A prospective study of maternal serum insulin-like growth factor-I in pregnancies with appropriately grown or growth restricted fetuses.
OBJECTIVE
To determine whether there is a relationship between maternal serum insulin-like growth factor-I and fetal growth, consistent with the hypothesis that insulin-like growth factor-I influences maternal constraint upon fetal growth by controlling placental transfer.


METHODS
A prospective, observational study.


METHODS
Fetal medicine unit and antenatal clinic of a large teaching hospital.


METHODS
One hundred and forty-one pregnant women identified as having small or normally grown fetuses.


METHODS
Fetuses were scanned every two weeks with maternal venesection at each visit. Cases (birthweight < 5th centile) were assigned to two groups: fetal growth restriction due to placental dysfunction (umbilical artery Doppler, growth velocity pulsatility index > +2 SD; n = 25) and normal small-for-gestational-age (normal Doppler, growth velocity and amniotic fluid; n = 27). Eighty-nine controls had birthweights between the 5th and the 95th centiles, normal Doppler, growth velocity and amniotic fluid. Insulin-like growth factor-I was measured by radioimmunoassay, and its relationship to gestational age and birthweight was assessed by regression analysis. Comparisons between case groups were made by Student's t test or analysis of covariance to allow for the effect of birthweight.


METHODS
The last insulin-like growth factor-I level before delivery within the different subgroups.


RESULTS
In controls, maternal insulin-like growth factor-I increased with gestational age (r = 0.40; P = 0.0001) but did not correlate with birthweight. Insulin-like growth factor-I was low in the mothers of growth restricted fetuses (-1.56 SD; P = 0.0001), but not in those with small-for-gestational age fetuses.


CONCLUSIONS
The control and small-for-gestational-age data suggest that maternal insulin-like growth factor-I is not associated with endocrine control of normal placental function. Low insulin-like growth factor-I relates to poor placental transfer, as indicated by Doppler, rather than to low birthweight. Whether this is a regulatory mechanism, a cause or a consequence of placental dysfunction needs further study.
Holmes
R P
RP
Fetal Medicine Research Unit, University of Bristol, St Michael's Hospital, UK.
Holly
J M
JM
Soothill
P W
PW
D015415:Biomarkers / Q000097:blood; D001724:Birth Weight; D005314:Embryonic and Fetal Development / Q000502:physiology*; D005260:Female; D005317:Fetal Growth Retardation / Q000378:metabolism*; D005865:Gestational Age; D006801:Humans; D007231:Infant, Newborn; D007236:Infant, Small for Gestational Age; D007334:Insulin-Like Growth Factor I / Q000378:metabolism*; D011247:Pregnancy; D011446:Prospective Studies
D015415:Biomarkers; D007334:Insulin-Like Growth Factor I