Follistatin serum concentrations during full-term labour in women--significant differences between spontaneous and induced labour.
Follistatin has been isolated from human placenta and has been identified in human foetal membranes and fluids. Serum follistatin levels in women rise during pregnancy particularly near term. In this study, we examined the effect of induction and stage of labour on maternal plasma concentrations of follistatin. Women who gave birth after a normal pregnancy were retrospectively divided into three groups: those who went in labour spontaneously (n = 33), needed induction by amniotomy and IV oxytocin (n = 18) or underwent planned caesarean section (n = 10). Serum was collected at 38-40 weeks of gestation, periodically through labour with a vaginal examination and once within 36 h postpartum and assayed for oestradiol, progesterone, prolactin and C-reactive protein. Follistatin was measured using a rabbit antiserum (#204) raised against purified 35 kDa bovine follistatin. Human recombinant follistatin was used as both standard and tracer. Concentrations of follistatin at 38-40 weeks of gestation were significantly different between groups. Those who had a spontaneous labour had concentrations higher than those who were induced. Similarly, those who were induced had concentrations higher than those who underwent a caesarean. In the spontaneous group, follistatin rose during labour, peaking at 57.9 +/- 5.48 ng/ml at > 3 cm of cervical dilation, and after delivery follistatin decreased to 26.16 +/- 3.4 ng/ml at 24 h post-delivery. In induced patients follistatin continued increasing to peak following delivery at 26.9 +/- 3.0 ng/ml and decreased at > 3 h post-delivery. Follistatin concentrations in caesarean section patients at 24 h post-surgery (18.53 +/- 3.74 ng/ml) were not different from that before the surgery and were comparable with the other two groups. Follistatin is clearly implicated in the onset of labour; however, further studies with a larger cohort of women are necessary to determine the nature of its role.
Rae
K
K
School of Biological, Biomedical and Molecular Sciences, University of New England, Armidale, New South Wales 2351, Australia. kym.rae@hnehealth.nsw.gov.au
Hollebone
K
K
Chetty
V
V
Clausen
D
D
McFarlane
J
J
D000704:Analysis of Variance; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000032:analysis; D020070:Cervical Ripening / Q000097:blood; D002585:Cesarean Section; D004958:Estradiol / Q000097:blood; D005260:Female; D038681:Follistatin / Q000097:blood*; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D007745:Labor Onset / Q000097:blood*; D007747:Labor Stage, First / Q000097:blood; D007748:Labor Stage, Second / Q000097:blood; D007749:Labor Stage, Third / Q000097:blood; D007751:Labor, Induced; D016014:Linear Models; D011247:Pregnancy; D011263:Pregnancy Trimester, Third / Q000097:blood; D011374:Progesterone / Q000097:blood; D011388:Prolactin / Q000097:blood
D015415:Biomarkers; D038681:Follistatin; D011374:Progesterone; D004958:Estradiol; D011388:Prolactin; D002097:C-Reactive Protein; D006854:Hydrocortisone