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 (El) 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 S E M 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 2 1 0 ng/ml S E M versus 144 + 10, p < 0.001, and 46 2 1 1 ng/ml S E M versus 136 2 23, p < .01, respectively). Umbilical venous El and EZ levels were not different from the control values. El, EZ, E3, and DHAS were measured in eight maternal venous samples obtained from mothers bearing fetuses with IUGR. In comparison with 11 control mothes, only E3 was significantly different (10.7 + 3.0 ng/ml S E M in mothers with IUGR fetuses versus 25.0 + 4.9 in control mothersp < 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 DEIAS to the estrogens El and EZ. 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. (Pediatr Res 20: 166-168, 1986) Abbreviations IUGR, intrauterine growth retardation DHAS, dehydroepiandrosterone sulfate E,, estrone E2, estradiol E3, estriol Women bearing fetuses with IUGR frequently have low serum E3 levels in late gestation (1, 2). One origin of the low E3 production in these pregnancies may be reduced secretion of fetal adrenal cortex-derived neutral steroid precursors of estriol synthesis in the placenta (3). However, there is evidence that placental conversion of the neutral precursors to estrogen may be low in association with a fetus with IUGR (4). In order to investigate the relative importance of these two possible causes of low Ej production, umbilical venous, and maternal venous neutral steroid and estrogen levels were assessed in a series of pregnancies in which the fetus had IUGR. MATERIALS AND METHODSPatients. All pregnant women studied in this investigation were hospitalized in the Oregon Health Sciences University Hospital. Fetuses with IUGR were diagnosed when their birth weights were more than 2 SD below the mean for gestational age, as...

Summaryumbilical cord, and evidence of fetal distress or anoxia. Stage 111 showed all the characteristics of the first two with evidence of The venous of d e h~-chronic asphyxia, a dirty yellow or yellow-green cord, and yellowdroepiandrosterone sulfate (DHAS), and unconjugated estriol stained nails and skin (2). Mortality was as high as 50% were compared in 54 37 POstterm9 and 22 POstmature in the acutely distressed stage I1 infants. Postmature newborns newborns. Pre-and postadrenocorticotropic hormone (ACTHI have twice the perinatal mortality as term babies (14), the stimulation levels of serum cortisol and DHAS were compared in overall postterm mortality rate at to 7% (13). Postmature newthe first t' days '' life in l9 postterm and '' POstmature borns are prone to develop hypoglycemia, asphyxic organ dysinfants. Comparison was also made between vaginally and cesar-function, and pulmonary aspiration syndrome. There is some can delivered postterm and postmature newborns. There evidence that postmature babies may have neurologic abnormalwere significantly greater cord blood cortisol levels in the post-ities which persist as learning disabilities when they reach school mature (260 * 22 n d m l (*S.E.)I, than in the normal (193 f 11 age (6).The possibility that the delayed onset of labor in pregnancies vaginally delivered infants. There were no significant differences a postmature fetus might be secondary to decreased fetal in the mean blood DHAS levels in the three groups (normal9 cortisol secretion was raised by Nwosu er al. (9, 10). They found *'" * POstterm9 U23 * nd* POstmature9that cortisol levels at 8 to 36 hr of age were lower in postmature d ) . Cortisol and DHAS responses to ACTHbabies than in their controls. Amniotic fluid analysis by the same were the same in the POstterm and POstmature groups. There was group, however, failed to demonstrate significantly lower cortisol a lower venous uncOnjugated estriO1 in the postmature than in the postterm babies (7). In spite of the level in the vaginally delivered postmature group (75 * 11 ndml) lower cortisol levels, a normal cortisol rise followed adreas compared in vagina'l~ delivered postterm * l4 noco~icotropic hormone (ACTH) administration in the postma-'dm' (' = 0'0')1 and * ndd ( ' < 0' *2)1 ture group (8). They concluded that there seemed to be no primary newborns. Stressed postmature infants cesarean set-adrenal insufficiency present in these babies, but that there was tion had higher uncOnjugated estriOl levels (83 * l2 than perhaps an inadequately functioning hypo~halamic-pituitary axis their unstressed, P s t t e m Cesarean section controls 140 * 9 n d (8). ln this study, we have examined function in ml (P < 0.01)1, but levels were still below those from vaginally postmature and postterm infants by measuring cortisol and dedelivered postterm infants. These findings substantiate normal hydroepiandrosterone sulfate (DHAS) before and after ACTH function in the fetus and newborn' stimulation. In addition, we have evaluated the function of the umbilical ve...

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