ECE2007 Poster Presentations (1) (659 abstracts)
1Semmelweis University, Budapest, Hungary; 2G. Richter Ltd, Budapest, Hungary.
Objevtives: Maternal hyperandrogenism occurs rarely during pregnancy as the consequense of maternal ovarian or adrenal disorders, or placental aromatase deficiency.
Case: A 33-year-old pregnant women was referred because of high serum testosterone (240 ng/dl; normal, 2060 ng/dl) measured at the 7th week of pregnancy. At presentation she had symptoms of moderate hyperandrogenism, which slightly increased until delivery. Abdominal and pelvic ultrasound exams showed no evidence for adrenal or ovarian masses. Serum hormone measurements indicated severe hyperandrogenism and marked increases of serum estradiol levels during the whole tenure of pregnancy. Serum hCG and SHBG levels were normal. The patient refused fetal karyotype exam. Fetal ultrasound indicated normal female external genitalia.
Mothers hormone levels during gestation | 13th week | 17th week | 28th week | 35th week | Postpartum 12 hours |
Testosterone ng/dl | 458 | 664 | 607 | 590 | 808 |
Estradiol pg/ml | 3139 | 11073 | 28973 | 33733 | 609 |
At 39 weeks of pregnancy she delivered a girl with normal female external genitalia. Umbilical cord hormone levels were normal, except a modest increase of testosterone (94 ng/dl). At the age of six weeks the babys androgen concentrations were normal and bone age was not accelerated. One week after delivery androgen levels of the mother decreased markedly, but they remained slightly above the upper limit of normal. Placental aromatase activity, measured by conversion of testosterone to estradiol in microsomal preparations was normal.
Conclusion: This case clearly shows that severe hyperandrogenism detected as early as 7 weeks of pregnancy and persisting until delivery presumably due to hyperreactio luteinalis does not necessarily cause virilization of a female fetus. The marked difference in maternal and umbilical blood testosterone levels, together with the largely increased maternal estradiol suggest that placental aromatase activity plays a key role in preventing fetal androgen excess.