Placental pathology in fetal thrombophilia.
The aim of this study was to test the hypothesis that placental vascular lesions of the fetal circulation are caused by fetal thrombophilic mutations. The study included 64 newborns of women with one or more of the following pregnancy complications: preeclampsia, placental abruption, and intrauterine growth restriction. The most prevalent inherited thrombophilias--factor V Leiden, factor II (prothrombin) G20210A, and homozygosity for methyltetrahydrofolate reductase C677T--were examined in maternal blood and fetal umbilical cord blood. One pathologist reviewed all of the slides for fetal vascular lesions. Associations between fetal thrombotic vasculopathy and fetal thrombophilia were tested for using Fisher's exact test; Z scores and gestational age were compared using the Student t-test. Fetal thrombophilic mutations were diagnosed in 19 of 64 newborns, 15 of whom had coexistent maternal thrombophilia. There was no statistical difference in the prevalence of thrombotic lesions of the fetal circulation between newborns with and without thrombophilia. The combination of maternal and fetal thrombophilia was also not associated with increased fetal vascular lesions. The results indicate that fetal thrombophilia alone, even in the context of maternal underperfusion, is not associated with fetal vascular lesions of the placenta, although it may represent an underlying risk factor for lesions triggered by other process(es).
Ariel
Ilana
I
Department of Pathology, Hadassah Hebrew University Medical Center, Mount Scopus, Jerusalem, Israel.
Anteby
Eyal
E
Hamani
Yaron
Y
Redline
Raymond W
RW
D005260:Female; D006801:Humans; D010922:Placenta Diseases / Q000209:etiology* / Q000473:pathology*; D016133:Polymerase Chain Reaction; D011247:Pregnancy; D011250:Pregnancy Complications, Hematologic / Q000473:pathology*; D019851:Thrombophilia / Q000150:complications* / Q000235:genetics