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Isaacsohn JL, Bakker-Arkema RG, Fayyad R, et al. Atorvastatin, a New HMG-CoA Reductase Inhibitor, Does Not Affect Glucocorticoid Hormones in Patients With Hypercholesterolemia. J Cardiovasc Pharmacol Ther. 1997;2(4):243-249doi: 10.1177/107424849700200402.
Isaacsohn, J. L., Bakker-Arkema, R. G., Fayyad, R., Whitcomb, R., & Black, D. M. (1997). Atorvastatin, a New HMG-CoA Reductase Inhibitor, Does Not Affect Glucocorticoid Hormones in Patients With Hypercholesterolemia. Journal of cardiovascular pharmacology and therapeutics, 2(4), 243-249. https://doi.org/10.1177/107424849700200402
Isaacsohn, et al. "Atorvastatin, a New HMG-CoA Reductase Inhibitor, Does Not Affect Glucocorticoid Hormones in Patients With Hypercholesterolemia." Journal of cardiovascular pharmacology and therapeutics vol. 2,4 (1997): 243-249. doi: https://doi.org/10.1177/107424849700200402
Isaacsohn JL, Bakker-Arkema RG, Fayyad R, Whitcomb R, Black DM. Atorvastatin, a New HMG-CoA Reductase Inhibitor, Does Not Affect Glucocorticoid Hormones in Patients With Hypercholesterolemia. J Cardiovasc Pharmacol Ther. 1997 Oct;2(4):243-249. doi: 10.1177/107424849700200402. PMID: 10684465.
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J Cardiovasc Pharmacol Ther. 1997 Oct;2(4):243-249. doi: 10.1177/107424849700200402.

Atorvastatin, a New HMG-CoA Reductase Inhibitor, Does Not Affect Glucocorticoid Hormones in Patients With Hypercholesterolemia.

Journal of cardiovascular pharmacology and therapeutics

Isaacsohn, Bakker-Arkema, Fayyad, Whitcomb, Black

Affiliations

  1. Metabolic and Atherosclerosis Research Center, Cinicnnati, Ohio, USA

PMID: 10684465 DOI: 10.1177/107424849700200402

Abstract

BACKGROUND: Atorvastatin calcium (Lipitor) is a new 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitor. The present study was conducted to examine the effect of pronounced cholesterol lowering on adrenal function in patients with severe hypercholesterolemia. METHODS AND RESULTS: Adrenal function was examined under basal conditions and following adrenal corticotropin hormone stimulation in 40 patients (36 with heterogeneous familial and 4 with polygenic hypercholesterolemia). The study was part of a larger study comparing the efficacy and safety of atorvastatin, colestipol, atorvastatin + colestipol, and simvastatin + colestipol treatment over a 1-year period. Maximum doses of all agents were studied: 80 mg atorvastatin once daily, 40 mg simvastatin once daily, and 20 g/day colestipol. At the end of the 1-year treatment period, reductions in low-density lipoprotein cholesterol were 57%, 54%, and 49% for the atorvastatin, colestipol + atorvastatin, and colestipol + simvastatin groups, respectively. No clinically significant changes in basal serum cortisol levels were seen in any treatment group during the 1-year treatment period. Mean serum cortisol concentrations and area under the curve for cortisol concentration versus time data following adrenal corticotropin hormone stimulation were not clinically different during treatment compared with values obtained at baseline for any of the treatment groups. CONCLUSIONS: Treatment with maximum doses of atorvastatin for 1-year did not have any adverse effects on adrenal function under basal conditions or during maximum stimulation. Similarly, colestipol therapy alone and in combination with either atorvastatin or simvastatin did not appear to affect adrenal function.

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