Roswin Drug Interactions

Vitamin K antagonists: As with other HMG-CoA reductase inhibitors, the initiation of treatment or dosage up-titration of rosuvastatin in patients treated concomitantly with Vitamin K antagonists (e.g. warfarin) may result in an increase in INR. Discontinuation or down-titration of rosuvastatin may result in a decrease in INR. In such situations, appropriate monitoring of INR is desirable.
Gemfibrozil: Concomitant use of rosuvastatin and gemfibrozil resulted in a 2-fold increase in rosuvastatin C_max and AUC (see DOSAGE & ADMINISTRATION).
Gemfibrozil, fenofibrate, other fibrates and lipid lowering doses > or equal to 1 g/day of niacin (nicotinic acid) increase the risk of myopathy when given concomitantly with HMG-CoA reductase inhibitors, probably because they can produce myopathy when given alone. The 40 mg dose is contraindicated with concomitant use of fibrate. These patients should also start with the 5 mg dose.
Protease inhibitors: Consideration should be given both to the benefit of lipid lowering by the use of rosuvastatin in HIV patients receiving protease inhibitors and the potential for increased rosuvastatin plasma concentrations when initiating and up-titrating rosuvastatin doses in patients treated with protease inhibitors.
Cyclosporin: During concomitant treatment with rosuvastatin and cyclosporin, rosuvastatin plasma levels were on average 7 times higher than those observed in healthy volunteers (see CONTRAINDICATIONS).
Concomitant administration of rosuvastatin and cyclosporin did not affect plasma concentration of cyclosporin.
Antacid: The simultaneous dosing of rosuvastatin with an antacid suspension containing aluminum and magnesium hydroxide resulted in a decrease in rosuvastatin plasma concentration of approximately 50%. This effect was mitigated when the antacid was dosed 2 hours after rosuvastatin. The clinical relevance of this interactions has not been studied.
Cytochrome P450 enzymes: Rosuvastatin is neither an inhibitor nor an inducer of cytochrome P450 isoenzymes. In addition, rosuvastatin is a poor substrate for these isoenzymes.
No interactions have been observed between rosuvastatin and either fluconazole (an inhibitor of CYP2C9 and CYP3A4) or ketoconazole (an inhibitor of CYP2A6 and CYP3A4).
Concomitant administration of itraconazole (an inhibitor of CYP3A4) and rosuvastatin resulted in a 28% increase in AUC of rosuvastatin. This small increase is not considered clinically significant. Therefore, drug interactions resulting from cytochrome P450-mediated metabolism are not expected.
Erythromycin: Concomitant use of rosuvastatin and erythromycin resulted in a 20% decrease in AUC_(0-t) and a 30% decrease in C_max of rosuvastatin. This interaction may be caused by the increase in gut motility caused by erythromycin.
Oral contraceptive/hormone replacement therapy (HRT): Concomitant use of rosuvastatin and an oral contraceptive resulted in an increase in ethinyl estradiol and norgestrel AUC of 26% and 34% respectively. These increased plasma levels should be considered when selecting oral contraceptive doses.