Effects of short-term glucocorticoids on cardiovascular biomarkers.
| Autor: | Brotman DJ; Department of General Internal Medicine, Cleveland Clinic Foundation, Cleveland, Ohio 44195, USA. dbrotma1@jhmi.edu, Girod JP, Garcia MJ, Patel JV, Gupta M, Posch A, Saunders S, Lip GY, Worley S, Reddy S |
|---|---|
| Jazyk: | angličtina |
| Zdroj: | The Journal of clinical endocrinology and metabolism [J Clin Endocrinol Metab] 2005 Jun; Vol. 90 (6), pp. 3202-8. Date of Electronic Publication: 2005 Mar 15. |
| DOI: | 10.1210/jc.2004-2379 |
| Abstrakt: | 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. |
| Databáze: | MEDLINE |
| Externí odkaz: |
|