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: 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; · 2.74 Impact Factor
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ABSTRACT: Context:Aromatase deficiency due to a CYP19A1 defect leads to fetoplacental inability to convert androgens into estrogens. Pregnant mothers experience virilization caused by excess nonaromatized fetal androgens entering the maternal circulation. Biochemical normalization is believed to take place shortly after delivery.Objective:We report prolonged postnatal hyperandrogenism and enlarged multicystic ovaries in the mother of an affected 46,XX infant and hypothesize a possible pathogenetic mechanism.Patients and Methods:We investigated the mother on days 12 and 20 after delivery. FSH, LH, T, estradiol (E2), androstenedione (A), dehydroepiandrosterone-sulfate (DHEA-S), and human chorionic gonadotropin (hCG) plasma levels were obtained, and ovarian ultrasonography and magnetic resonance imaging were performed.Results:T (1040 ng/dL), A (6940 ng/dL), and E2 (2787 pg/mL) levels were markedly elevated on day 12 after delivery, whereas LH and FSH were suppressed (<0.1 IU/L). On day 20, all hormones had decreased significantly; however, T, A, and E2 still remained 3.5-, 2.2-, and 1.4-fold elevated, respectively, as compared to upper reference values. hCG (18.9 U/L) was still increased. DHEA-S was normal on both occasions. Sonography and magnetic resonance imaging revealed enlarged ovaries, with several cysts up to 4 cm. There was no history of polycystic ovary syndrome.Conclusions:We hypothesize that persistent ovarian overstimulation by hCG had occurred in the mother during pregnancy, leading to prolonged autonomous excess production of androgens during the first weeks after delivery. As a causative mechanism, we propose that gestational hyperandrogenism and hypoestrogenism reduced inhibition of placental GnRH and hCG secretion by progesterone, resulting in persistently elevated hCG.The Journal of Clinical Endocrinology and Metabolism 07/2013; · 6.31 Impact Factor
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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. · 2.49 Impact Factor