Objective: To determine whether implementation of a metabolic monitoring training program (MMTP) in an urban community-based setting improved monitoring in children treated with second-generation antipsychotics (SGAs) and changed prescription rates of SGAs to children.
Method: The MMTP was implemented in the Vancouver Coastal Health Child and Youth Mental Health Teams (CYMHTs) on January 1, 2009. A retrospective review of paper charts and electronic records for children seen at the CYMHTs from September 1, 2007, to May 1, 2010, was performed to collect the following data: age, sex, foster care, immigrant status, Axis I diagnosis, and medications. In SGA-treated children, anthropometric measurements and blood work completed at baseline and 3, 6, and 12 months were also collected.
Results: Among the 1114 children seen pre-MMTP and 1262 children seen post-MMTP implementation, 174 (15.4%) and 81 (6.4%), respectively, were SGA-treated (P < 0.001). Among the SGA-treated children seen at the CYMHTs after MMTP implementation, 38.3% had a copy of the MMTP in their paper chart. Metabolic monitoring increased by up to 40% at baseline (P < 0.01), 20% at 3 (P < 0.01) and 6 months (P < 0.01), and 18% at 12 months after MMTP implementation.
Conclusions: Implementation of an MMTP was associated with significantly improved monitoring rates of anthropometric and blood work parameters at baseline and the 3- and 6-month time points, with a trend for improvement at the 12-month time point, in SGA-treated children cared for in urban community mental health clinics. In addition, a 56% decrease in SGA prescriptions was observed following MMTP implementation in this population.
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http://dx.doi.org/10.1177/070674371205700504 | DOI Listing |
Background: Abnormal glucose metabolism in AD brains correlates with cognitive deficits. The glucose changes are consistent with brain thiamine (vitamin B1) deficiency. In animals, thiamine deficiency causes multiple AD-like changes including memory loss, neuron loss, brain inflammation, enhanced phosphorylation of tau, exaggerated plaque formation and elevated advanced glycation end products (AGE).
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