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Angiogenic factors in maternal circulation and preeclampsia with or without fetal growth restriction

Authors

  • LARS J. VATTEN,

    1. Department of Public Health, Norwegian University of Science and Technology, Trondheim
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  • BJØRN O. ÅSVOLD,

    1. Department of Public Health, Norwegian University of Science and Technology, Trondheim
    2. Department of Endocrinology, Trondheim University Hospital, Trondheim
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  • ANNE ESKILD

    1. Department of Obstetrics and Gynecology, Akershus University Hospital and the Faculty of Medicine, University of Oslo, Oslo
    2. Divisions of Epidemiology and Mental Health, Norwegian Institute of Public Health, Oslo, Norway
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  • Conflict of interest The authors have stated explicitly that there are no conflicts of interest in connection with this article.

  • Please cite this article as: Vatten LJ, Åsvold BO, Eskild A. Angiogenic factors in maternal circulation and preeclampsia with or without fetal growth restriction. Acta Obstet Gynecol Scand. 2012;91: DOI: 10.1111/j.1600-0412.2012.01516.x

Bjørn O. Åsvold, Department of Public Health, Norwegian University of Science and Technology, N-7491 Trondheim, Norway. E-mail: bjorn.o.asvold@ntnu.no

Abstract

Objective. To study associations of placental growth factor (PlGF) and soluble fms-like tyrosine kinase 1 (sFlt-1) in maternal circulation with the risk of preeclampsia with and without fetal growth restriction. Design. Nested case-control study. Setting. A cohort of 29 948 pregnant women in Norway. Sample. Cases were identified through linkage to the Medical Birth Registry of Norway. We selected 69 preterm and 36 term preeclampsia cases with delivery of a small-for-gestational-age (SGA) infant, 83 preterm and 154 term preeclampsia cases without SGA delivery, and 384 normotensive controls. Methods. We measured PlGF and sFlt-1 in maternal serum samples from each trimester. Main outcome measures. Odds ratios of preeclampsia subtypes by tertile categories of PlGF and sFlt-1. Results. Low (lowest third) PlGF and sFlt-1 levels in the first trimester, and low (lowest third) increase in PlGF and strong (highest third) increase in sFlt-1 from first to second trimester were associated with increased risk of preterm preeclampsia, both with and without SGA offspring. For term preeclampsia with SGA offspring, the associations were similar to the findings for preterm preeclampsia. For term preeclampsia without SGA offspring, low increase in PlGF from first to second trimester and high sFlt-1 in the third trimester were associated with increased risk. Conclusions. Low PlGF and high sFlt-1 levels in maternal circulation are associated with subsequent development of preeclampsia, regardless of whether fetal growth is affected or not. For term preeclampsia without fetal growth restriction, the imbalance in angiogenic factors seems to appear later in pregnancy than for preterm preeclampsia.

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