Maternal serum leptin concentrations do not correlate with cord blood leptin concentrations in normal pregnancy

OBJECTIVE: To determine whether there is a difference in maternal leptin concentration and cord blood concentration, consistent with the hypothesis of a noncommunicating, two-compartement model of fetoplacental leptin regulation. METHODS: Blood samples were collected from 139 women, identified as having an uncomplicated pregnancy, from an antecubital vein at delivery. Cord blood samples were taken from the umbilical vein. Leptin was measured by radioimmunoassay, and its relationship to fetal and maternal anthropometrics was assessed by Spearman correlation. Differences in maternal and cord blood leptin levels between male and female infants were tested with the Mann-Whitney Utest. Maternal and cord blood leptin were compared by the Wilcoxon signed rank test. The outcome measures were maternal and cord blood leptin at delivery, fetal birth weight, length, weight/length ratio, and ponderal index, maternal prepregnancy body mass index, pregnancy weight gain, relative weight gain, and body mass index at delivery. RESULTS: No correlations were found between maternal and cord blood leptin concentrations. Fetal leptin level correlated with birth weight (rho = 0.665; P <.0001), length (rho = 0.490; P <.0001), ponderal index (rho = 0.260; P =.002), and weight/length ratio (rho = 0.625; P <.0001). Median leptin concentrations were higher in female (9.3 ng/mL, range 1.5-34.4 ng/mL) than in male (8.2 ng/mL, range 1.6-38.3 ng/mL) neonates, but this difference was statistically not significant. Logistic regression analysis showed a significant influence on umbilical venous leptin concentration for birth weight (P <.0001) but not for gender. Maternal leptin concentrations were significantly higher than cord leptin concentrations (P <.0005 for the male and female neonates and the entire group). CONCLUSION: There was no correlation between maternal and cord leptin, which supports the hypothesis of a noncommunicating, two-compartment model of fetoplacental leptin regulation.     

Maternal and umbilical cord copeptin levels in pregnancies complicated by fetal growth restriction

Objective: The aim of this study was to compare maternal and fetal serum copeptin concentrations in pregnancies complicated by isolated fetal growth restriction (FGR), and uncomplicated pregnancies, and to investigate relationships between copeptin levels and clinical parameters.

Methods: Maternal and fetal serum copeptin levels were measured in 21 women with pregnancies complicated by isolated FGR and 20 women with normal pregnancies (control group). Doppler assessment of the uterine and umbilical arteries was performed in each patient.

Results: Maternal serum copeptin levels were significantly higher in women with isolated FGR compared to controls (p?=?0.042). In addition, maternal copeptin levels were inversely correlated with the uterine artery pulsatility and resistance indices and positively correlated with neonatal birth weight. Umbilical vein copeptin levels were significantly increased in neonates with adverse outcomes (p?=?0.001).

Conclusions: Increased maternal copeptin concentration may reflect a response to stress, thus serving as a compensatory mechanism in pregnancies complicated by FGR.     

Maternal serum copeptin as a marker for fetal growth restriction

ObjectivesCopeptin is a hormone of endogenous stress. The aim was to evaluate whether the measurement of maternal serum copeptin is useful for differentiation between fetal growth retardation and constitutionally small fetuses among small for gestational age fetuses.Study Designprospective case control clinical study.Patients and MethodsMaternal serum copeptin levels were measured by ELISA technique in 53 pregnant females subdivided into a control group (group 1) of 20 women with normal gestation & a group of 33 pregnant women with small for gestational age fetuses. The small for gestational age fetuses were subclassified into constitutionally small fetuses (17 cases) with normal umbilical artery Doppler studies (group 2), and fetal growth restriction with abnormal umbilical artery Doppler studies (16 idiopathic cases) as group 3.ResultsThe fetal growth restricted group had a significantly higher maternal serum copeptin levels as compared with the control group (P < 0.01). The maternal serum copeptin levels in fetal growth restriction were significantly higher than in constitutionally small fetus (P < 0.05).ConclusionMaternal serum copeptin level can differentiate between the normal sized and small for gestational age fetuses. Also, it can differentiate between constitutionally small and growth restricted fetuses.     

Maternal serum activin A levels in association with intrauterine fetal growth restriction

Objective To assess maternal serum activin A as a potential marker of fetal growth restriction.
Design A cohort study.
Setting A maternal–fetal medicine unit, university teaching hospital.
Population Fifty-seven women with a small fetus (less than 10th centile for gestation) referred for assessment of fetal size by ultrasound biometry.
Methods At the time of presentation for fetal biometry, maternal blood was collected for activin A measurement. The case records of each woman were independently reviewed after delivery and the pregnancy grouped into one of three groups: constitutionally small fetus, intrauterine growth restricted (IUGR) fetus or IUGR fetus and maternal pre-eclampsia (IUGR–pre-eclampsia). Activin A levels in the three groups were compared.
Main outcome measures Maternal serum activin A levels.
Results Sixteen of the 57 pregnancies were classified as constitutionally small, 17 as IUGR and 24 as IUGR–pre-eclampsia. Expressed as multiples of a normal median (MoMs), the median (95% CI) activin A level in the constitutionally small pregnancies was 1.12 (0.72–1.39) MoMs significantly lower than the level in both the IUGR pregnancies, 3.00 (1.84–4.11) MoMs, and the IUGR–pre-eclampsia pregnancies, 7.96 (5.73–10.62) MoMs (   P = 0.002 and 0.0001 for IUGR vs constitutionally small and IUGR–pre-eclampsia vs constitutionally small, respectively  ).
Conclusions Maternal serum activin A may be useful in the assessment of the small for gestational age fetus.     

Maternal and fetal leptin and ghrelin levels: relationship with fetal growth

Purpose  

In our study, we investigated the influence of plasma levels ghrelin, leptin and other metabolic hormones (ILGF-1 and ILGF-2) in pregnants in regulating fetal body weight and mode of delivery.     

Maternal venous procalcitonin levels do not correlate with umbilical cord blood and venous blood concentrations in the neonate

BACKGROUND: To compare procalcitonin (PCT) concentrations between maternal blood and levels in umbilical cord or venous blood of neonates who were born with or without infection. METHODS: Forty-six women with singleton pregnancies, complicated by premature rupture of membranes, preterm delivery and/or chorioamnionitis, were enrolled in this study. The study group comprised 15 patients and their infected newborns. The control group consisted of 31 women and their healthy newborns. We compared PCT concentrations between maternal, umbilical cord and neonatal serum, in both study and control groups. Additionally, PCT levels were compared between the corresponding compartments. RESULTS: PCT concentrations in the umbilical cord and venous blood in infected newborns, but not in non-infected neonates, were significantly higher than maternal serum PCT levels. PCT concentrations of mothers who delivered infected newborns were comparable to those in the controls. However, PCT concentrations in the umbilical cord and in the venous blood of the infected newborns were higher than in healthy newborns. CONCLUSION: Measurement of maternal PCT concentration during labor does not contribute to early prediction of infection in the neonate. However, umbilical cord PCT concentrations, as well as its neonatal venous levels on the second day of life, seem to be related to intrauterine infection, and may be a useful tool in the diagnosis of early neonatal infection.     

Maternal cardiac function in fetal growth restriction

OBJECTIVE: To assess the maternal central haemodynamics in normotensive women with pregnancies complicated by severe fetal growth restriction (FGR). DESIGN: Cross-sectional study. SETTING: A tertiary referral fetal medicine unit. POPULATION: The study groups comprised 107 women with normal singleton pregnancies and 20 with singleton pregnancies complicated by FGR at 25-37 weeks. In the latter group, assessment was carried out within 10 days prior to their delivery. All the women were normotensive, without any medical problems. METHODS: Two-dimensional and M-mode echocardiography of the left ventricle. MAIN OUTCOME MEASURES: Maternal left ventricular systolic and diastolic function. RESULTS: In the FGR group, compared with the normal group, there was increased total vascular resistance (TVR), reduced systolic function characterised by lower cardiac output, stroke volume, heart rate, ejection time and septal and lateral long-axis shortening. Mean arterial pressure (MAP) was not significantly different between the groups. CONCLUSIONS: Severe FGR is associated with reduced maternal systolic function and increased TVR but no change in MAP. TVR may be a useful tool in the classification and management of FGR. The findings suggest that in FGR, there is increased blood viscosity due to lack of intravascular space expansion.     

Maternal serum ferritin and fetal growth

OBJECTIVE: To determine the relationship between maternal serum ferritin and concentrations and specific types of fetal growth restriction (FGR). METHODS: Serum ferritin concentrations were measured at approximately 25 and 36 weeks' gestation in 480 multiparas with singleton fetuses who participated in a study of risk factors for repeated FGR. Asymmetric FGR was defined by low birth weight for gestational age criteria and a ponderal index less than 2.32, and symmetric FGR was defined by the same birth weight for gestational age criteria and a ponderal index of at least 2.32. RESULTS: Among 480 infants, 370 were appropriate for gestational age (AGA), 58 had asymmetric FGR, and 52 had symmetric FGR. Higher ferritin concentrations were associated with black race, maternal age 25 years or older, and smoking. Mothers of asymmetric-FGR infants had higher mean ferritin levels than mothers of AGA infants at 25 weeks' (38.0 versus 20.2 microg/L, P < .01) and 36 weeks' gestation (21.0 versus 13.3 microg/L, P < .01), whereas mothers of symmetric-FGR infants had significantly lower ferritin levels at 36 weeks (8.3 microg/L). For mothers with serum ferritin levels of at least 26 microg/L (highest quartile at 25 weeks), the adjusted odds ratio (OR) for asymmetric-FGR infants was 3.4, 95% confidence interval (CI) 1.6, 7.2. There was a similar association between the highest quartile of serum ferritin at 36 weeks (at least 20 microg/L) and asymmetric FGR (adjusted OR 2.7, 95% CI 1.3, 5.8). Women with serum ferritin levels less than 3 microg/L (lowest quartile at 36 weeks) had an adjusted OR for symmetric-FGR infants of 2.2, 95% CI 1.01, 4.6. CONCLUSION: High maternal serum ferritin levels are associated with asymmetric FGR, whereas low serum ferritin levels are associated with symmetric FGR.     

Maternal blood pressure and fetal growth

Eleven thousand eighty-two term, singleton pregnancies were analyzed for clues to how different levels of maternal blood pressure affect fetal growth. Birth weights progressively increased with increasing pressures until the hypertensive range was reached when maternal edema and proteinuria were absent. Pressure-associated increases in fetal growth were even more rapid when mothers were edematous, and slower when 2+ or greater proteinuria was present. Birth weights leveled off or decreased when pressures reached the hypertensive range. The pressure threshold at which growth slowed increased from diastolic 75 mm Hg in the lowest maternal pregnancy weight gain category to nearly 100 mm Hg in the highest weight gain category. Decreases in birth weight associated with hypertension were most severe when mothers were thin and had low pregnancy weight gains. Diuretics reduced birth weights in low maternal weight gain pregnancies but not in high weight gain ones.     

Leptin concentrations in maternal serum and cord blood: relationship to maternal anthropometry and fetal growth.

OBJECTIVE: To determine 1. the relationship between maternal serum leptin concentrations and maternal anthropometry and 2. the relationship between cord serum leptin concentrations at birth and neonatal anthropometry. DESIGN: Prospective cohort study of fetal growth in low-risk pregnancies. SETTING: University teaching hospital. SAMPLE: Thirty-nine women and their babies taking part in a fetal growth study. METHODS: Blood was taken from the women between 10-20 weeks of gestation and from the umbilical cord of their babies at delivery. Serum leptin was measured by radio-immunoassay. Maternal anthropometric measurements were recorded at booking. Neonatal anthropometric measurements were recorded within 48 hours after delivery. Linear regression analysis was used to explore the relationship between serum leptin concentrations and anthropometric measures and multiple regression analysis then applied to determine which variables remained independently associated with leptin. RESULTS: The median (range) leptin concentration in maternal serum was 11.8 ng/mL (1.7-39.7) and in cord blood was 4.2 ng/mL (0.6-21.4). Maternal leptin levels correlated with maternal weight, body mass index, midarm circumference and skinfold thickness, but not with birthweight, placental weight or maternal height. Body mass index and midarm circumference remained significant after multiple regression analysis. Cord leptin levels correlated with birthweight, birthlength, placental weight and skinfold thickness but not with ponderal index. Birthweight and subscapular skinfold thickness remained significant after multiple regression analysis. Cord leptin concentrations did not correlate with maternal leptin concentrations. CONCLUSIONS: We suggest that there are very strong associations between maternal leptin and maternal adiposity in pregnancy, and between cord leptin at delivery and birthweight, as well as other anthropometric markers of fetal growth.     

beta-Endorphin and beta-lipotropin concentrations in umbilical cord blood

Antisera suitable for human beta-endorphin and beta-lipotropin radioimmunoassay were developed, and radioimmunoassays were established to measure these peptides in umbilical cord plasma, with silicic acid extraction and gel chromatography used to separate the beta-endorphin from the beta-lipotropin fraction. These two peptides were determined in umbilical venous plasma from 64 newborn infants. Umbilical vein beta-endorphin and beta-lipotropin concentrations averaged 38.5 +/- 3.2 and 50.4 +/- 4.1 (+/- SE) fmoles/ml in the 54 newborn infants without and 115 +/- 18 and 110 +/- 25 fmoles/ml in the 10 newborn infants with apparent fetal distress. Neither the presence or absence of labor nor the route or mode of delivery was found to affect umbilical vein beta-endorphin or beta-lipotropin concentrations. However, cord plasma levels of both peptides were significantly elevated in conjunction with fetal distress, as evidenced by prolonged bradycardia, late and prolonged variable fetal heart rate decelerations, or fetal acidosis. In 18 of 22 pairs of simultaneously measured umbilical venous and arterial beta-endorphin and beta-lipotropin concentrations in newborn infants without apparent intrapartum distress, the venous beta-endorphin concentrations, which averaged 40.4 +/- 3.5 fmoles/ml, were significantly higher than the arterial beta-endorphin levels, with a mean of 28.5 +/- 4.2 fmoles/ml. No significant umbilical arteriovenous concentration difference could be observed for beta-lipotropin. This suggests that at least a portion of the coad plasma beta-endorphin is derived from the placenta. The ratio of umbilical arterial to venous beta-endorphin concentrations rose as the absolute cord plasma beta-endorphin levels increased. Furthermore, both the molar umbilical venous and arterial beta-lipotropin to beta-endorphin ratios decreased significantly in association with intrapartum fetal distress. These data indicate tat the stress-related increase in umbilical plasma beta-endorphin exceeds that of beta-lipotropin and may be, at least in part, of fetal origin. Umbilical venous beta-endorphin and beta-lipotropin levels of neonates whose mothers did not receive meperidine or other narcotics agents did not differ from those of neonates whose mothers were given meperidine or other narcotics during labor. Our data, in conjunction with those of others, are consistent with the hypothesis that fetal hypoxia causes the release of neurotransmitters such as beta-endorphin, which may modulate the regulation of fetal heart rate patterns.     

Maternal snoring during pregnancy is not associated with fetal growth restriction

A small number of studies have, thus far, evaluated the association between maternal snoring and fetal growth revealing conflicting results. No study has compared fetal growth between women with habitual snoring who snored before pregnancy and women with habitual snoring that started to snore during pregnancy.

Objectives: To examine the effect of maternal snoring on fetal outcome and to investigate the differences between “chronic snorers” and “new-onset snorers”. Methods: Women of singleton, uncomplicated, full-term pregnancies completed a questionnaire. Obstetric and labor records were reviewed. Newborn records were reviewed for gestational age, birth weight, Apgar score and gender. Results: 246 low risk women were studied. Mean BMI at the beginning of pregnancy was 22.3?±?3.5?kg/m². 32% reported habitual snoring. Of those, 26% were chronic snorers and 74% were new-onset snorers. Neither significant difference in fetal growth was found between snorers and non-snorers nor between chronic snorers and new-onset snorers. Increased rate of nulliparous women was found in new-onset snorers compared with both chronic snorers and non-snorers (54 vs. 25 and 29% respectively; p?=?0.001). Conclusions: In pregnant women with no apparent risk factors, maternal snoring does not affect fetal growth. No differences in maternal characteristics or fetal outcome were found between chronic snorers and new-onset snorers.     

Maternal and fetal plasma endothelin levels in intrauterine growth restriction: relation to umbilical artery Doppler flow velocimetry

The objective of this study was to examine maternal and fetal endothelin-1 (ET-1) in pregnancies complicated with intrauterine growth restriction (IUGR) and to correlate these data with umbilical artery Doppler flow velocity waveforms (FVW). Higher mean maternal (13.8 +/- 6.4 vs 9.2 +/- 3.4 pmol/L, p < 0.05) and fetal (18.5 +/- 9.6 vs 11.7 +/- 6.9 pmol/L, p < 0.05) ET-1 levels were found in pregnancies complicated with IUGR than in controls. Fetal ET-1 level was related to birth weight percentile for gestational week. Maternal and fetal ET-1 concentrations were not related to umbilical artery Doppler flow S/D ratio, PI and RI. Maternal or fetal ET-1 concentrations were also not related to umbilical artery pH, PO2 and PCO2. Pregnancy-induced hypertension was significantly associated with an elevated fetal and maternal ET-1 concentration. In conclusion, increased production and secretion of ET-1 may play a role in the pathophysiology of idiopathic IUGR. Over-production of ET-1 in IUGR is not associated with increased placental resistance as reflected in abnormal umbilical artery Doppler FVW.