Abstract
ABSTRACT. The goal of the study was the determination of the relative roles of the placenta and the fetus in causing low serum estriol (E3) levels in women bearing fetuses with intrauterine growth retardation (IUGR). Umbilical venous levels of E3 and dehydroepiandrosterone sulfate (DHAS) were measured in 31 samples from fetuses with IUGR, 21 of whom were vaginally delivered and 10 who were delivered by cesarean section. In addition, estrone (E1) and estradiol (E2) were measured in 11 of the samples. The results were compared with 11 samples from cesarean section delivered control term infants and 54 samples from vaginally delivered control infants. The vaginally delivered IUGR group had a significantly lower mean umbilical venous DHAS level than did their control group (2128 ± 158 ng/ml SEM versus 2645 ± 130, p<0.05). Both the vaginally delivered and cesarean section delivered IUGR infants had umbilical venous E3 levels significantly lower than in their control groups (70 ± 10 ng/ml SEM versus 144 ± 10, p<0.001, and 46 ± 11 ng/ml SEM versus 136 ± 23, p<.01, respectively). Umbilical venous E1 and E2 levels were not different from the control values. E1, E2, E3, and DHAS were measured in eight maternal venous samples obtained from mothers bearing fetuses with IUGR. In comparison with 11 control mothers, only E3 was significantly different (10.7 ± 3.0 ng/ml SEM in mothers with IUGR fetuses versus 25.0 ± 4.9 in control mothers p< 0.01). The study provides evidence for reduced DHAS secretion in one group of the fetuses with IUGR, and no evidence for decreased placental conversion of DHAS to the estrogens E1 and E2. The significantly low E3 values in both umbilical and maternal samples are postulated to result not only from the reduced fetal adrenal DHAS secretion, but also underactive 16a-hydroxylase activity in fetal liver or low efficiency of 16a-OH-DHAS, relative to DHAS, as a substrate for placental conversion to an estrogen.
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Reynolds, J., Barnhart, B. & Carlson, C. Feto-Placental Steroid Metabolism in Growth Retarded Human Fetuses. Pediatr Res 20, 166–168 (1986). https://doi.org/10.1203/00006450-198602000-00015
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DOI: https://doi.org/10.1203/00006450-198602000-00015