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. Design A prospective, obse...
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Veröffentlicht in: | BJOG : an international journal of obstetrics and gynaecology 1998-12, Vol.105 (12), p.1273-1278 |
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Zusammenfassung: | 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. |
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ISSN: | 1470-0328 0306-5456 1471-0528 1365-215X |
DOI: | 10.1111/j.1471-0528.1998.tb10005.x |