Testosterone exposure in childhood: discerning pathology from physiology.
ABSTRACT Introduction: Testosterone (T) drives normal male sexual development both in utero and at puberty. Aberrant T exposure manifests as virilization of a female fetus, contrasexual precocity in girls, and isosexual precocity in boys. Evidence of pathologic T exposure warrants a prompt evaluation. Areas covered: The authors introduce the topic of T exposure in children by reviewing its physiology in the fetus and during childhood and adolescence. Pathologic conditions leading to virilization of a female fetus as well as androgen-mediated gonadotropin-independent precocious puberty in both genders are then discussed. The authors finish by noting exogenous T exposure in children and adolescents, focusing specifically on secondary exposure to topical T preparations. Expert opinion: Contrasexual precocity in a girl or sexual precocity in a boy should prompt evaluation for causes of gonadotropin-independent pubertal changes. Initial biochemical evaluation includes a bone age, T, 17-hydroxyprogesterone, androstenedione, dehydroepiandrosterone sulfate (DHEA-S) and high sensitivity gonadotropin levels. The provider must query exposure to topical androgen-containing preparations as unintentional secondary exposure to topical T must be considered. Hyperandrogenism is temporally related to exposure of topical T and removal of exposure results in a marked decrease in serum T as well as resolution or stabilization of the signs and symptoms.
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ABSTRACT: A newborn with female pseudohermaphroditism (profound masculinization of the external genitalia and preservation of the internal female genitalia) is presented. During pregnancy progressive hirsutism was noted in the mother, and polycystic ovaries were found at cesarean section. The serum testosterone level in the cord blood was elevated markedly (1,232 ng./dl). After birth the serum testosterone levels of the mother and newborn decreased dramatically. Over-all it appears that the polycystic ovaries were the source of the excessive androgen secretion that caused maternal and fetal masculinization during the pregnancy.The Journal of Urology 12/1986; 136(5):1098-100. · 3.75 Impact Factor
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ABSTRACT: A recently described, distinct form of male sexual precocity is characterized by premature Leydig and germinal cell maturation in the absence of pituitary gonadotropin stimulation. Analysis of a nine-generation kindred with at least 28 affected males supports sex-limited autosomal dominant transmission. Three boys, with precocious sexual development at 1 to 4 years of age, had low basal plasma gonadotropin values without pubertal-type pulsatility and a minimal rise in luteinizing hormone after acute stimulation with luteinizing hormone releasing factor or its potent analog D-Trp6-Pro9-NEt-LRF, distinguishing them from boys with true precocious puberty. Two affected adults had a mature luteinizing hormone response to LRF. Testicular biopsies showed a progression of abnormalities in the seminiferous tubules from childhood to maturity; in one adult this disorder was associated with marked oligospermia and selective elevation of plasma follicle-stimulating hormone. The findings are consistent with an inherited intratesticular defect. Furthermore, the majority of cases of familial male sexual precocity seem to be examples of this disorder rather than central or true precocious puberty.Journal of Pediatrics 02/1985; 106(1):33-40. DOI:10.1016/S0022-3476(85)80460-1 · 3.74 Impact Factor
American Journal of Obstetrics and Gynecology 05/1984; 149(1):99-100. DOI:10.1097/00006254-198502000-00017 · 3.97 Impact Factor