3 alpha-Androstanediol glucuronide in premature and normal pubarche. 1991

L M Riddick, and L R Garibaldi, and M E Wang, and A R Senne, and P E Klimah, and A T Clark, and L S Levine, and S E Oberfield, and S Y Pang
Department of Pediatrics, University of Illinois College of Medicine, Chicago 60612.

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.

UI MeSH Term Description Entries
D007223 Infant A child between 1 and 23 months of age. Infants
D008297 Male Males
D011629 Puberty, Precocious Development of SEXUAL MATURATION in boys and girls at a chronological age that is 2.5 standard deviations below the mean age at onset of PUBERTY in the population. This early maturation of the hypothalamic-pituitary-gonadal axis results in sexual precocity, elevated serum levels of GONADOTROPINS and GONADAL STEROID HORMONES such as ESTRADIOL and TESTOSTERONE. Familial Precocious Puberty,Idiopathic Sexual Precocity,Precocious Puberty,Precocious Puberty, Central,Precocious Puberty, Male Limited,Precocious Puberty, Male-Limited,Pubertas Praecox,Sexual Precocity,Testotoxicosis,Central Precocious Puberties,Central Precocious Puberty,Familial Precocious Puberties,Idiopathic Sexual Precocities,Male-Limited Precocious Puberties,Male-Limited Precocious Puberty,Praecox, Pubertas,Precocious Puberties,Precocious Puberties, Central,Precocious Puberties, Familial,Precocious Puberties, Male-Limited,Precocious Puberty, Familial,Precocities, Idiopathic Sexual,Precocities, Sexual,Precocity, Idiopathic Sexual,Precocity, Sexual,Puberties, Central Precocious,Puberties, Familial Precocious,Puberties, Male-Limited Precocious,Puberties, Precocious,Puberty, Central Precocious,Puberty, Familial Precocious,Puberty, Male-Limited Precocious,Sexual Precocities,Sexual Precocities, Idiopathic,Sexual Precocity, Idiopathic
D002648 Child A person 6 to 12 years of age. An individual 2 to 5 years old is CHILD, PRESCHOOL. Children
D002675 Child, Preschool A child between the ages of 2 and 5. Children, Preschool,Preschool Child,Preschool Children
D003687 Dehydroepiandrosterone A major C19 steroid produced by the ADRENAL CORTEX. It is also produced in small quantities in the TESTIS and the OVARY. Dehydroepiandrosterone (DHEA) can be converted to TESTOSTERONE; ANDROSTENEDIONE; ESTRADIOL; and ESTRONE. Most of DHEA is sulfated (DEHYDROEPIANDROSTERONE SULFATE) before secretion. Dehydroisoandrosterone,Prasterone,5-Androsten-3-beta-hydroxy-17-one,5-Androsten-3-ol-17-one,Androstenolone,DHEA,Prasterone, 3 alpha-Isomer,5 Androsten 3 beta hydroxy 17 one,5 Androsten 3 ol 17 one,Prasterone, 3 alpha Isomer
D005260 Female Females
D006801 Humans Members of the species Homo sapiens. Homo sapiens,Man (Taxonomy),Human,Man, Modern,Modern Man
D000312 Adrenal Hyperplasia, Congenital A group of inherited disorders of the ADRENAL GLANDS, caused by enzyme defects in the synthesis of cortisol (HYDROCORTISONE) and/or ALDOSTERONE leading to accumulation of precursors for ANDROGENS. Depending on the hormone imbalance, congenital adrenal hyperplasia can be classified as salt-wasting, hypertensive, virilizing, or feminizing. Defects in STEROID 21-HYDROXYLASE; STEROID 11-BETA-HYDROXYLASE; STEROID 17-ALPHA-HYDROXYLASE; 3-beta-hydroxysteroid dehydrogenase (3-HYDROXYSTEROID DEHYDROGENASES); TESTOSTERONE 5-ALPHA-REDUCTASE; or steroidogenic acute regulatory protein; among others, underlie these disorders. Congenital Adrenal Hyperplasia,Hyperplasia, Congenital Adrenal,Adrenal Hyperplasias, Congenital,Congenital Adrenal Hyperplasias,Hyperplasias, Congenital Adrenal
D000324 Adrenocorticotropic Hormone An anterior pituitary hormone that stimulates the ADRENAL CORTEX and its production of CORTICOSTEROIDS. ACTH is a 39-amino acid polypeptide of which the N-terminal 24-amino acid segment is identical in all species and contains the adrenocorticotrophic activity. Upon further tissue-specific processing, ACTH can yield ALPHA-MSH and corticotrophin-like intermediate lobe peptide (CLIP). ACTH,Adrenocorticotropin,Corticotropin,1-39 ACTH,ACTH (1-39),Adrenocorticotrophic Hormone,Corticotrophin,Corticotrophin (1-39),Corticotropin (1-39),Hormone, Adrenocorticotrophic,Hormone, Adrenocorticotropic

Related Publications

L M Riddick, and L R Garibaldi, and M E Wang, and A R Senne, and P E Klimah, and A T Clark, and L S Levine, and S E Oberfield, and S Y Pang
August 1992, The Journal of reproductive medicine,
L M Riddick, and L R Garibaldi, and M E Wang, and A R Senne, and P E Klimah, and A T Clark, and L S Levine, and S E Oberfield, and S Y Pang
February 1993, Journal of endocrinological investigation,
L M Riddick, and L R Garibaldi, and M E Wang, and A R Senne, and P E Klimah, and A T Clark, and L S Levine, and S E Oberfield, and S Y Pang
May 1997, Journal of endocrinological investigation,
L M Riddick, and L R Garibaldi, and M E Wang, and A R Senne, and P E Klimah, and A T Clark, and L S Levine, and S E Oberfield, and S Y Pang
March 1997, Journal of endocrinological investigation,
L M Riddick, and L R Garibaldi, and M E Wang, and A R Senne, and P E Klimah, and A T Clark, and L S Levine, and S E Oberfield, and S Y Pang
October 1987, The Journal of clinical endocrinology and metabolism,
L M Riddick, and L R Garibaldi, and M E Wang, and A R Senne, and P E Klimah, and A T Clark, and L S Levine, and S E Oberfield, and S Y Pang
December 1999, Nihon rinsho. Japanese journal of clinical medicine,
L M Riddick, and L R Garibaldi, and M E Wang, and A R Senne, and P E Klimah, and A T Clark, and L S Levine, and S E Oberfield, and S Y Pang
July 2010, Nihon rinsho. Japanese journal of clinical medicine,
L M Riddick, and L R Garibaldi, and M E Wang, and A R Senne, and P E Klimah, and A T Clark, and L S Levine, and S E Oberfield, and S Y Pang
August 2005, Nihon rinsho. Japanese journal of clinical medicine,
L M Riddick, and L R Garibaldi, and M E Wang, and A R Senne, and P E Klimah, and A T Clark, and L S Levine, and S E Oberfield, and S Y Pang
December 1997, Wiener klinische Wochenschrift,
L M Riddick, and L R Garibaldi, and M E Wang, and A R Senne, and P E Klimah, and A T Clark, and L S Levine, and S E Oberfield, and S Y Pang
January 1997, Hormone research,
Copied contents to your clipboard!