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 (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.
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 (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.
Authors: L Piao; C-P Chen; C-C Yeh; M Basar; R Masch; Y C Cheng; C J Lockwood; F Schatz; S J Huang Journal: Placenta Date: 2015-02-24 Impact factor: 3.481
Authors: Soyhan Bagci; Erwin Brosens; Dick Tibboel; Annelies De Klein; Hanneke Ijsselstijn; Charlotte H W Wijers; Nel Roeleveld; Ivo de Blaauw; Paul M Broens; Iris A L M van Rooij; Alice Hölscher; Thomas M Boemers; Marcus Pauly; Oliver J Münsterer; Eberhard Schmiedeke; Mattias Schäfer; Benno E Ure; Martin Lacher; Vera Choinitzki; Johannes Schumacher; Nadine Zwink; Ekkehart Jenetzky; David Katzer; Joerg Arand; Peter Bartmann; Heiko M Reutter Journal: Eur J Pediatr Date: 2016-03-16 Impact factor: 3.183
Authors: Lorelei A Mucci; Paul W Dickman; Mats Lambe; Hans-Olov Adami; Dimitrios Trichopoulos; Tomas Riman; Chung-Cheng Hsieh; Sven Cnattingius Journal: Cancer Epidemiol Biomarkers Prev Date: 2007-09 Impact factor: 4.254