Effects of short-term glucocorticoids on cardiovascular biomarkers

J Clin Endocrinol Metab. 2005 Jun;90(6):3202-8. doi: 10.1210/jc.2004-2379. Epub 2005 Mar 15.


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 C-reactive protein, 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, 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: Short-term glucocorticoids elicits both favorable and unfavorable effects on different cardiovascular risk factors. Manipulation of specific glucocorticoid-responsive physiological pathways deserves further study.

Publication types

  • Clinical Trial
  • Randomized Controlled Trial

MeSH terms

  • Adult
  • Biomarkers / blood*
  • Blood Pressure / drug effects
  • Body Weight
  • Brachial Artery / drug effects
  • Brachial Artery / physiology
  • Cardiovascular System / drug effects*
  • Dexamethasone / pharmacology*
  • Double-Blind Method
  • Glucocorticoids / pharmacology*
  • Heart Rate / drug effects
  • Humans
  • Lipids / blood
  • Lipoproteins / blood
  • Lipoproteins / drug effects
  • Male
  • Placebos


  • Biomarkers
  • Glucocorticoids
  • Lipids
  • Lipoproteins
  • Placebos
  • Dexamethasone