Maternal hyperandrogenism beginning from early pregnancy and progressing until delivery does not produce virilization of a female newborn
ABSTRACT A 33-year-old primagravida with a history of polycystic ovary syndrome was referred because of symptoms of moderate hyperandrogenism. Serum hormone levels, measured regularly from the 7th week of pregnancy until delivery, showed very high increases of testosterone, androstenedione and estradiol. Ultrasound showed no evidence of adrenal or ovarian masses. She delivered a female newborn with normal female external genitalia. Umbilical cord hormone levels were normal, except for a modest increase of serum testosterone. After delivery the androgen levels of the mother returned to normal and the symptoms of hyperandrogenism were also slightly improved.
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ABSTRACT: Transdermal testosterone gels are used in the treatment of hypoandrogenism of males. Virilization due to exposure to testosterone gels has been reported in children resulting in a US Food and Drug Administration (FDA) warning about secondary exposure to these products. At present, we are unaware of prenatal virilization associated with unintentional testosterone gel exposure. We report prenatal virilization in a female infant due to secondary maternal exposure to the father's testosterone gel. We also describe postnatal virilization of the child's twin sister.International Journal of Pediatric Endocrinology 10/2010; 2010:867471. DOI:10.1155/2010/867471
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ABSTRACT: To describe a possible mechanism underlying the partial virilization of a 46, XX infant by a functional maternal adrenocortical carcinoma (ACC). We performed immunocytochemical staining of tumor sections for luteinizing hormone (LH)/human chorionic gonadotropin (hCG) receptors. In addition, related reports in the literature are discussed. A previously healthy mother developed a large cortisol- and androgen-producing stage III adrenal tumor that did not interfere with conception or early morphogenesis. The tumor eluded detection until after delivery of a partially virilized 46, XX female infant with ambiguous genitalia. Immunohistochemical staining of tumor sections revealed overexpression of the LH/hCG receptor. Virilization of the genetically female fetus may have resulted from hCG-stimulated steroid secretion by the ACC. Because hypercortisolism and hyperandrogenism are associated with menstrual disturbances and spontaneous abortion, pregnancy in patients with functional adrenal tumors is uncommon. Rarely, maternal steroid excess from a functional adrenal tumor has caused 46, XX disordered sex differentiation. This unusual case demonstrates the influence of hCG on the functionality of an ACC and demonstrates the rare phenomenon of virilization of a female infant by a functional maternal adrenal tumor.Endocrine Practice 02/2011; 17(2):e26-31. DOI:10.4158/EP10209.CR · 2.59 Impact Factor
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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.Expert Opinion on Drug Safety 03/2013; DOI:10.1517/14740338.2013.782000 · 2.74 Impact Factor