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Submitted on December 7, 2004
Accepted on March 7, 2005
Departments of General Internal Medicine (DJB, JPG, CSH); Cardiovascular Medicine (MG); Endocrinology, Diabetes and Metabolism (MG, AP, SR), and Biostatistics and Epidemiology (SW), Cleveland Clinic Foundation, Cleveland, OH; Department of Cardiology (JPG), University of Pittsburgh Medical Center, Pittsburgh, PA; Haemostasis Thrombosis and Vascular Biology Unit, University Department of Medicine, City Hospital, Birmingham, UK (JVP, GYHL)
* To whom correspondence should be addressed. E-mail: dbrotma1{at}jhmi.edu.
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: 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: Randomized, double-blind, placebo-controlled study.
SETTING: Tertiary care hospital.
STUDY SUBJECTS: 25 healthy male volunteers, ages 19-39.
INTERVENTION: Subjects received either dexamethasone 3 mg twice daily vs. placebo for 5 days. Subjects also underwent a low-dose (0.5 mg) overnight dexamethasone suppression test.
MEASURES: Parameters examined before and after the 5-day intervention included: heart rate, blood pressure, weight, fasting lipid variables, homocysteine, renin, aldosterone, insulin resistance (HOMA), high-sensitivity C-reactive protein (hs-CRP), B-type natriuretic peptide (BNP), flow-mediated and nitroglycerin-mediated brachial artery dilatation, and heart rate recovery following exercise. All measurements were done in the morning hours in the fasting state.
RESULTS: Dexamethasone increased systolic blood pressure, weight, BNP, and high-density-lipoprotein-cholesterol. Dexamethasone decreased resting heart rate, hs-CRP, and aldosterone, and tended to attenuate nitroglycerin-mediated vasodilatation. There was no effect on flow-mediated vasodilatation, diastolic blood pressure, triglycerides, low-density-lipoprotein-cholesterol, non-esterified 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: Short-term glucocorticoids elicits both favorable and unfavorable effects on different cardiovascular risk factors. Manipulation of specific glucocorticoid-responsive physiological pathways deserves further study.
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