No abstract

Context: Glucocorticoids are known to acutely increase blood pressure, suppress inflammation, and precipitate insulin resistance. However, the short-term effects of glucocorticoids on other cardiovascular risk factors remain incompletely characterized.Objective: Our objective was to determine the effects of a short course of dexamethasone on multiple cardiovascular biomarkers and to determine whether suppression of morning cortisol in response to low-dose dexamethasone is correlated with cardiovascular risk markers in healthy volunteers. Design:We conducted a randomized, double-blind, placebo-controlled study. Setting:The study took place in a tertiary care hospital. Study subjects: Twenty-five healthy male volunteers, ages 19 -39 yr, participated in the study.Intervention: Subjects received either 3 mg dexamethasone twice daily or placebo for 5 d. Subjects also underwent a low-dose (0.5 mg) overnight dexamethasone suppression test. Measures:Parameters examined before and after the 5-d intervention included heart rate, blood pressure, weight, fasting lipid variables, homocysteine, renin, aldosterone, insulin resistance (homeostasis model assessment), high-sensitivity C-reactive protein, B-type natriuretic peptide, flow-mediated and nitroglycerin-mediated brachial artery dilatation, and heart rate recovery after exercise. All measurements were done in the morning hours in the fasting state.Results: Dexamethasone increased systolic blood pressure, weight, B-type natriuretic peptide, and high-density-lipoprotein-cholesterol. Dexamethasone decreased resting heart rate, high-sensitivity Creactive protein, and aldosterone and tended to attenuate nitroglycerin-mediated vasodilatation. There was no effect on flow-mediated vasodilatation, diastolic blood pressure, triglycerides, low-densitylipoprotein-cholesterol, nonesterified fatty acids, homocysteine, or heart rate recovery. The response of circulating cortisol to low-dose dexamethasone had no significant correlation with any of the cardiovascular risk markers. Conclusions

No abstract

Aims: Urease-producing microorganisms may lower urea nitrogen (UN) during dialysate-side dosing. We investigated the impact of 3 proven preservatives (acetic acid, ceftazidime, thimerosal) on UN concentration, and the concentrations of creatinine (CR) and β₂-microglobulin (β₂M). Methods: The UN, CR and β₂M concentrations were assayed in 3 separate aliquots from 20 spent dialysate samples (ceftazidime, 125 mg/l, or 1% thimerosal, 1 ml/l, vs. control). The β₂M concentration was assayed in 10 further spent dialysate collections (concentrated glacial acetic acid, 5 ml/l, vs. control). Solute concentrations were compared with the concordance correlation coefficient (r_c). Results: Ceftazidime and thimerosal had little effect on the concentrations of UN and CR (r_c >0.97). For the β₂M concentration, agreement remained good (r_c >0.96) for ceftazidime and thimerosal (although the former tended to lower concentrations) but acetic acid was less optimal (r_c = 0.893). Conclusions: Ceftazidime and thimerosal may be used as dialysate preservatives without affecting the UN or CR concentrations. Thimerosal is to be preferred when studying β₂M. Acetic acid produces unacceptable inaccuracy when measuring β₂M.