A US Food and Drug Administration (FDA) drug safety communication was released in March 2013, warning prescribers of the risk of QT prolongation associated with azithromycin. Overall azithromycin utilization and adherence to an inpatient QTc monitoring guideline during 8-month time periods before and after the warning were assessed to evaluate the impact of this warning on inpatient azithromycin utilization and QTc monitoring. Fifty-five patients were included in the prewarning time period and 50 were included in the postwarning period. A significant reduction in utilization in days of therapy per 1,000 patient days was observed (31.2 prewarning vs 17.5 postwarning, p < .001) in these groups. No changes in QTc monitoring among patients receiving azithromycin were identified. FDA warnings of severe, life-threatening toxicities can have a profound impact on utilization and prescribing of medications, however they may not necessarily change monitoring practices.

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Acrylamide is a monomer with established human neurotoxic actions. Public concern was lately heightened by the finding that acrylamide is formed in starch‐based foods cooked at high temperatures. However, the extent of neurotoxicity particularly in children is not understood. The primary objective of this project was to assess gene expression and translational changes induced by acrylamide in juvenile rats. Animals were administered acrylamide daily (p.o., 30 mg/kg doses, n=6) for 21 days. Neurobehavioral effects were assessed and gene expression changes were evaluated in different brain regions, spinal cord, and sciatic nerve. Quantitative RT‐PCR followed by western blot analyses were conducted. Acrylamide treatment induced significant behavioral symptoms. Gene expression changes identified differentially expressed genes that play a role in neuronal development, pain pathways, and control of motor function. Western blot analyses revealed a significant decrease (p<0.05) in expression of kappa opioid receptors (KOR) in motor cortex and cerebellar tissues, while the expression was significantly increased in the sciatic nerve (p<0.01). The current study revealed that acrylamide‐caused down regulation of KOR expression in motor cortex and cerebellum. Such an effect might be responsible for the enhanced pain sensation observed in animal studies as well as in workers who have high acrylamide exposure.