The effect of rosuvastatin on oestrogen & progestin pharmacokinetics in healthy women taking an oral contraceptive

Article date: March 2004

By: Steven G. Simonson, Paul D. Martin, Mike J. Warwick, Patrick D. Mitchell, Dennis W. Schneck, in Volume 57, Issue 3, pages 279-286


To assess the effect of rosuvastatin on oestrogen and progestin pharmacokinetics in women taking a commonly prescribed combination oral contraceptive steroid (OCS); the effect on endogenous hormones and the lipid profile was also assessed.


This open‐label, nonrandomised trial consisted of 2 sequential menstrual cycles. Eighteen healthy female volunteers received OCS (Ortho Tri‐Cyclen®) on Days 1–21 and placebo OCS on Days 22–28 of Cycles A and B Rosuvastatin 40 mg was also given on Days 1–21 of Cycle B.


Co‐administration did not result in lower exposures to the exogenous oestrogen or progestin OCS components. Co‐administration increased AUC[0–24] for ethinyl oestradiol (26%; 90% CI ratio 1.19–1.34), 17‐desacetyl norgestimate (15%; 90% CI 1.10–1.20), and norgestrel (34%; 90% CI 1.25–1.43), and increased Cmax for ethinyl oestradiol (25%; 90% CI 1.17–1.33) and norgestrel (23%; 90% CI 1.14–1.33). The increases in exposure were attributed to a change in bioavailability rather than a decrease in clearance. Luteinizing and follicle‐stimulating hormone concentrations were similar between cycles. There were no changes in the urinary excretion of cortisol and 6β‐hydroxycortisol. Rosuvastatin significantly decreased low‐density lipoprotein cholesterol [‐55%], total cholesterol [‐27%], and triglycerides [‐12%], and significantly increased high‐density lipoprotein cholesterol[11%]. Co‐administration was well tolerated.


Rosuvastatin can be coadministered with OCS without decreasing OCS plasma concentrations, indicating that contraceptive efficacy should not be decreased. The results are consistent with an absence of induction of CYP3A4 by rosuvastatin. The expected substantial lipid‐regulating effect was observed in this study, and there was no evidence of an altered lipid‐regulating effect with OCS coadministration.

DOI: 10.1046/j.1365-2125.2003.02015.x

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