Increase in plasma high-density lipoprotein concentration following complete androgen blockage in men with prostatic carcinoma

Abstract

There is evidence that endogenous estrogens have a positive effect on plasma high density lipoprotein (HDL) concentration, whereas the relation between HDL and male sex hormones is unclear, since both positive and negative effects have been reported. This study examined the effects of LHRH agonist in combination with an antiandrogen on plasma lipids and lipoproteins in 17 elderly men with prostatic carcinoma. Subjects were examined prior to and after therapy at 4-week intervals up to 16 weeks. Prior to therapy, their lipid and lipoprotein profiles were not significantly different from a control group composed of individuals of similar age and living in the same community area. Following therapy plasma levels of testosterone and dihydrotestosterone were markedly decreased (above 90%) and their residual activity neutralized through effective use of an antiandrogen. Plasma estradiol decreased between 65% and 85% and the concentration of cortisol was unaffected. The very low density lipoprotein (VLDL) apo-B decreased and low density lipoprotein (LDL) apo-B increased; thus, no change was observed in the total plasma apo-B levels. Total plasma cholesterol increased by 6% (baseline v peak values, mg/dL, mean ± SEM; 219 ± 9 v 233 ± 9, P < 0.05) due to a significant rise in HDL cholesterol concentration (45.5 ± 2.8 v 56.5 ± 3.6, P < 0.01). Both VLDL and LDL cholesterol levels remained unchanged. The mean elevation of 21% in HDL cholesterol was accompanied by a significant rise in HDL apo-A concentration (161 ± 6 v 193 ± 10, P < 0.01), thus suggesting an increase in HDL mass and/or particle number. The opposite changes in the concentration of apo-B in the VLDL and LDL fractions, together with a corresponding increase in HDL concentration, are suggestive of stimulation in VLDL hydrolysis. The favorable effect of this antihormonal therapy on plasma lipoprotein profile is indicated by decrease in the atherogenic index ratios. Finally, the data suggests that suppression of endogenous androgens in men increases HDL concentration and hence, it may be concluded that the low levels of HDL in men (relative to women) might be the result of the metabolic actions of androgens.