- Aust Prescr 2004;27:101-5
- 1 August 2004
- DOI: 10.18773/austprescr.2004.082
Lipidil (Laboratoires Fournier SA)
67 mg capsules
160 mg film-coated tablets
Approved indication: dyslipidaemia
Australian Medicines Handbook section 6.6
Although HMG CoA reductase inhibitors are the drugs of choice for patients with hypercholesterolaemia, fibrates are sometimes considered if the high density lipoprotein (HDL)-cholesterol is low. Fibrates such as fenofibrate are more likely to be used for hypertriglyceridaemia as their main action is to decrease serum triglycerides.
After absorption fenofibrate is rapidly metabolised to fenofibric acid. By acting on the perioxisome proliferator activated receptor, fenofibric acid reduces total cholesterol, low density lipoprotein (LDL)-cholesterol, triglycerides, apolipoprotein B and very low density lipoprotein (VLDL). Fenofibric acid increases HDL. These effects make fenofibrate suitable, as an adjunct to diet, for the treatment of type II, III, IV and V dyslipidaemia, and the dyslipidaemia associated with type 2 diabetes. It can also be prescribed if dietary changes have not controlled hypercholesterolaemia.
Several placebo-controlled trials have confirmed the effect of fenofibrate on lipids. Some trials have compared fenofibrate with HMG CoA reductase inhibitors. In one study of 265 patients with primary hyperlipidaemia, fenofibrate was as effective as pravastatin in reducing total cholesterol and LDL-cholesterol. Fenofibrate had a greater effect than pravastatin on HDL-cholesterol (13.2% versus 5.6% increase) and triglycerides (38.7% versus 11.8% decrease).1 Another 12-week trial of 181 patients found that fenofibrate increased HDL-cholesterol more than atorvastatin (13.3% versus 5.3%).2 In patients with type 2 diabetes and mixed hyperlipoproteinaemia the increase in HDL-cholesterol was similar with fenofibrate and atorvastatin (10% versus 11%), but atorvastatin caused a greater reduction in total cholesterol (24% versus 16%).3 Although gemfibrozil is currently the first-choice fibrate for hypertriglyceridaemia, there are no published comparisons with fenofibrate.
In the clinical trials the most common complaint was abdominal pain, but laboratory tests revealed that 7.5% of patients develop liver function abnormalities. Liver function should be monitored, as cholestatic and chronic active hepatitis have occurred during treatment. As fenofibrate is metabolised in the liver and excreted in the urine, it is contraindicated in patients with hepatic or severe renal dysfunction.
Fenofibrate affects the clotting process3 and will prolong the prothrombin time. Patients taking warfarin will need to reduce their dose of anticoagulant. Although fibrates rarely cause rhabdomyolysis themselves, concomitant treatment with an HMG CoA reductase inhibitor should usually be avoided because of the increased risk of muscle damage.
Although fenofibrate has been available overseas for several years, there is not much information about its effect on cardiovascular disease. It should probably not be the first-choice fibrate until more outcome data are available.