Aim Glucocorticoids play a major role in regulating the stress response, and an imbalance of glucocorticoids has been implicated in stress‐related disorders. Within mouse models, CpGs across the genome have been shown to be differentially methylated in response to glucocorticoid treatment, and using the Infinium 27K array, it was shown that humans given synthetic glucocorticoids had DNA methylation (DNAm) changes in blood. However, further investigation of the extent to which glucocorticoids affect DNAm across a larger proportion of the genome is needed. Methods Buccal samples were collected before and after synthetic glucocorticoid treatment in the context of a dental procedure. This included 30 tooth extraction surgery patients who received 10 mg of dexamethasone. Genome‐wide DNAm was assessed with the Infinium HumanMethylationEPIC array. Results Five CpGs showed genome‐wide significant DNAm changes that were >10%. These differentially methylated CpGs were in or nearest the following genes: ZNF438, KLHDC10, miR‐544 or CRABP1, DPH5, and WDFY2. Using previously published datasets of human blood gene expression changes following dexamethasone exposure, a significant proportion of genes with false‐discovery‐rate‐adjusted significant CpGs were also differentially expressed. A pathway analysis of the genes with false‐discovery‐rate‐adjusted significant CpGs revealed significant enrichment of olfactory transduction, pentose and glucuronate interconversions, ascorbate and aldarate metabolism, and steroid hormone biosynthesis pathways. Conclusion High‐dose synthetic glucocorticoid administration in the setting of a dental procedure was significantly associated with DNAm changes within buccal samples. These findings are consistent with prior findings of an influence of glucocorticoids on DNAm in humans.

doi: medRxiv preprint NOTE: This preprint reports new research that has not been certified by peer review and should not be used to guide clinical practice.

Background/Objectives: We aim to confirm the association between the high risk score on bispectral electroencephalogram (BSEEG) and mortality by comparing outcomes for those with “diffuse slowing” and normal findings on standard EEG. Design: This is a retrospective study conducted with patient chart data from March 2015 to March 2017. Setting: Single center study at a tertiary care academic hospital in the Midwest region of the USA. Participants: 1069 subjects aged 55 years and older who were on an inpatient floor or intensive care unit and received a standard 24-hour EEG. Measurements: Primary outcome was all-cause mortality at 30-, 90-, 180-, and 365- days. Secondary outcomes were time-to-discharge, and discharge to home. Results: Patients with “diffuse slowing” on standard EEG was significantly associated with 30-, 90-, 180-, and 365-day mortality (P < .001) compared to those with normal EEG findings when controlling for age, sex, and Carlson Comorbidity Index. Those with diffuse slowing also had a longer time to discharge (P < 0.001) and were less likely to discharge to home (P < 0.001) when controlling for the same factors. Findings were similar when limiting the study to only patients whose clinical status indicated “awake” at time of EEG, except for 30-day mortality. Conclusion: Our findings show that a standard EEG finding of “diffuse slowing” for inpatients 55 year or older is associated with greater mortality. This study strengthens the importance of the association found between high BSEEG score and mortality.