- Aust Prescr 1999;22:95-8
- 1 August 1999
- DOI: 10.18773/austprescr.1999.076
Some of the views expressed in the following notes on newly approved products should be regarded as preliminary, as there may have been limited published data at the time of publication, and little experience in Australia of their safety or efficacy. However, the Editorial Executive Committee believes that comments made in good faith at an early stage may still be of value. Before new drugs are prescribed, the Committee believes it is important that more detailed information is obtained from the manufacturer's approved product information, a drug information centre or some other appropriate source.
200 and 300 microgram tablets
Approved indication: hypercholesterolaemia
Australian Medicines Handbook Section 6.6.1
Cerivastatin adds to the choice of HMG-CoA reductase inhibitors available for the treatment of hypercholesterolaemia. It reduces low-density lipoprotein(LDL) cholesterol concentrations in the plasma by reducing hepatic cholesterol production. Plasma triglycerides and apolipoprotein B may be reduced while high-density lipoprotein-cholesterol concentrations may increase.
The drug should only be prescribed to patients who are following a cholesterol-lowering diet. Other causes of hypercholesterolaemia, such as diabetes, should be excluded.
Cerivastatin is given each evening. Food does not affect the pharmacokinetics of this drug, but bioavailability is reduced to 60% by first-pass metabolism. Cerivastatin is almost completely metabolised by the liver. Although there is no unchanged drug excreted in the urine, some of the metabolites are renally excreted. A reduced dose is recommended for patients with significant renal dysfunction. Cerivastatin is contraindicated in liver disease.
The hepatic metabolism of cerivastatin includes cytochrome P450 3A4. There is a potential for interactions with other drugs involved with this enzyme system. Erythromycin will increase the concentration of cerivastatin and a similar effect may be expected with other inhibitors of this system e.g. ketoconazole.
Cerivastatin has been studied in randomised double-blind placebo-controlled trials. The drug significantly reduced concentrations of total and LDL cholesterol after one week. LDL cholesterol concentrations reduced by 20-30% compared to placebo. The effect peaked after 4 weeks and was then maintained.
A blood sample should be taken after 6 weeks of treatment to assess the response and also to check liver function. As treatment should be discontinued if liver enzyme concentrations exceed 3 times normal, liver function should also be checked before treatment, after 12 weeks, and periodically thereafter.
Approximately 3% of patients left the clinical trials because of adverse effects. The overall incidence of adverse effects is similar to placebo. Prescribers should be alerted by complaints of muscle aches as myopathy has been reported with other HMG-CoA reductase inhibitors.
Cerivastatin does lower cholesterol, but its effect on cardiovascular disease is not yet known. As data are accumulating on the long-term effects of other HMG-CoA reductase inhibitors, there seems to be little reason for prescribing cerivastatin until such outcome data are available.