ISSN:
1471-0528
Source:
Blackwell Publishing Journal Backfiles 1879-2005
Topics:
Medicine
Notes:
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.Results In controls, maternal insulin-like growth factor-I increased with gestational age (p= 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.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1111/j.1471-0528.1998.tb10005.x
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