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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.Design A prospective, observational study. Setting Fetal medicine unit and antenatal clinic of a large teaching hospital. Population 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. Outcome measure The last insulin-like growth factor-I level before delivery within the different subgroups. ResultsIn 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 = O.OOOl), but not in those with small-forgestational 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.

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