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Am J Obstet Gynecol. 2011 Jun;204(6):546.e1-4. doi: 10.1016/j.ajog.2011.02.027. Epub 2011 Apr 20.

Placental expression of angiogenic factors in Trisomy 13.

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  • 1Department of Obstetrics and Gynecology/Maternal-Fetal Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.



Increased levels of soluble fms-like tyrosine kinase (sFlt-1) in Trisomy 13 pregnancies are thought to be mediated by the placenta. This study aimed to compare sFlt-1 expression in Trisomy 13 (n = 7) placentas with that in control placentas (Trisomy 21, n = 11, and euploid, n = 6).


This was a retrospective case-control study analyzing paraffin-embedded placental blocks that were stained with hematoxylin and eosin and antibodies to sFlt-1. Their staining intensity was compared using a semiquantitative technique. The Kruskal-Wallis test and Wilcox rank sum test were used for statistical analysis.


The median staining was significantly higher in Trisomy 13 compared with control specimens (P = .008) (for Trisomy 13 vs Trisomy 21, P = .003, and Trisomy 13 vs euploid, P = .004).


Our study demonstrates that Trisomy 13 placentas express more sFlt-1 than control placentas. These results strengthen the hypothesis that the increased incidence of preeclampsia in Trisomy 13 pregnancies is secondary to placental up-regulation of sFlt-1.

Copyright © 2011 Mosby, Inc. All rights reserved.

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