due to lithium appears to be a rare, idiosyncratic event. Lithium-induced cardiovascular teratology appears to be less common than previously thought. Optimal lithium dosing may be once daily, this agent appears to bestow a robust suicide-lowering effect, and emerging data hint at neurotrophic and neuroprotective effects. CONCLUSION: Lithium remains an effective and integral agent in the treatment of BD. Its ability to lower suicide rates in persons with BD warrants clinical attention.

Adverse Drug Reaction Reporting Systems↗
PubMed2001

Clinical guidelines for the treatment of depressive disorders. VII. Comorbidity.

BACKGROUND: The Canadian Psychiatric Association and the Canadian Network for Mood and Anxiety Treatments partnered to produce clinical guidelines for psychiatrists for the treatment of depressive disorders. METHODS: A standard guidelines development process was followed. Relevant literature was identified using a computerized Medline search supplemented by review of bibliographies. Operational criteria were used to rate the quality of scientific evidence, and the line of treatment recommendations included consensus clinical opinion. This section, on Axis I, Axis II, and Axis III comorbidity, is 1 of 7 articles that were drafted and reviewed by clinicians. Revised drafts underwent national and international expert peer review. RESULTS: Comorbid depression on Axis I is particularly prevalent in patients with anxiety disorders, substance use disorders, and eating disorders, but it also occurs in patients with schizophrenia, attention-deficit hyperactivity disorder (ADHD), and dementia. Depressive comorbidity has implications for assessment, management, and outcome. The relation between depression and personality disorders is complex. Patient with this comorbidity often require longer, more intense, and multimodal therapies. Depression is also prevalent in medical illnesses, requires careful diagnosis, and responds to standard antidepressant treatments. CONCLUSIONS: Comorbidity can influence the course and outcome of both associated conditions. Depression-specific psychotherapy and/or pharmacotherapy should be considered when comorbid depression is diagnosed.

Antidepressive Agents↗
PubMed2001

Mechanisms of antipsychotic-induced weight gain.

The estimated percentage of persons with schizophrenia who are overweight is higher than the percentage of persons in the general population who are overweight. The increased mortality rate for persons with schizophrenia is largely due to obesity-related diseases. The atypical antipsychotics offer an improved therapeutic index when compared with the conventional agents, but may impart serious adverse events such as weight gain. This brief review is intended to provide the practicing clinician with an update of disparate research paradigms under investigation in an attempt to delineate the biological mechanisms that presage weight gain. Research success in this area may invite novel prevention strategies and hint at potential mechanisms of antipsychotic drug action.

Antipsychotic Agents↗
PubMed2001

Genetic dissection of atypical antipsychotic-induced weight gain: novel preliminary data on the pharmacogenetic puzzle.

Atypical antipsychotics such as clozapine represent a significant improvement over typical antipsychotics in the treatment of schizophrenia, particularly regarding extrapyramidal symptoms. Despite their benefits, use is limited by the occurrence of adverse reactions such as sedation and weight gain. This article provides a comprehensive review and discussion of obesity-related pathways and integrates these with the known mechanisms of atypical antipsychotic action to identify candidate molecules that may be disrupted during antipsychotic treatment. Novel preliminary data are presented to genetically dissect these obesity pathways and elucidate the genetic contribution of these candidate molecules to clozapine-induced weight gain. There is considerable variability among individuals with respect to the ability of clozapine to induce weight gain. Genetic predisposition to clozapine-induced weight gain has been suggested. Therefore, genetic variation in these candidate molecules may predict patient susceptibility to clozapine-induced weight gain. This hypothesis was tested for 10 genetic polymorphisms across 9 candidate genes, including the serotonin 2C, 2A, and 1A receptor genes (HTR2C/2A/1A); the histamine H1 and H2 receptor genes (H1R/H2R); the cytochrome P450 1A2 gene (CYPIA2); the beta3 and alpha,alpha-adrenergic receptor genes (ADRB3/ADRAIA); and tumor necrosis factor alpha (TNF-alpha). Prospective weight gain data were obtained for 80 patients with schizophrenia who completed a structured clozapine trial. Trends were observed for ADRB3, ADRA1A, TNF-alpha, and HTR2C; however, replication in larger, independent samples is required. Although in its infancy, psychiatric pharmacogenetics will in the future aid clinical practice in the prediction of response and side effects, such as antipsychotic-induced weight gain, and minimize the current "trial and error" approach to prescribing.

Adult↗