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唐氏综合征妊娠中胎盘雌三醇的合成。

Placental synthesis of oestriol in Down's syndrome pregnancies.

作者信息

Newby D, Aitken D A, Howatson A G, Connor J M

机构信息

Institute of Medical Genetics, Yorkhill NHS Trust, Glasgow, G3 8SJ, UK.

出版信息

Placenta. 2000 Mar-Apr;21(2-3):263-7. doi: 10.1053/plac.1999.0469.

Abstract

In the second trimester, oestriol is synthesized in the placenta and secreted into the maternal circulation. 16alpha-hydroxy dehydroepiandrosterone sulphate (16alpha-OH-DHEAS) is formed in the fetal liver by hydroxylation of dehydroepiandrosterone sulphate (DHEAS) and transported to the placenta where it undergoes desulphation by steroid sulphatase (STS) and aromatization to oestriol. Maternal serum levels of unconjugated oestriol (UE3) are lower in Down's syndrome pregnancies than in unaffected pregnancies in the second trimester. The underlying cause of this variation was investigated in placenta, fetal liver, maternal serum and amniotic fluid from Down's syndrome pregnancies by measuring the levels of UE3, DHEAS and STS in appropriate tissues and in corresponding samples from unaffected pregnancies. UE3 levels, expressed as multiples of the control median at the appropriate gestation (MOM), were lower in placental tissue (0.52 MOM), maternal serum (0.65 MOM) and amniotic fluid (0.61 MOM) than in unaffected pregnancies. There was a significant correlation between placental and maternal serum levels of UE3 in the Down's syndrome cases. The median STS activity in placental tissue from Down's syndrome pregnancies (1.14 MOM) was not significantly different from that of the control pregnancies (1. 01 MOM), suggesting that placental turnover of the fetal precursor DHEAS is not reduced. However, levels of DHEAS were reduced in maternal serum (0.69 MOM), placental tissue (0.54 MOM) and fetal liver (0.65 MOM) from Down's syndrome pregnancies. Thus, a diminished supply of the fetal precursor DHEAS may be the cause of the decreased placental production of UE3 in Down's syndrome pregnancies in the second trimester.

摘要

在妊娠中期,雌三醇在胎盘合成并分泌进入母体循环。硫酸脱氢表雄酮(DHEAS)在胎儿肝脏中经羟基化形成16α-羟基硫酸脱氢表雄酮(16α-OH-DHEAS),然后转运至胎盘,在胎盘处它被类固醇硫酸酯酶(STS)脱去硫酸根并芳香化生成雌三醇。与未受影响的妊娠中期孕妇相比,唐氏综合征孕妇母体血清中未结合雌三醇(UE3)水平较低。通过测量唐氏综合征孕妇胎盘、胎儿肝脏、母体血清和羊水以及未受影响妊娠相应样本中UE3、DHEAS和STS的水平,对这种差异的潜在原因进行了研究。以相应孕周对照中位数倍数(MOM)表示的UE3水平,在胎盘组织(0.52 MOM)、母体血清(0.65 MOM)和羊水(0.61 MOM)中低于未受影响的妊娠。在唐氏综合征病例中,胎盘和母体血清中UE3水平之间存在显著相关性。唐氏综合征妊娠胎盘组织中的STS活性中位数(1.14 MOM)与对照妊娠(1.01 MOM)无显著差异,这表明胎儿前体DHEAS的胎盘周转率未降低。然而,唐氏综合征妊娠的母体血清(0.69 MOM)、胎盘组织(0.54 MOM)和胎儿肝脏(0.65 MOM)中DHEAS水平降低。因此,胎儿前体DHEAS供应减少可能是唐氏综合征妊娠中期胎盘产生UE3减少的原因。

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