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The 4-vessel Sampling Approach to Integrative Studies of Human Placental Physiology In Vivo
Published on: August 2, 2017
Alterations in maternal sFlt-1 and PlGF: Time to labor onset in term-/late-term pregnancies with and without
Birgitte Mitlid-Mork1, Sophie Bowe1, Anne Cathrine Staff1
1Division of Obstetrics and Gynaecology, Oslo University Hospital, Ullevål, Oslo, Norway; University of Oslo, Faculty of Medicine, Oslo, Norway.
Objectives:
To investigate the placenta-associated biomarkers placental growth factor (PlGF) and soluble fms-like tyrosine kinase-1 (sFlt-1) longitudinally in late third trimester extending to late-term pregnancies, and their correlation with time to labor onset in pregnancies with and without placental syndromes (ie preeclampsia and/or fetal growth restriction). Also, to compare whether time to labor onset after induction differ between these groups.
Study Design:
Pregnant women (n = 338, of which 75 had a placental syndrome) with serial blood samples from gestational week ≥37 until labor onset were included. Maternal serum PlGF and sFlt-1 concentrations were analyzed by immunoassay postpartum.
Main Outcome Measures:
Rate of alteration in sFlt-1, PlGF and the sFlt-1/PlGF ratio prior to labor onset. Secondary outcome was rates of delivery within 48 h of labor induction.
Results:
In placental syndrome pregnancies, sFlt-1 and sFlt-1/PlGF ratio increased more rapidly between the two last samples prior to labor onset compared to uncomplicated pregnancies (both p < 0.01), but there was no difference in the PlGF decrease (p = 0.513). Time to labor onset was significantly shorter in pregnancies with placental syndromes compared to those without (p = 0.001). In the induced deliveries, there was no difference in delivery within 48 h between the two groups.
Conclusions:
An increase in sFlt-1 and sFlt-1/PlGF ratio at term prior to labor onset is more rapid in pregnancies with placental syndromes. This more rapid antiangiogenic shift might indicate a pregnancy more prone to acute placental failure and more inflammatory prepared for labor onset. Effect of labor induction was not impacted by placental dysfunction.
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