Human Reproduction, Vol. 14, No. 11, 2881-2885,
November 1999
© 1999 European Society of Human Reproduction and Embryology
The role of insulin-like growth factor binding protein-1 phosphoisoforms in pregnancies with impaired placental function identified by Doppler ultrasound
1 Harris Birthright Research Centre for Fetal Medicine, Department of Obstetrics & Gynaecology, King's College Hospital, Denmark Hill, London SE5 9RS and 2 Department of Medicine, Guy's, King's College & St Thomas' Medical School, Bessemer Road, London SE5 9PJ, UK
This study was performed to investigate the hypothesis that insulin-like growth factor binding protein-1 (IGFBP-1) is involved in the pathogenesis of trophoblast invasion and impaired placentation in human pregnancy. The role of total and non-phosphorylated IGFBP-1 in women with fetal growth restriction and in high risk pregnancies identified by uterine artery Doppler ultrasound screening was examined. This was a prospective study of women booked for antenatal care having second trimester anomaly scans and Doppler screening between 22–26 weeks gestation. Women were divided into three groups and compared: normal uterine artery Doppler and normal fetal growth (control group, n = 10); abnormal Doppler and normal fetal growth [bilateral uterine artery notches (BN; n = 16); abnormal Doppler and intrauterine growth restriction (IUGR; n = 8)]. Maternal serum was collected, stored and assayed simultaneously for total and non-phosphorylated IGFBP-1. There was elevated total and non-phosphorylated IGFBP-1 (mean 44.99 ± 12.19 and 29.61 ± 10.38 µg/l respectively) in the IUGR group compared with controls (mean 17.96 ± 3.24 and 12.18 ± 1.55 µg/l, P < 0.05). This finding suggests that the various IGFBP-1 isoforms, the degree of phosphorylation and the ratios of these different forms locally may be important during trophoblast invasion and may be implicated in clinical manifestations of impaired placentation later in the second trimester.
Key words: Doppler ultrasound/insulin-like growth factor binding protein-1/intrauterine growth restriction/trophoblast invasion
3 Present address: Genetics Unit, Massachusetts General Hospital, 55 Fruit Street, Warren 801, Boston, MA 02114-2696, USA
4 To whom correspondence should be addressed
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