Adherence to guidelines for glucose assessment in starting second-generation antipsychotics

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Meyers Primary Care Institute

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Adolescent; Antipsychotic Agents; Blood Glucose; Child; Child, Preschool; Cohort Studies; Diabetes Mellitus; Female; Humans; Hyperglycemia; Male; Practice Guidelines as Topic; Retrospective Studies


Endocrine System Diseases | Health Services Research | Pediatrics | Psychiatric and Mental Health | Psychiatry


OBJECTIVES: In 2003, the US Food and Drug Administration issued warnings about hyperglycemia and diabetes with second-generation antipsychotics (SGAs); guidelines have recommended metabolic screening since 2004. However, little is known of contemporary practices of glucose screening among youth initiating SGAs. Our objective was to evaluate baseline glucose assessment among youth in the Mini-Sentinel Distributed Database starting an SGA.

METHODS: The cohort included youth ages 2 through 18 newly initiating SGAs January 1, 2006, through December 31, 2011, across 10 sites. Baseline glucose was defined as fasting/random glucose or hemoglobin A1c (GLU) measurement occurring relative to first SGA dispensing. Differences in GLU assessment were evaluated with chi(2) tests and logistic regression.

RESULTS: The cohort included 16,304 youth; 60% boys; mean age 12.8 years. Risperidone was most commonly started (43%). Eleven percent (n = 1858) had GLU assessed between 90 days before and 3 days after first dispensing. Assessment varied across SGAs (olanzapine highest), sites (integrated health care systems higher), ages (16-18 highest), years (2007 highest), and gender (female higher; all P < .001). GLU assessment among those starting olanzapine was more likely than among those starting quetiapine (odds ratio [OR]: 1.72 [95% confidence interval (CI): 1.37-2.18]), aripiprazole (OR: 1.49 [95% CI: 1.18-1.87]), or risperidone (OR: 1.61 [95% CI: 1.28-2.03]).

CONCLUSIONS: Few children and adolescents starting SGA have baseline glucose assessed. This is concerning because those at high diabetes risk may not be identified. Further, lack of screening impedes determining the contribution of SGAs to hyperglycemia development.

DOI of Published Version



Pediatrics. 2014 Nov;134(5):e1308-14. doi: 10.1542/peds.2014-0828. Epub 2014 Oct 6. Link to article on publisher's site

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