Jebbink Jiska, Veenboer Geertruda, Boussata Souad, Keijser Remco, Kremer Andreas E, Elferink Ronald Oude, van der Post Joris, Afink Gijs, Ris-Stalpers Carrie
Women's and Children's Clinic, Academic Medical Center, University of Amsterdam, PO Box 22660, Amsterdam 1100 DD, The Netherlands; Department of Obstetrics and Gynaecology, Onze Lieve Vrouwe Gasthuis, PO Box 95500, Amsterdam 1090 HM, The Netherlands.
Reproductive Biology Laboratory, Academic Medical Center, University of Amsterdam, PO Box 22660, Amsterdam 1100 DD, The Netherlands.
Biochim Biophys Acta. 2015 Jan;1852(1):131-6. doi: 10.1016/j.bbadis.2014.11.008. Epub 2014 Nov 12.
To investigate total bile acid (TBA) levels in maternal (MB) and umbilical cord blood (UCB) in normotensive, preeclamptic (PE), and PE pregnancies complicated by hemolysis elevated liver enzymes and low platelets (HELLP) syndrome in the context of ABCG2 placental gene expression levels, a recently reported placental bile acid transporter.
TBA levels were determined in 83 paired MB and UCB samples of normotensive, PE and PE/HELLP pregnancies and in 22 paired arterial and venous UCB samples from uncomplicated term pregnancies. ABCG2 gene expression was measured in 104 human placentas by reverse transcriptase quantitative polymerase chain reaction.
Overall, TBA levels in MB are higher compared to levels in UCB (p<0.0001), but this comparison looses statistical significance for the 11 PE/HELLP cases. TBA levels in maternal blood are increased in PE/HELLP compared to PE pregnancies (p=0.016). TBA levels in arterial and venous UCB from 22 normotensive pregnancies are not statistically different. ABCG2 expression is reduced in pregnancies where preeclampsia is further complicated by HELLP syndrome. ABCG2 expression in human placenta is not correlated with TBA levels in either the maternal or fetal compartment.
Increased maternal TBA levels in PE/HELLP pregnancies indicate a relation between bile acids in the maternal circulation and HELLP syndrome. As overall TBA levels in maternal blood are increased compared to UCB, we conclude that the placenta partly protects the fetus from increased maternal TBA levels. This consistent difference in TBA levels between the maternal and fetal compartment is unrelated to the placental expression of ABCG2.
在ABCG2胎盘基因表达水平（一种最近报道的胎盘胆汁酸转运体）的背景下，研究正常血压、先兆子痫（PE）以及合并溶血、肝酶升高和血小板减少（HELLP）综合征的PE孕妇的母血（MB）和脐带血（UCB）中的总胆汁酸（TBA）水平。
测定了83对正常血压、PE和PE/HELLP孕妇的MB和UCB样本，以及22对来自无并发症足月妊娠的动脉和静脉UCB样本中的TBA水平。通过逆转录定量聚合酶链反应测定了104个人类胎盘中ABCG2基因的表达。
总体而言，MB中的TBA水平高于UCB中的水平（p<0.0001），但在11例PE/HELLP病例中，这种比较失去了统计学意义。与PE妊娠相比，PE/HELLP孕妇母血中的TBA水平升高（p=0.016）。22例正常血压妊娠的动脉和静脉UCB中的TBA水平无统计学差异。在子痫前期进一步合并HELLP综合征的妊娠中，ABCG2表达降低。人类胎盘中ABCG2的表达与母胎双方的TBA水平均无相关性。
PE/HELLP妊娠中母血TBA水平升高表明母血循环中的胆汁酸与HELLP综合征之间存在关联。由于母血中的总体TBA水平高于UCB，我们得出结论，胎盘部分保护胎儿免受母血TBA水平升高的影响。母胎双方TBA水平的这种持续差异与ABCG2的胎盘表达无关。
