MD Conference Express ADA 2011 - (Page 27)

diabetes was 26% higher than in the placebo group, and in the SPARCL trial, the risk was increased 44% with atorvastatin 80 mg versus placebo [Waters DD et al. J Am Coll Cardiol 2011]. In JUPITER, the absolute risk was 7 new cases of diabetes per 10 patients who were protected from major cardiovascular (CV) events (CV death, stroke, and myocardial infarction) with rosuvastatin. In SPARCL, there was an approximate absolute risk of 9 new cases of diabetes per 10 patients who were protected from a CV event with atorvastatin [SPARCL Investigators. N Engl J Med 2006]. A recent pooled analysis of five statin trials, involving 32,752 patients without diabetes at baseline but with a high risk for CV events, showed that high-dose statins were associated with a 12% increase in the risk of diabetes compared with low-dose statins [Preiss D et al. JAMA 2011], in keeping with a dose-dependent effect. At the same time, high-dose statins led to a 16% reduction in major CV events compared with low-dose statins. Overall benefit was still clear in this high-risk group, although there was one additional case of diabetes for every three patients who were protected from a major CV event. These findings indicate that clinicians should continue to follow recommended statin prescribing, and there are no changes that are needed for the treatment of patients with established diabetes. It appears sensible to screen patients who are taking statins for diabetes, especially for those with intensive statin regimens. Perhaps most important, Dr. Preiss added, is to inform patients of the link between new-onset diabetes and statins, so that patients can weigh the benefits and risks and participate in decision-making. Antipsychotic Drugs Severe mental illness is associated with a 2- to 3-fold increase in the prevalence of diabetes; this association was recognized over a century ago in the preantipsychotic era. However, following the introduction of antipsychotic medication in the 1950s, a number of reports that link antipsychotics and diabetes mellitus and/or impaired glucose tolerance have emerged. This association came to be generally accepted by the late 1960s, and the term “phenothiazine diabetes” was coined [ThonnardNeumann E. Am J Psychiatr 1968]. There are a number of potential mechanisms for dysglycemia with antipsychotic drugs, including weight gain, insulin resistance, and β-cell failure, said Richard I.G. Holt, PhD, FRCP, University of Southampton School of Medicine, Southampton, United Kingdom. Such side effects have been reported to be more common with second-generation antipsychotics. For example, olanzapine and clozapine have been associated with greater weight gain compared with placebo and first-generation antipsychotics as well as other second-generation antipsychotics. In a meta-analysis of a series of head-to-head randomized controlled trials, olanzapine has also been associated with greater increases in serum glucose, weight gain, and dyslipidemia than other second-generation antipsychotics, with the exception of clozapine [Rummel-Kluge C. Schizophr Res 2010]. The increased risk of dysglycemia and/or diabetes calls for clinicians to screen for diabetes and to educate their patients who take antipsychotics about the need for lifestyle modifications. Screening guidelines have been published in both the United States and Europe; these guidelines recommend determining a baseline fasting or random glucose level (or HbA1C level) before antipsychotic treatment begins, with follow-up levels determined at 3 to 4 months and then annually [De Hert M et al. Eur Psychiatry 2009; ADA. Diabetes Care 2004]. The risk of diabetes must be balanced with the benefits of treatment with antipsychotic drugs, added Prof. Holt. Before deciding to stop an antipsychotic, the potential role of the antipsychotic, the duration of treatment, and other risk factors must be weighed against the risk of relapse and the benefits of treatment. If diabetes does develop, the management of schizophrenia or bipolar illness and diabetes requires a multidisciplinary approach. Preventing Drug-Induced Dysglycemia Dr. Ponte described several strategies to prevent druginduced dysglycemia (Table 3). He emphasized the need for clinicians to monitor a patient when interacting drugs can not be avoided, adding that if an interaction results in a morbid event, clinicians should reduce the dose or discontinue the offending drug(s) and manage the hyperglycemia or hypoglycemia appropriately. Table 3. Strategies to Prevent Drug-Induced Dysglycemia. • Review current prescription and nonprescription drug regimens • Evaluate concomitant medication/comorbid conditions that may interfere with the pharmacokinetics/pharmacodynamics of the drug in question • Evaluate comorbid condition(s) that may be affected by the drug choice • Obtain baseline data (such as weight, fasting blood glucose level) when initiating drugs with known effects on glucose regulation • Limit patient exposure to drugs with effects on glucose regulation (limiting the number, dose, and duration) • Continue prospective monitoring of high-risk patients • Use the appropriate tools to assist in evaluating drug-drug interaction potential (compendia available as online references, mobile applications, colleagues, etc) Peer-Reviewed Highlights from the American Diabetes Association 71st Annual Scientific Sessions 27  http://www.mdconferencexpress.com

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