title: Avascular villi, increased syncytial knots, and hypervascular villi are associated with pregnancies complicated by factor V Leiden mutation.
abstract: There is controversy about whether pathologic abnormalities are associated with pregnancies complicated by factor V Leiden (FVL) mutation. The purpose of this study was to evaluate 105 placentas delivered to mothers heterozygous for FVL mutation to determine if there are pathologic changes suggestive of hypoxia or thrombosis, which correlate with mutation status. We examined placentas obtained as part of a prospective study of 5188 pregnancies analyzed for the presence of FVL mutation in either the mother or the infant. One hundred five placentas from mothers heterozygous for the mutation were compared with 225 controls matched for maternal age, race, and geographic site. Of the 330 pregnancies, 50 infants were FVL mutation heterozygotes. Maternal FVL heterozygote status was associated with more frequent increased numbers of syncytial knots (13% vs 4%); the difference remained significant after controlling for hypertension, preeclampsia, small-for-gestational-age infants, and delivery prior to 35 weeks of gestation (odds ratio 3.6, 95% confidence interval 1.5-8.7, P  =  0.004). Maternal FVL heterozygotes had more hypervascular villi (10% vs 3%), with significance retained controlling for delivery route (odds ratio 3.4, 95% confidence ratio 1.2-9.4, P  =  0.018). Placentas from infants heterozygous for FVL mutation had more avascular villi than controls (odds ratio 2.9, 95% confidence interval 1.5-5.6, P  =  0.001). Fetal or maternal FVL heterozygosity was not associated with infarcts, small-for-gestational-age placentas, or fetal thrombotic vasculopathy. This analysis demonstrates that pathologic findings associated with placental hypoxia, specifically focal avascular villi, increased numbers of syncytial knots, and hypervascular villi, also correlate with FVL heterozygosity in infants or mothers.
authors.affiliation: Department of Pathology, Children's Medical Center, Dallas, TX, USA. beverly.rogers@childrens.com
authors.forename: Beverly Barton
authors.initials: BB
authors.lastname: Rogers
authors.forename: Valerija
authors.initials: V
authors.lastname: Momirova
authors.forename: Donna
authors.initials: D
authors.lastname: Dizon-Townson
authors.forename: Katharine
authors.initials: K
authors.lastname: Wenstrom
authors.forename: Philip
authors.initials: P
authors.lastname: Samuels
authors.forename: Baha
authors.initials: B
authors.lastname: Sibai
authors.forename: Catherine
authors.initials: C
authors.lastname: Spong
authors.forename: Steve N
authors.initials: SN
authors.lastname: Caritis
authors.forename: Yoram
authors.initials: Y
authors.lastname: Sorokin
authors.forename: Menachem
authors.initials: M
authors.lastname: Miodovnik
authors.forename: Mary J
authors.initials: MJ
authors.lastname: O'Sullivan
authors.forename: Deborah
authors.initials: D
authors.lastname: Conway
authors.forename: Ronald J
authors.initials: RJ
authors.lastname: Wapner
mesh_terms: D005165:Factor V / Q000235:genetics*; D005260:Female; D006579:Heterozygote; D006801:Humans; D009154:Mutation; D010922:Placenta Diseases / Q000235:genetics*; D011247:Pregnancy; D019851:Thrombophilia / Q000150:complications / Q000235:genetics
chemical_list: C095381:factor V Leiden; D005165:Factor V