Paternoster D, Vanin M
Department of Obstetrics and Gynecology, University of Padua, Italy.
Minerva Ginecol. 1997 Jun;49(6):293-7.
The paper describes a case of polycystic ovarian syndrome (PCOS) characterised by normal blood insulin levels and LH hypersecretion which explains the etiopathogenesis of the two voluminous ovarian masses originating from micro-cysts existing prior to pregnancy and undergoing abnormal growth during gestation owing to stimulation by beta-HCG (beta human chorionic gonadotropin). The ability of HCG ti stimulate ovarian steroidogenesis in pregnancy can result in enhanced testosterone and androstenedione levels. Our findings, like those of another recent report, emphasise the correlation between beta-HCG levels and testosterone values; the quantitative increase in beta-HCG probably plays an essential part in determining the abnormal development of the ovarian cysts, which remained morphologically unchanged up to delivery. Our patient's virilisation is explained by the increase in total testosterone in circulation. Fetal virilisation cannot be assessed in this patient because the mother gave birth to a male.
本文描述了一例多囊卵巢综合征（PCOS）病例，其特征为血液胰岛素水平正常但促黄体生成素（LH）分泌过多，这解释了两个巨大卵巢肿物的发病机制，这两个肿物起源于妊娠前就已存在的微囊肿，并在孕期因β-人绒毛膜促性腺激素（β-HCG）的刺激而异常生长。HCG在孕期刺激卵巢甾体激素生成的能力可导致睾酮和雄烯二酮水平升高。我们的研究结果与最近另一篇报告的结果一样，强调了β-HCG水平与睾酮值之间的相关性；β-HCG的定量增加可能在决定卵巢囊肿的异常发育中起关键作用，这些囊肿在分娩前形态上一直未变。我们患者的男性化表现可通过循环中总睾酮的增加来解释。由于该母亲分娩的是一名男婴，因此无法评估胎儿的男性化情况。
