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pubmed-article:1870809pubmed:abstractTextGenetic predisposition and abnormal trophoblastic function are thought to contribute to the development of preeclampsia. A multipara developed severe preeclampsia and subsequently delivered a live growth-retarded infant with trisomy 13. Biopsy of the placental bed taken immediately after delivery demonstrated inadequate trophoblastic remodeling of the maternal uterine vasculature, with an absence of normal physiologic changes in the spiral arteries. This case suggests that fetal trisomy 13 can be associated with preeclampsia in multiparous women and that abnormal trophoblastic invasion may contribute to the pathophysiology.lld:pubmed
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pubmed-article:1870809pubmed:authorpubmed-author:FeinbergR FRFlld:pubmed
pubmed-article:1870809pubmed:authorpubmed-author:CohenA WAWlld:pubmed
pubmed-article:1870809pubmed:authorpubmed-author:KlimanH JHJlld:pubmed
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pubmed-article:1870809pubmed:dateRevised2009-10-26lld:pubmed
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pubmed-article:1870809pubmed:year1991lld:pubmed
pubmed-article:1870809pubmed:articleTitlePreeclampsia, trisomy 13, and the placental bed.lld:pubmed
pubmed-article:1870809pubmed:affiliationDepartment of Obstetrics and Gynecology, University of Pennsylvania Medical Center, Philadelphia.lld:pubmed
pubmed-article:1870809pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:1870809pubmed:publicationTypeCase Reportslld:pubmed
pubmed-article:1870809pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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