Fetal Risk Summary
Cerivastatin is a synthetic inhibitor of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase. It is indicated as an adjunct to diet to reduce total cholesterol, low-density lipoprotein (LDL) cholesterol, apolipoprotein B, and triglyceride levels in patients with primary hypercholesterolemia and mixed dyslipidemia. It has the same mechanism of action as atorvastatin, fluvastatin, lovastatin, pravastatin, and simastatin. The parent drug and some of the metabolites are pharmacologically active in humans (1).
Reproduction studies have been conducted in pregnant rats and rabbits (1). At doses producing plasma levels about 6 and 3 times, respectively, the human exposure at a dose of 0.8 mg (HE), a significant increase in incomplete ossification of the lumbar center of the vertebrae was observed in rats, but no malformations were seen in rabbits.
It is not known if cerivastatin crosses the human placenta. The molecular weight (about 482) is low enough that transfer to the fetus should be expected. Cerivastatin crossed the rat placenta and was found in the fetal liver, gastrointestinal tract, and kidneys after a single maternal dose that resulted in about 17 times the HE (1).
No published cases involving the use of cerivastatin during human pregnancy have been located. The interruption of cholesterol-lowering therapy during pregnancy should have no effect on the long-term treatment of hyperlipidemia. Moreover, because cholesterol and products synthesized by cholesterol are important during fetal development, and because of the human pregnancy data reported with a similar drug (see Lovastatin), the use of cerivastatin is contraindicated during pregnancy.
Breast Feeding Summary
Cerivastatin is excreted into human breast (1). The milk:plasma ratio was 1.3 (1). Because of the potential for adverse effects in a nursing infant, women who are taking cerivastatin should not breast feed.
- Product information. Baycol. Bayer, 2001.