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Maternal serum insulin‐like growth factor‐binding protein‐1 (IGFBP‐1) at 11–13 weeks in pre‐eclampsia
Author(s) -
Sifakis Stavros,
Akolekar Ranjit,
Kappou Dimitra,
Mantas Nikitas,
Nicolaides Kypros H.
Publication year - 2011
Publication title -
prenatal diagnosis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.956
H-Index - 97
eISSN - 1097-0223
pISSN - 0197-3851
DOI - 10.1002/pd.2682
Subject(s) - eclampsia , insulin like growth factor binding protein , placental growth factor , medicine , endocrinology , binding protein , insulin like growth factor , growth factor , pregnancy , chemistry , biology , biochemistry , receptor , vascular endothelial growth factor , vegf receptors , genetics , gene
Objective The aim of this study was to determine the maternal serum concentration of insulin‐like growth factor‐binding protein‐1 (IGFBP‐1) at 11–13 weeks' gestation in pregnancies that subsequently develop pre‐eclampsia (PE) and to examine the possible association with uterine artery pulsatility index (PI). Methods Maternal serum concentration of IGFBP‐1 and uterine artery PI were measured in 60 cases that developed PE, including 20 that required delivery before 34 weeks (early‐PE) and 120 unaffected controls. The measured IGFBP‐1 concentration and uterine artery PI were converted into a multiple of the expected median (MoM) in unaffected pregnancies and median MoM values were compared in the outcome groups. Regression analysis was used to determine the significance of association of IGFBP‐1 MoM with uterine artery PI MoM. Results In the early‐ and late‐PE groups, the median IGFBP‐1 was decreased (0.63 and 0.67 MoM, respectively) and uterine artery PI was increased (1.31 and 1.19 MoM, respectively). In the group that developed PE there were no significant associations between serum IGFBP‐1 with uterine artery PI ( p = 0.210). Conclusion In pregnancies that develop PE, the serum IGFBP‐1 is decreased from the first trimester suggesting that IGFBP‐1 may be implicated in the pathogenesis of PE in a mechanism unrelated to impaired placental perfusion. Copyright © 2011 John Wiley & Sons, Ltd.

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