Zevas Use In Pregnancy & Lactation

Atherosclerosis is a chronic disease and does not affect long-term treatment results of primary hypercholesterolemia even if the administration of lipid-lowering drugs is stopped during pregnancy. In addition, cholesterol and other producing substance of cholesterol biosynthesis pathways are essential for fetal development, such as steroids and cell membrane synthesis.
HMG-CoA reductase inhibitors, including rosuvastatin, may reduce cholesterol synthesis and other producing substance of the cholesterol biosynthetic pathway and should not be administered to pregnant or lactating women. Because the safety of this drug for pregnant women is not established, the administration should be discontinued immediately when the pregnancy is confirmed and the patient should be informed of the potential risks to the fetus.
It is not known whether the component of this drug is excreted into human breast milk, the drug should not be used in nursing mothers unless the potential benefit justifies the potential risk to the infant.
Rosuvastatin: Rosuvastatin is contraindicated in pregnancy and lactation since the safety of this drug for pregnant women is not established.
Woman of childbearing potential should use appropriate contraceptive measures. Since cholesterol and other products of cholesterol biosynthesis are essential for the development of the foetus, the potential risk from inhibition of HMG-CoA reductase outweighs the advantage of treatment during pregnancy. Animal studies provide limited evidence of reproductive toxicity. If a patient becomes pregnant during use of this product, treatment should be discontinued immediately. Rosuvastatin is excreted in the milk of rats. There are no data with respect to excretion in milk in humans.
Ezetimibe: No clinical data are available on the use of ezetimibe during pregnancy and lactation. Ezetimibe should be used during pregnancy only if the potential benefit justifies the risk to the fetus.
In oral embryo-fetal development studies of ezetimibe conducted in rats and rabbits during organogenesis, there was no evidence of embryofetal effects at the doses tested (250, 500, 1000 mg/kg/day). In rats, increased incidences of common fetal skeletal findings (extra pair of thoracic ribs, unossified cervical vertebral centra, shortened ribs) were observed at 1000 mg/kg/day (10 x the human exposure at 10 mg daily based on AUC0-24hr for total ezetimibe). In rabbits treated with ezetimibe, an increased incidence of extra thoracic ribs was observed at 1000 mg/kg/day (150 x the human exposure at 10 mg daily based on AUC0-24hr for total ezetimibe).
Ezetimibe crossed the placenta when pregnant rats and rabbits were given multiple oral doses.
All HMG-CoA reductase inhibitors and fenofibrate are contraindicated in pregnant and lactating women. When ezetimibe is administered with a statin or fenofibrate in a woman of childbearing potential, refer to the pregnancy category and product labeling for the HMG-CoA reductase inhibitor and fenofibrate.
Multiple-dose studies of ezetimibe given in combination with statins in rats and rabbits during organogenesis result in higher ezetimibe and statin exposures. Reproductive abnormal findings occur at lower doses in combination therapy compared to monotherapy.
Studies on rats have shown that ezetimibe is excreted into breast milk. In rat studies, exposure to total ezetimibe in nursing pups was up to half of that observed in maternal plasma. It is not known whether ezetimibe is excreted into human breast milk. Therefore, ezetimibe should not be used in nursing mothers unless the potential benefit justifies the potential risk to the infant.