Fetal gender effects on maternal serum prolactin levels

Circulating maternal prolactin (PRL) levels have been reported to be higher in term pregnancies yielding male infants. The mechanism for this gender difference is unknown, but we theorized that it was mediated through the fetal adrenal cortex. To test this theory we measured circulating PRL and estriol (E3) concentrations with radioimmunoassay in 37 pregnant women at 34 and 36 weeks' gestation. We then separated the groups by newborn gender. Maternal serum PRL levels were significantly higher in the women bearing male fetuses. There was no significant difference by gender in E3 concentrations, and there was no PRL surge corresponding to the E3 surge at 34-36 weeks' gestational age. There was no correlation between E3 and PRL levels. Transmission of the fetal gender effect on maternal PRL does not appear to be mediated through the fetal adrenal as measured by the fetoplacental production of E3. The effect probably is mediated by the fetal gonad.     

Estrogens in intrahepatic cholestasis of pregnancy

OBJECTIVE: To determine whether estrogen production and excretion are impaired in gravidas with intrahepatic cholestasis. METHODS: Plasma and urine samples were collected from 13 women from the United States and Chile at 35-38 weeks' gestation with mild (n = 9) or severe (n = 4) intrahepatic cholestasis of pregnancy. Urinary and plasma steroid levels from women with cholestasis were compared with levels from 27 normal pregnant women within the same gestational age range. Urinary concentrations of dehydroepiandrosterone (DHEA), estrone (E1), estradiol (E2), estriol (E3), estetrol, progesterone, and 16-hydroxy-pregnenolone were measured by gas chromatography mass spectrometry, and plasma concentrations of DHEA sulfate, progesterone, unconjugated E1, unconjugated E2, unconjugated E3, sulfated E3 derivatives, glucuronidated E3 derivatives, and total E3 were measured by radioimmunoassay. RESULTS: Compared with normal pregnant women, women with cholestasis had significantly lower plasma levels of estrogens and DHEA sulfate, the precursor to placental estrogen production synthesized by the fetal adrenal gland (Hotelling-Lawley trace = 0.81; F4,19 = 3.9; P = .02). The mean plasma DHEA sulfate, unconjugated E2, unconjugated E3, and total E3 concentrations were 0.271, 10.21, 9.80, and 99.53 ng/mL, respectively, in women with cholestasis compared with 0.802, 18.98, 16.28, and 145.07 ng/mL for controls. CONCLUSION: Fetal adrenal production of DHEA sulfate, and in response, downstream placental production of estrogens, was compromised by intrahepatic cholestasis of pregnancy.     

Hormones and cervical ripening: dehydroepiandrosterone sulfate, estradiol, estriol, and progesterone

Fetal adrenal steroids have been shown to be important in the timing of parturition. Since dehydroepiandrosterone sulfate is converted to estrogen, which is important in cervical softening, levels of dehydroepiandrosterone sulfate together with those of estradiol, estriol, and progesterone were measured and compared in pregnant women undergoing induction of labor with ripe and unripe uterine cervices. While there were no differences between the levels of estradiol, estriol and progesterone in the two groups of women, dehydroepiandrosterone sulfate was significantly elevated in the group of women with ripe cervices. These findings suggest that cervical changes preceding the onset of labor are associated with a significant elevation of maternal dehydroepiandrosterone sulfate levels. Changes in maternal plasma estradiol, estriol, and progesterone levels do not appear to be clinically related to cervical ripeness.     

Randomized investigation of magnesium sulfate for prevention of preterm birth

One hundred fifty-six women with preterm labor between 24 and 34 weeks' gestation were randomized to receive either intravenous magnesium sulfate or no tocolytic therapy. Magnesuim sulfate infusions of up to 3 gm/hr were used in 76 pregnancies and resulted in a mean serum magnesium concentration of 5.5 +/- 1.4 mEq/L (mean +/- SEM). Compared with 80 control pregnancies, magnesium sulfate tocolysis had no significant effect on duration of gestation, birth weight, neonatal morbidity, and perinatal mortality. We conclude that clinically safe infusions of magnesium sulfate are ineffective when used to prevent preterm birth.     

Intrauterine infection and preterm delivery: evidence for activation of the fetal hypothalamic-pituitary-adrenal axis

OBJECTIVE: We studied pregnant women in preterm labor with and without intrauterine infection to determine whether fetal hypothalamic-pituitary-adrenal axis activation occurs in the setting of infection-induced preterm parturition.Study Design: Amniotic fluid collected by amniocentesis and maternal blood from patients in preterm labor with intact membranes at 24 to 34 weeks' gestation were analyzed by radioimmunoassay for the steroid hormones estrone, estradiol, progesterone, androstenedione, dehydroepiandrosterone, dehydroepiandrosterone sulfate, and cortisol. Amniotic fluid was also obtained for microbial culture and for interleukin 6 measurements by enzyme immunoassay. RESULTS: Patients with intrauterine infection (n = 11) had significantly higher amniotic fluid concentrations of dehydroepiandrosterone (539 +/- 79 pg/mL) and of cortisol (5.28 +/- 1.0 microg/dL) than did patients with preterm labor and preterm delivery without infection (n = 11; 273 +/- 82 pg/mL and 1.61 +/- 1.05 microg/dL, respectively) or patients with preterm labor and subsequent term delivery (n = 11; 202 +/- 79 pg/mL and 1.82 +/- 1.0 microg/dL, respectively). Furthermore those patients who were delivered within 7 days after enrollment (who were also more likely to have intrauterine infection) had higher amniotic fluid concentrations than did those who were not delivered within 7 days of both estrone (586 +/- 101 pg/mL vs 314 +/- 98 pg/mL) and estradiol (238 +/- 44 pg/mL vs 91 +/- 43 pg/mL). CONCLUSION: Intrauterine infection was associated with increased fetal adrenal androgen and cortisol biosynthesis, and delivery within 7 days after the onset of preterm labor was associated with increased placental estrogen synthesis. These data are consistent with fetal hypothalamic-pituitary-adrenal axis activation in the setting of infection-associated preterm delivery.     

Fetoplacental steroid metabolism in prolonged pregnancies

The response to an intravenous load of 50 mg of dehydroepiandrosterone sulfate given to women with a pregnancy prolonged to more than 42 weeks was compared to the response in control pregnant women at 40 weeks. The half-life of dehydroepiandrosterone sulfate was longer in the prolonged pregnancy group than in the control group (mean +/- SEM, 3.64 +/- 0.24 hour versus 2.78 +/- 1.08 hour, p less than 0.05), and the rises of serum free estrone and free estradiol 4 hours after infusion were less in the prolonged pregnancy group than in the control group. Maternal venous and umbilical venous estrone, estradiol, free estriol, and dehydroepiandrosterone sulfate levels were compared in samples from control, postmature, and postterm groups. Umbilical estriol concentrations were significantly less in the postmature group (67.8 +/- 9.5 ng/ml, mean +/- SEM) than in the control group (136 +/- 22.8 ng/ml, mean +/- SEM, p less than 0.01), but there were no significant differences between dehydroepiandrosterone sulfate, estrone, and estradiol levels. Maternal venous estriol levels were lower in the postmature group (13.3 +/- 2.1, p less than 0.05) than in the control group (25.0 +/- 4.9). A reduction in overall placental estrogen production was indicated by the results of the dehydroepiandrosterone sulfate loads in the patients with prolonged pregnancy, yet the normal umbilical venous estrone and estradiol levels do not fit this conclusion. There is no explanation for the discrepancy at this time.     

Reduced estriol and dehydroepiandrosterone sulphate plasma levels in methadone-addicted pregnant women

The plasma levels of human chorionic somatomammotropin (hCS), estriol (E3), dehydroepiandrosterone sulphate (DHA-S), cortisol and the circadian changes of the two last adrenal hormones were studied in 25 pregnant methadone-addicted women (MA) and 21 pregnant drug-naive controls (C) at different periods of gestation and in 13 non-pregnant women (7 MA and 6 drug-naive). MA pregnant women showed normal plasma levels of hCS both at the second (6.9 +/- 0.1 vs. 7.2 +/- 0.1 micrograms/ml) and third (9.6 +/- 0.2 vs. 9.3 +/- 0.2) trimester, while plasma concentrations of E3 at term were lower than normal (MA: 4.4 +/- 0.8; C: 8.2 +/- 1.0 ng/ml, P less than 0.05). DHA-S plasma levels of MA pregnant women were half the normal values in three trimesters of gestation, while there were no differences in non-pregnant subjects. Circadian variations of cortisol and DHA-S plasma levels were present in both MA and C. The blunted DHA-S but normal cortisol plasma levels found in MA pregnant women indicate that opiate abuse interferes with adrenal function, mainly of the fetus. Due to the scarce availability of adrenal precursors, these data suggest that E3 measurements should not be considered as a useful index of fetal well-being in the presence of opiate addiction.     

Studies on the interrelation of fetal heart rate change, placental findings and fetal outcome

The relation between antepartum fetal heart rate (FHR) non stress test (NST), maternal serum estriol, intrapartum FHR change, birth weight, placental findings and Apgar score were studied in 168 normal gestations and 36 high-risk pregnancies including 25 EPH-gestosis cases. The frequency of placental infarcts was higher in severe gestosis than in other high-risk pregnancies and normal gestation. Abnormal NST was more frequent in high-risk pregnancy than normal. Light for date (LFD) infants were more numerous in high-risk pregnancy than normal, and also frequent in the cases of placental infarcts. Particularly in high-risk pregnancy patients with abnormal NST and placental infarcts, 3 out of 5 showed LFD infants. Intrapartum fetal distress was more common in the cases of abnormal NST than normal. The five minute Apgar score was lower in the patients with abnormal NST and in the cases of placental infarcts than normal. The placental infarct ratio was higher in high-risk pregnancies with abnormal NST than normal. The maternal serum estriol level was not changed in cases of high-risk pregnancy, abnormal NST or placental infarcts when compared to normal gestation. The cases of succeeding fetal death, however, showed a low serum estriol level. In conclusion, antepartum abnormal NST suggests severe placental dysfunction caused by its infarcts and the prognosis is poor in patients with high-risk pregnancies, particularly EPH-gestosis. Coping with abnormal antepartum NST is regarded as important in fetal management.     

Fetal and maternal endocrine responses to experimental intrauterine infection in rhesus monkeys

OBJECTIVE: Our purpose was to describe the temporal and quantitative relationships among intrauterine infection, fetal-placental steroid biosynthesis, and preterm labor in a nonhuman primate model. STUDY DESIGN: On approximately day 130 of gestation (term 167 days) chronically instrumented rhesus monkeys (Macaca mulatta) were infected with 10⁶ colony-forming units of group B streptococci either by intraamniotic (n = 4) or choriodecidual (n = 2) inoculation. As controls, four additional chronically instrumented noninfected monkeys were followed up to spontaneous parturition. Amniotic fluid and maternal and fetal arterial blood were serially sampled in all monkeys (both before and after infection) for progesterone, estrone, estradiol, dehydroepiandrosterone, dehydroepiandrosterone sulfate, androstenedione, and cortisol by specific radioimmunoassays, and uterine activity was continuously recorded. RESULTS: Spontaneous parturition was preceded by gradual and significant increases in the plasma concentrations of fetal dehydroepiandrosterone, dehydroepiandrosterone sulfate, and androstenedione and fetal and maternal levels of estrone, estradiol, and progesterone but not by changes in cortisol. In contrast, infection-associated parturition (either intraamniotic or choriodecidual) was characterized by abrupt increases in fetal dehydroepiandrosterone, dehydroepiandrosterone sulfate, androstenedione, progesterone, and cortisol but not by increases in maternal or fetal estrone or estradiol. Infection-associated steroid changes occurred concurrently with or after increases in uterine activity. CONCLUSION: Infection-associated preterm parturition is associated with dramatic increases in fetal adrenal steroid biosynthesis but not by corresponding increases in placental estrogen biosynthesis. This suggests that fetal stress is accompanied by placental dysfunction and that infection-associated parturition is not dependent on the increased estrogen biosynthesis observed in spontaneous parturition. (Am J Obstet Gynecol 1996;174:1725-33.)     

Multicenter trial of a simplified mifepristone medical abortion regimen

OBJECTIVE: Atherosis and placental infarction have been observed in pregnancies complicated by fetal growth restriction (FGR). Low-density lipoprotein (LDL) oxidation plays a central role in the pathogenesis of atherosclerosis; therefore, it could be involved in the placental alterations observed in FGR. The aims of the present study were to estimate LDL susceptibility to oxidation in pregnancies complicated by FGR and to evaluate their relationship with fetal growth and placental hormone secretion. METHODS: A cohort prospective study was carried out in 50 women with uncomplicated pregnancies and 55 women with FGR. Blood was drawn at 15, 24, and 32 weeks of gestation. Low-density lipoprotein oxidation was initiated by the addition of CuCl2 and formation of conjugated dienes was monitored. Cholesterol, triglycerides, vitamin E, estradiol, progesterone, and placental lactogen were determined. RESULTS: Women with FGR showed a lag phase (minutes from addition of CuCl2) similar to the control group in the first trimester of pregnancy (85.3 +/- 3.3 versus 81.3 +/- 5.6). But in the second and third trimester, they showed a lower lag phase than the control group: 69.6 +/- 3.6 versus 84.4 +/- 3.5 (P < .05) and 69.9 +/- 3.4 versus 95.6 +/- 3.4 (P < .001). During the third trimester, pregnancies complicated with FGR showed lower levels of estradiol, progesterone, and human placental lactogen than those in the control group. In the third trimester, a positive correlation was found between the lag phase and the birth weight (P = .001) and with the plasma levels of estradiol (P = .002). CONCLUSION: Fetal growth restriction is associated with an increased LDL susceptibility to oxidation, a process that could damage the placenta, leading to alterations in placental endocrine function and fetal weight. Pregnancies complicated by fetal growth restriction show an increased LDL susceptibility to oxidation, a process that may lead to placental dysfunction and growth delay.     

Circadian hormonal interactions among the mother, fetus, and amniotic fluid

Circadian rhythms and hormonal interactions among the maternal, fetal, and amniotic fluid compartments were studied in long-term catheterized rhesus macaque monkeys between days 127 and 138 of gestation (term = 167 days). Blood samples were collected at 3-hour intervals for 48 hours and analyzed by radioimmunoassay for estrone, estradiol, cortisol, progesterone, dehydroepiandrosterone sulfate, and prolactin. Distinct circadian rhythms were present for cortisol and progesterone in the maternal circulation and for progesterone and dehydroepiandrosterone sulfate in the fetal circulation (p less than 0.05). Although maternal and fetal estrogen levels were higher in AM samples than in PM samples, a statistically significant circadian rhythm was not present (p greater than 0.10). Fetal levels of progesterone and dehydroepiandrosterone sulfate and maternal levels of progesterone were highest between 9:00 PM and 3:00 AM and lowest between 9:00 AM and 3:00 PM. Maternal levels of cortisol were highest between 6:00 AM and 9:00 AM and lowest between 6:00 PM and 12 midnight. The circadian patterns of maternal cortisol and progesterone were inversely related to each other (r = -0.68; p less than 0.01). Amniotic fluid cortisol levels were highest between 9:00 AM and 12 noon and lowest between 6:00 PM and 3:00 AM (p less than 0.10). With the possible exception of cortisol, amniotic fluid steroid hormones did not demonstrate distinct diurnal fluctuations, nor did they correlate with steroid changes in maternal or fetal blood. Because the rhesus placenta is permeable to glucocorticoids it is likely that transplacental passage of maternal cortisol influences the activity of the fetal pituitary and adrenal so that the circadian rhythm in the fetal axis is 180 degrees out of phase with that of the maternal axis. The circadian rhythms in fetal dehydroepiandrosterone sulfate and progesterone in late gestation parallel the biorhythm in uterine contraction frequency and amplitude, with peaks during periods of darkness between 9:00 PM and 3:00 AM.     

Intrauterine growth retardation and urinary elimination of estriol

33 measurements of urinary estriol from 30-40 weeks' gestation in 22 pregnancies where dysmaturity was diagnosed in utero are shown graphically. The mean estriol excretion was about 2-3 mg below the lower limit of normal; it increased more slowly with gestational age: and it declined precipitously from 34-38 weeks. 1/3 of the women delivered at 38 weeks, either spontaneously or by induction. The mean estriol curve in the remaining women rose during treatment until delivery at 40 weeks. No correlation could be discerned in individual cases between the estriol excretion curve (or especially between an individual estriol value) and fetal weight, maturity, fetal distress in labor, or fetal death (1 case).     

Umbilical cord plasma concentrations of deoxycorticosterone sulfate in anencephalic fetuses

In the present investigation, we determined the levels of deoxycorticosterone sulfate in mixed umbilical cord plasma of anencephalic abortuses and newborn infants. The anencephalic fetus is an interesting model with respect to the production of deoxycorticosterone and deoxycorticosterone sulfate on several accounts. There is profound adrenal atrophy in most such fesuses, and, in consequence, there also is relatively profound hypoestrogenism. This is an important consideration in the formation of deoxycorticosterone and deoxycorticosterone sulfate since it is known that estrogen acts to stimulate extra-adrenal steroid 21-hydroxylase and 21-hydroxysteroid sulfotransferase activities. The plasma levels of deoxycorticosterone sulfate in 22 anencephalic abortuses and newborn infants delivered between 21.5 and 45.5 weeks of gestation ranged from 1.8 to 30.3 ng/ml. The concentrations of deoxycorticosterone sulfate in umbilical cord plasma of anencephalic fetuses and newborn infants were not related to gestational age or method of delivery and, at term, were less than 13% of those in umbilical cord plasma of normal newborn infants. These data can be interpreted to indicate (1) that deoxycorticosterone sulfate normally is secreted directly by the fetal adrenal or (2) that placental estrogen normally derived largely from fetal adrenal dehydroisoandrosterone sulfate is essential for the maintenance of plasma deoxycorticosterone sulfate levels in the fetus by stimulating extra-adrenal deoxycorticosterone sulfate production from plasma progesterone, or both.     

Changes in rates of salivary estriol increases before parturition at term

OBJECTIVE: The aim of this study was to characterize the increases of salivary estriol concentrations before the onset of labor at term. STUDY DESIGN: Salivary estriol concentrations were measured in weekly patient-collected samples by means of a sensitive (mean +/- SD threshold, 0.025 +/- 0.001 ng/mL; coefficient of variation, 3.8%) direct enzyme immunoassay in a microtiter plate format. The salivary estriol concentrations in 16 healthy pregnant women were characterized from 30 weeks' gestation until the time of parturition and delivery. Samples were stored frozen at collection and analyzed in batches after delivery. RESULTS: The median salivary estriol concentration profile revealed a nonlinear rise beginning from 30 weeks' gestation (0.89 ng/mL) until term (2.70 ng/mL, an increase of 201%). At 35 weeks' gestation the salivary estriol concentration median value increased sharply (positive inflection point, 50%-93% increase) at a demarcation between a slower increase during early pregnancy and a more rapid increase during late pregnancy. This positive inflection point associated with a late pregnancy increase characterized subgroups of pregnancies according to the lengths of gestation as follows: early term (delivered at <38 weeks 1 day's gestation), middle term (delivered at 38 weeks 1 day-40 weeks' gestation), and late term (delivered at >40 weeks' gestation). Five weeks before delivery the mean (+/-SEM) rate of rise in salivary estriol concentration was 0.50 +/- 0.13 ng/mL per week to 0.84 +/- 0.26 ng/mL per week in the early term group. The increase in rate for the middle term group was 0.32 +/- 0.06 ng/mL per week to 0.37 +/- 0.26 ng/mL per week, whereas in the late term group the rate of salivary estriol concentration rise was 0.37 +/- 0.03 ng/mL per week to -0.03 +/- 0.25 ng/mL per week. CONCLUSION: These data demonstrate in normal pregnancies (1) that a direct, nonradiometric measure of salivary estriol concentration can be used to monitor the late pregnancy increase in estriol production, (2) that 35 weeks' gestation marks a positive inflection point of the onset of increased estriol production, and (3) that the late pregnancy rise in salivary estriol concentration shows distinct patterns that tend to be characteristic of the length of pregnancy. These data support the concept that the rate of increase of estriol production is related to the timing of the onset of labor.     

Alterations in saliva steroid hormone levels after oral mifepristone administration in women with pregnancies of greater than 41 weeks' gestation

The objective of this study is to describe the effects of oral mifepristone administration on saliva levels of estradiol, estriol, progesterone, and cortisol in women with postdates pregnancy. As an adjunct to a randomized controlled trial comparing 200 mg oral mifepristone to placebo for cervical ripening and labor induction in women with pregnancies greater than 41 weeks' gestation, saliva samples were obtained before drug administration and every 6 hours thereafter for 24 hours. Estradiol, estriol, progesterone, and cortisol levels were measured by radioimmunoassay. Ninety-seven participants received mifepristone, and 83 received placebo. Saliva steroid hormone data were available for 71 mifepristone-and 60 placebo-treated women. Mean baseline saliva estradiol, estriol, progesterone, and cortisol levels were similar between study groups. At 24 hours after study medication administration, saliva estradiol, estriol, progesterone, and cortisol levels in the mifepristone group were significantly elevated compared with baseline. There was no significant change in hormone levels in the placebo group. Oral mifepristone significantly increased saliva estradiol, estriol, progesterone, and cortisol compared with placebo. This may reflect mifepristone's antiglucocorticoid properties. These hormone elevations may contribute to the mechanism by which mifepristone causes cervical ripening and increases myometrial activity.     

Erythroblastosis and reticulocytosis in anemic fetuses

The fetal blood erythroblast and reticulocyte counts were determined in umbilical cord samples obtained at 17 to 36 weeks' gestation from 127 pregnancies complicated by red blood cell isoimmunization. The reticulocyte count increased linearly with fetal anemia, and the erythroblast count increased exponentially. Significant erythroblastosis was observed only when the hemoglobin concentration deficit was greater than 7 gm/dl. Of the 52 fetuses with a hemoglobin concentration deficit greater than 7 gm/dl, 35 had ultrasonographic evidence of hydrops. These data suggest that medullary hematopoiesis is stimulated by mild anemia and that recruitment of extramedullary sites occurs when anemia is severe. Extensive hepatic erythropoiesis may be the cause of fetal hydrops in red blood cell isoimmunization.     

Plasma progesterone, dehydroepiandrosterone sulfate and estriol levels during labor induction with a sustained-release prostaglandin E2 vaginal insert.

OBJECTIVE: To measure plasma progesterone, dehydroepiandrosterone sulfate (DHEAS) and estriol levels in women induced for labor with a sustained-release vaginal polymer prostaglandin E2 insert, and to analyze the relationships between the changes in hormone levels and Bishop score. METHODS: Twelve primipara and 12 multipara were treated with a sustained-release polymer vaginal prostaglandin E2 insert (0.3 mg/h) for up to 24 h. The Bishop score was assessed at the start and end of therapy, and serum samples were collected at 4-h intervals. Plasma levels of progesterone, DHEAS and estriol were measured by specific radioimmunoassays. RESULTS: Exposure averaged 13.5 +/- 7.2 h. Progesterone levels decreased in the majority of patients (79.2%) after the start of therapy. Higher baseline DHEAS and estriol levels were observed among women who achieved an improvement in Bishop score of at least 4 during prostaglandin E2 treatment. CONCLUSIONS: Higher DHEAS and estriol levels prior to labor induction with prostaglandin E2 may be indicators of a favorable labor outcome. Additional studies are needed to substantiate the decrease in progesterone levels observed in this study and the importance of this phenomenon for the mechanism of labor induction with prostaglandin E2.     

Sonographic evaluation of fetal abdominal growth: predictor of the large-for-gestational-age infant in pregnancies complicated by diabetes mellitus

Serial ultrasound examinations were performed during the third trimester in 79 pregnant women with diabetes to establish the onset of accelerated fetal growth. At least three ultrasound examinations were performed, with a minimum scan interval of 2 weeks. Growth curves constructed for femur length and head circumference were similar for fetuses appropriate for gestational age (n = 48) and fetuses large for gestational age (n = 31). The mean changes in femur length and head circumference (expressed as centimeters per week during the early and late third trimesters) did not differ statistically between these two groups. Abdominal circumference growth was clearly accelerated at 32 weeks' gestation in the large for gestational age group (mean +/- SD, 1.36 +/- 0.16 cm/wk) compared with the appropriate for gestational age group (0.901 +/- 0.21 cm/wk, p less than 0.001). With use of a receiver operator characteristic curve, a change in abdominal circumference of 1.2 cm/wk over the period of 32 to 39 weeks' gestation was determined to be an optimal cutoff for detecting excessive fetal growth (sensitivity 84%, specificity 85%). A change in abdominal circumference 1.2 cm/wk was present in 4/4 large-for-gestational age fetuses (less than 4000 gm), in 17/21 (81%) of fetuses with birth weights 4000 to 4499 gm, and in 5/6 (83%) whose weight exceeded 4500 gm. It appears that improved detection of the fetus large for gestational age in diabetic pregnancies may be accomplished by the use of serial ultrasonography during the third trimester.     

Human placental lactogen and unconjugated estriol concentrations in twin pregnancy: monitoring of fetal development in intrauterine growth retardation and single intrauterine fetal death

Human placental lactogen and unconjugated estriol concentrations in maternal serum were evaluated in 100 uneventful twin pregnancies, and these values were compared with those observed in 16 twin pregnancies associated with intrauterine growth retardation or single intrauterine fetal death. In pregnancies associated with intrauterine growth retardation (n = 8), human placental lactogen levels were at the lower limit of normal range for singleton pregnancies, whereas estriol levels were normal in most cases. When one of the fetuses had died before week 33 of pregnancy (n = 5), both human placental lactogen and estriol levels were low and they were almost at the levels in singleton pregnancy. When intrauterine fetal death occurred after week 36 of pregnancy (n = 3), both hormone levels remained normal until term. Thus human placental lactogen rather than estriol is a good indicator of intrauterine growth retardation in twin pregnancy. Both human placental lactogen and estriol are useful for the monitoring of the surviving fetus in the case of single intrauterine fetal death.     

Plasma and placental levels of interleukin-10, transforming growth factor-beta1, and epithelial-cadherin in preeclampsia

OBJECTIVE: To investigate the plasma and placental levels of interleukin-10 (IL-10), transforming growth factor-beta1 (TGF-beta1), and epithelial-cadherin (E-cadherin) in normotensive and preeclamptic pregnancies. METHODS: The study population consisted of 33 women with normotensive pregnancy and 35 women with preeclampsia. Peripheral venous blood samples were collected before labor (35.3 +/- 1.1 and 34.2 +/- 3.4 weeks' gestation for normotensive and preeclamptic pregnancies, respectively), and placental tissues were obtained after delivery. Maternal plasma and placental homogenate IL-10, TGF-beta1, and E-cadherin levels were determined by enzyme-linked immunosorbent assay. RESULTS: The mean plasma and placental levels of IL-10, TGF-beta1, and E-cadherin were significantly higher in preeclamptic than normotensive patients (P <.001). The plasma and placental levels of IL-10, TGF-beta1, and E-cadherin significantly increased with the increments in diastolic blood pressure (P <.001). CONCLUSION: IL-10, TGF-beta1, and E-cadherin may be involved in the pathologic process of preeclampsia. The pathophysiologic changes associated with preeclampsia may stem in part from the overproduction of these placental mediators.