Plasma C19 steroid sulphate levels and indices of androgen bioavailability in female pattern androgenic alopecia.
Female pattern androgenic alopecia (AA) is a relatively common endocrine abnormality in premenopausal women. However, unlike hirsutism, little is known about the androgen metabolism and plasma C19 steroid sulphate profiles in this disorder. We have therefore measured the plasma levels of dehydroepiandrosterone sulphate (DHEA-S), 5-androstene-3 beta,17 beta-diol sulphate (5-ADIOL-S), 5 alpha-androstane-3 alpha, 17 beta-diol sulphate (3 alpha-DIOL-S), androstenedione (AD), total testosterone (T), free testosterone (FT), sex hormone binding globulin (SHBG), non-SHBG bound T, luteinizing hormone (LH) and follicle stimulating hormone (FSH), and have calculated the free androgen index (FAI): 100 x T (nmol/l) divided by SHBG (nmol/l), in premenopausal women with AA (n = 25-45) and in normal premenopausal women (n = 17-73). While mean plasma concentrations of DHEA-S and T were not significantly different from controls, mean SHBG concentrations were significantly lower (47 +/- 3 vs 64 +/- 3 nmol/l) and the mean free androgen index (4.4 +/- 0.4 vs 2.4 +/- 0.2), and mean concentrations of free testosterone (45 +/- 5 vs 26 +/- 1.4 pmol/l), non-SHBG bound T (0.9 +/- 0.2 vs 0.6 +/- 0.1 nmol/l) and androstenedione (4.3 +/- 0.3 vs 3.4 +/- 0.2 nmol/l) were significantly elevated in women with AA. Furthermore, mean plasma concentrations of 5-ADIOL-S (512 +/- 42 nmol/l) and 3 alpha-DIOL-S (76 +/- 7 nmol/l) were significantly higher than levels found in normal women (272 +/- 12 nmol/l and 52 +/- 2 nmol/l respectively). The nature of the hyperandrogenism associated with AA may thus only be revealed by a comprehensive plasma androgen and androgen sulphate profile, which may explain apparently aberrant data for a given patient. In addition, 5-ADIOL-S and 3 alpha-DIOL-S may serve as excellent plasma markers of both the existence of the disorder and the efficacy of its treatment.
Montalto
J
J
Department of Clinical Biochemistry, Royal Children's Hospital, Parkville, Victoria, Australia.
Whorwood
C B
CB
Funder
J W
JW
Yong
A B
AB
Callan
A
A
Davies
H E
HE
Connelly
J F
JF
D000293:Adolescent; D000328:Adult; D000505:Alopecia / Q000378:metabolism*; D000728:Androgens / Q000378:metabolism*; D015113:Androstane-3,17-diol / Q000031:analogs & derivatives / Q000097:blood; D015114:Androstenediol / Q000031:analogs & derivatives / Q000097:blood; D000735:Androstenedione / Q000097:blood; D001682:Biological Availability; D003687:Dehydroepiandrosterone / Q000031:analogs & derivatives / Q000097:blood; D019314:Dehydroepiandrosterone Sulfate; D005260:Female; D005640:Follicle Stimulating Hormone / Q000097:blood; D006801:Humans; D007986:Luteinizing Hormone / Q000097:blood; D008875:Middle Aged; D011863:Radioimmunoassay / Q000379:methods; D012738:Sex Hormone-Binding Globulin / Q000032:analysis; D013739:Testosterone / Q000097:blood
D000728:Androgens; D012738:Sex Hormone-Binding Globulin; C056506:androstane-3,17-diol 17-sulfate; D015113:Androstane-3,17-diol; D013739:Testosterone; D000735:Androstenedione; D003687:Dehydroepiandrosterone; D019314:Dehydroepiandrosterone Sulfate; C033537:5-androstene-3 beta,17 beta-diol sulfate; D007986:Luteinizing Hormone; D005640:Follicle Stimulating Hormone; D015114:Androstenediol