MICRONIZED FENOFIBRATE - REVIEW OF ITS PHARMACODYNAMIC PROPERTIES ANDCLINICAL EFFICACY IN THE MANAGEMENT OF DYSLIPIDEMIA

Micronised fenofibrate is a new formulation of the fibric acid derivat ive fenofibrate. It is indicated for the treatment of patients with ty pe IIa, IIb, III or IV dyslipidaemia who have failed to respond to die tary control or other nonpharmacological interventions. Micronised fen ofibrate has improved absorption characteristics compared with the sta ndard preparation, allowing a lower daily dosage and once-daily admini stration. The lipid-modifying profile of micronised fenofibrate is cha racterised by a decrease in low density lipoprotein (LDL) and total ch olesterol levels, a marked reduction in elevated plasma triglyceride l evels and an increase in high density lipoprotein (HDL) cholesterol le vels. Consistent with the standard formulation, which is administered as 300mg daily in divided doses, the micronised preparation has demons trated efficacy in the treatment of type IIa, IIb and IV primary dysli pidaemias but at a lower daily dosage of 200mg once daily. Because of its significant triglyceride-lowering effect, micronised fenofibrate a ppears to be of greatest benefit in patients with hypertriglyceridaemi a (with or without hypercholesterolaemia), including patients with typ e 2 (non-insulin-dependent) diabetes mellitus and dyslipidaemia. In th e comparisons available, micronised fenofibrate 200mg once daily was o f similar efficacy to or less effective than the HMG-CoA reductase inh ibitors simvastatin 20mg daily and pravastatin 20mg daily at reducing LDL and total cholesterol levels. However, micronised fenofibrate prod uced greater improvements in triglyceride and, generally, HDL choleste rol levels than both simvastatin and pravastatin. Data on the long ter m tolerability of micronised fenofibrate are limited. However, data fr om a large short term (3-month) study have indicated that gastrointest inal disorders are the most frequent adverse events associated with th erapy. Elevations in serum transaminase and creatine phosphokinase lev els have been reported rarely with micronised fenofibrate. In conclusi on, available data suggest that the more convenient lower once-daily d osage of micronised fenofibrate remains the beneficial lipid-modifying effects of the standard formulation. Further studies are required to determine whether the lipid changes achieved with micronised fenofibra te result in a reduction in cardiovascular morbidity and mortality.