Effects of transdermal application of DHEA on the levels of steroids, gonadotropins and lipids in men.
In order to ascertain the kinetics of absorption and metabolism of transdermally administered dehydroepiandrosterone (DHEA), 10 men 29-72 years old (mean 52.4+/-14.5) received 50 mg DHEA/day in a gel applied onto the skin of the abdomen for 5 consecutive days. The objective was to establish the extent to which DHEA influences the levels of gonadotropins, sex hormone-binding globulin and lipids. It was found that DHEA is well absorbed and rapidly metabolized to its sulfate (DHEAS), androstenedione, and consequently to testosterone and estradiol. The DHEA levels that markedly increased after the first doses gradually declined already during the application, and this decline proceeded even after it was discontinued, reaching levels significantly lower than the original ones. On the other hand, the levels of DHEA metabolites (with the exception of DHEAS) rose during the application and reached values significantly higher than the basal ones within 5 weeks. This effect was accompanied by significantly decreased levels of LH. The serum levels of lipids, namely of cholesterol (both HDL and LDL cholesterol), triglycerides, apolipoproteins A-I and B and lipoprotein(a) after DHEA application were not changed significantly, and the atherogenic index (AI) remained unaltered. However, some correlations between hormones and lipids were found. Negative correlations concerned the following indices: DHEA/Lp(a); DHEAS/cholesterol; DHEA, DHEAS, testosterone/TG; testosterone/AI. On the other hand, LH, FSH/cholesterol, FSH, SHBG/LDL cholesterol, FSH/Apo B, Lp(a) correlated positively. It can be concluded that transdermal short-time application of DHEA results in a decrease of endogenous DHEA after finishing the treatment, with a parallel marked increase in the levels of sex hormones. Using this application protocol, exogenous DHEA neither altered the lipid spectrum, nor did it influence the atherogenic index.
Institute of Endocrinology, AREKO, Ltd., First Faculty of Medicine, Charles University, Prague, Czech Republic. jsulcova@endo.cz
J
J
Sulcová
M
M
Hill
R
R
Hampl
Z
Z
Masek
A
A
Novácek
R
R
Ceska
L
L
Stárka
D000279:Administration, Cutaneous; D000328:Adult; D000368:Aged; D000735:Androstenedione / Q000097:blood; D016632:Apolipoprotein A-I / Q000097:blood; D001055:Apolipoproteins B / Q000097:blood; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D003687:Dehydroepiandrosterone / Q000008:administration & dosage* / Q000097:blood / Q000493:pharmacokinetics; D019314:Dehydroepiandrosterone Sulfate / Q000097:blood; D004958:Estradiol / Q000097:blood; D005640:Follicle Stimulating Hormone / Q000097:blood; D005782:Gels; D006065:Gonadotropins, Pituitary / Q000097:blood*; D006801:Humans; D007700:Kinetics; D008055:Lipids / Q000097:blood*; D017270:Lipoprotein(a) / Q000097:blood; D007986:Luteinizing Hormone / Q000097:blood; D008297:Male; D008875:Middle Aged; D013256:Steroids / Q000097:blood*; D013739:Testosterone / Q000097:blood; D014280:Triglycerides / Q000097:blood
D016632:Apolipoprotein A-I; D001055:Apolipoproteins B; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D005782:Gels; D006065:Gonadotropins, Pituitary; D008055:Lipids; D017270:Lipoprotein(a); D013256:Steroids; D014280:Triglycerides; D013739:Testosterone; D000735:Androstenedione; D003687:Dehydroepiandrosterone; D004958:Estradiol; D019314:Dehydroepiandrosterone Sulfate; D007986:Luteinizing Hormone; D005640:Follicle Stimulating Hormone