Maternal serum androgens in pregnant women with polycystic ovarian syndrome:: possible implications in prenatal androgenization

被引:312
作者
Sir-Petermann, T
Maliqueo, M
Angel, B
Lara, HE
Pérez-Bravo, F
Recabarren, SE
机构
[1] Univ Chile, Sch Med, Hosp San Juan Dios, Dept Internal Med,Div Endocrinol, Santiago, Chile
[2] Univ Chile, Fac Chem & Pharmaceut Sci, Lab Neurobiochem, Santiago, Chile
[3] Univ Chile, INTA, Lab Energy Metab & Stable Isotopes, Santiago, Chile
[4] Univ Concepcion, Sch Vet Med, Lab Anim Physiol & Endocrinol, Chillan, Chile
关键词
androgens; fetal androgen excess; insulin; PCOS; pregnancy;
D O I
10.1093/humrep/17.10.2573
中图分类号
R71 [妇产科学];
学科分类号
100211 ;
摘要
BACKGROUND: The aim of this study was to evaluate the peripheral serum androgen concentrations in normal and polycystic ovarian syndrome (PCOS) women during pregnancy, in order to establish if PCOS may induce gestational hyperandrogenism and therefore constitute a potential source of androgen excess for the fetus. METHODS: Twenty pregnant PCOS (PPCOS) women and 26 normal pregnant (NP) women of similar age with singleton pregnancies were selected for the study. During gestational weeks 10-16 and 22-28, a 2 h, 75 g oral glucose tolerance test (OGTT) was performed. For the OGTT, glucose and insulin were measured in each sample and testosterone, androstenedione, dehydroepiandrosterone sulphate (DHEAS), estradiol, progesterone and sex hormone-binding globulin were determined in the fasting sample. RESULTS: In the first study period (gestational weeks 10-16), the levels of androstenedione, testosterone and DHEAS and the free androgen index tended to be higher in the PCOS group. These differences became significant in the second study period (gestational weeks 22-28). In this second period, 2 h insulin concentrations were also significantly higher in PPCOS than in N-P women. CONCLUSIONS: The present study demonstrates a significant increase in androgen concentrations during pregnancy in PCOS women. We propose that these androgen concentrations could provide a potential source of androgen excess for the fetus, without leading to fetal virilization.
引用
收藏
页码:2573 / 2579
页数:7
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