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a Fetal Medicine
Research Unit, University of Bristol,
St Michael's Hospital,
Southwell Street,
Bristol BS2 8EG, UK, b Department of Surgery,
University of Bristol,
Bristol Royal Infirmary
Correspondence to: Professor P Soothill email: Peter.Soothill{at}bristol.ac.uk
Accepted 31
July 1999
AIM
To examine the
hypothesis that the maternal insulin-like growth factor system may
constrain fetal growth.
METHODS
A prospective
observational study of maternal serum insulin-like growth factor
binding protein-1 (IGFBP-1) and fetal growth was undertaken in neonates
with birthweights below the 5th centile. They had been classified
either as having fetal growth restriction (FGR) due to placental
dysfunction (increased umbilical artery Doppler pulsatility index (PI);
n = 25) or as being small for gestational age (SGA; normal umbilical
artery PI, growth velocity and amniotic fluid; n = 27). Eighty nine
controls had normal birthweights (5th-95th centile), umbilical artery
PI, growth velocity, and amniotic fluid. IGFBP-1 was measured by radioimmunoassay.
RESULTS
Among the
controls, there was no significant correlation between IGFBP-1 and
birthweight after allowing for body mass index (BMI). Maternal BMI was
high in FGR and after adjusting for this, IGFBP-1 was increased (109 ng/ml) compared with SGA babies (69 ng/ml) and controls (57 ng/ml) and
correlated with the umbilical artery PI.
CONCLUSIONS
Maternal
IGFBP-1 is probably not part of normal placental function. Its increase
in FGR could be the cause or consequence of impaired placental
perfusion, but high IGFBP-1 concentrations might further reduce the
availability of maternal IGF-I to the placenta. This could worsen
placental function and so adversely affect fetal growth.
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