Objective: To determine the effects of fluvastatin, a synthetic 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor, combined with moderate alcohol consumption on lipid profiles and hepatic function in patients with primary hypercholesterolemia.
Design: Randomized, placebo-controlled, crossover study.
Setting: Lipid clinic of a university hospital.
Patients: 31 patients with primary hypercholesterolemia (low-density lipoprotein cholesterol levels ≥ 4.2 mmol/L) who had previously received a lipid-lowering diet.
Interventions: After a dietary baseline period, 26 patients were randomly assigned to receive 6 weeks of treatment with either 1) fluvastatin, 40 mg/d, added to 20 g of ethanol and diluted to 20% with orange juice or 2) fluvastatin added to orange juice alone. After a 6-week washout period, the two groups crossed over.
Main Outcome Measures: Plasma fluvastatin levels, lipid levels, and clinical variables were determined at the end of each treatment period.
Results: Six patients left the study prematurely. The remaining patients (15 men, 5 women; mean age ±SD, 49.1 ±14.5 years; mean body mass index ±SD 24.5 ±2.2 kg/m2) completed the study. Fluvastatin, alone and combined with alcohol, resulted in similar decreases in levels of total cholesterol (22% and 23%, respectively; P < 0.001 when compared with baseline), low-density lipoprotein cholesterol (28% and 29%, respectively; P < 0.001 compared with baseline), and apolipoprotein B (17% and 20%, respectively; P < 0.001 compared with baseline). High-density lipoprotein cholesterol and triglyceride levels were not changed. Fluvastatin with alcohol resulted in a significantly greater area under the plasma concentration curve (23.4 ±4.7 compared with 18.2 ±3.2 × 103 ng x min/mL) and in a greater time to maximum concentration (187.5 ±16.6 min compared with 130.9 ±7.0 min) than fluvastatin alone. Terminal half-life tended to increase. No important adverse clinical effects were observed.
Conclusion: Six weeks of daily, moderate alcohol consumption influenced the metabolism of fluvastatin but did not interfere with its lipid-lowering efficacy and had no adverse effects.