3 alpha-Androstanediol glucuronide in premature and normal pubarche.
To investigate the role of adrenal androgens in 3 alpha-androstanediol glucuronide (3AG) production in childhood, we compared serum 3AG and androgen levels [dehydroepiandrosterone (DHEA), DHEA sulfate (DS), androstenedione (delta 4-A), and testosterone (T)] in 32 children with premature pubarche due to idiopathic premature adrenarche (IPA; n = 26), partial 21-hydroxylase deficiency (n = 2), or 3 beta-hydroxysteroid dehydrogenase deficiency (n = 4) with those in 36 normal prepubertal (18 males and 18 females) and 22 normal pubertal Tanner II-III subjects (10 males and 12 females). Serum 3AG (2.7 +/- 2.0 nmol/L) and all androgen concentrations in children with IPA were significantly higher (P less than 0.05-0.001) than those in normal prepubertal children (3AG, 0.8 +/- 0.5 nmol/L). Serum 3AG and androgen levels, except T, in all children with premature pubarche due to 21-hydroxylase deficiency or 3 beta-hydroxysteroid dehydrogenase deficiency were higher than those in the normal prepubertal children. Serum 3AG and all androgen levels in normal Tanner II-III male (3AG, 3.8 +/- 1.7 nmol/L) or female (3AG, 1.74 +/- 0.52 nmol/L) subjects were also significantly higher (P less than 0.05-0.001) than those in prepubertal children. Serum 3AG, DHEA, DS, and delta 4-A levels in children with IPA were similar to those in normal Tanner II-III females or males, but serum T in children with IPA (0.37 +/- 0.2 nmol/L) was significantly lower (P less than 0.05-0.001) than that in normal pubertal females (0.71 +/- 0.37 nmol/L) or males (4.5 +/- 2.6 nmol/L). In the combined group (n = 88), 3AG levels correlated better with serum DS (r = 0.7), DHEA (r = 0.6), and delta 4-A (r = 0.52), than with T (r = 0.31) levels. These data suggest that the weak adrenal androgens DS, DHEA, and delta 4-A contribute substantially to 3AG production in premature and normal pubarche.
Riddick
L M
LM
Department of Pediatrics, University of Illinois College of Medicine, Chicago 60612.
Garibaldi
L R
LR
Wang
M E
ME
Senne
A R
AR
Klimah
P E
PE
Clark
A T
AT
Levine
L S
LS
Oberfield
S E
SE
Pang
S Y
SY
D015096:3-Hydroxysteroid Dehydrogenases / Q000172:deficiency; D000312:Adrenal Hyperplasia, Congenital; D000324:Adrenocorticotropic Hormone; D000728:Androgens / Q000097:blood*; D015113:Androstane-3,17-diol / Q000031:analogs & derivatives* / Q000097:blood; D000735:Androstenedione / Q000097:blood; D002648:Child; D002675:Child, Preschool; D003687:Dehydroepiandrosterone / Q000031:analogs & derivatives / Q000097:blood; D019314:Dehydroepiandrosterone Sulfate; D005260:Female; D006801:Humans; D007223:Infant; D008297:Male; D011629:Puberty, Precocious / Q000097:blood* / Q000209:etiology; D013739:Testosterone / Q000097:blood
D000728:Androgens; D015113:Androstane-3,17-diol; C028895:androstane-3,17-diol glucuronide; D013739:Testosterone; D000735:Androstenedione; D003687:Dehydroepiandrosterone; D019314:Dehydroepiandrosterone Sulfate; D000324:Adrenocorticotropic Hormone; D015096:3-Hydroxysteroid Dehydrogenases