Naltrexone exerts a favourable effect on plasma lipids in abstinent patients with alcohol dependence

Epidemiological studies suggest that abstinence periods in some patients with alcohol dependence may increase their cardiovascular risk via proatherogenic changes in plasma lipid levels. Because of this, drugs administered in withdrawal therapy should not exacerbate these effects. The aim of this study was to estimate the influence of naltrexone, carbamazepine, and lithium carbonate on plasma lipid levels in 160 alcohol-dependent males during withdrawal therapy. Plasma concentrations of total cholesterol (TC), HDL cholesterol (HDL-C), LDL cholesterol (LDL-C), and triglycerides (TGL) were determined every 2 weeks for 20 weeks. Pharmacotherapy (naltrexone 50 mg, carbamazepine 600-800 mg, lithium carbonate 500-1000 mg once per day or placebo) was given within the framework of a double-blind study between the fourth and twentieth weeks of the study. The results of 116 patients who maintained abstinence during the whole 20-week observation period were analysed. In patients treated with naltrexone significant decreases in TC (239 +/- 58 vs 216 +/- 52 mg/dl; P < 0.01) and TGL (125 +/- 68 vs 86 +/- 33 mg/dl; P < 0.02) concentrations after 16 weeks of pharmacotherapy were observed. In patients treated with carbamazepine, significant increases in TC (224 +/- 39 vs 243 +/- 54 mg/dl, P < 0.04) and HDL (40 +/- 10 vs 44 +/- 8 mg/dl, P < 0.01) after 16 weeks of pharmacotherapy were observed. After 16 weeks of pharmacotherapy, patients treated with naltrexone had lower mean TC (P < 0.03) and LDL-C (P < 0.01) concentrations than patients treated with carbamazepine, lower mean LDL-C levels than patients treated with lithium carbonate (149 +/- 54 vs 164 +/- 57 mg/dl, P < 0.01), and lower TGL concentrations than patients of the remaining pharmacotherapy groups. We conclude that naltrexone, by its hypolipaemic effect, could be useful for withdrawal therapy in alcoholic patients, because it may decrease the cardiovascular risk in abstinent patients with alcohol dependence by lipid mechanisms.