Allometric Metabolic Scaling and Fetal and Placental Weight

BackgroundWe tested the hypothesis that the fetal–placental relationship scales allometrically and identified modifying factors of that relationship.Materials and methodsAmong women delivering after 34 weeks but prior to 43 weeks' gestation, 24,601 participants in the Collaborative Perinatal Project (CPP) had complete data for placental gross proportion measures, specifically, placental weight (PW), disk shape, larger and smaller disk diameters and thickness, and umbilical cord length. The allometric metabolic equation was solved for α and β by rewriting PW = α(BW)β as ln(PW) = ln α + β[ln(BW)]. α_ι was then the dependent variable in regressions with p < 0.05 significant.ResultsMean β was 0.78 + 0.02 (range 0.66, 0.89), which is consistent with the scaling exponent 0.75 predicted by Kleiber's Law. Gestational age, maternal age, maternal BMI, parity, smoking, socioeconomic status, infant sex, and changes in placental proportions each had independent and significant effects on α.ConclusionsWe find an allometric scaling relation between the placental weight and the birthweight in the CPP cohort with an exponent approximately equal to 0.75, as predicted by Kleiber's Law. This implies that: (1) placental weight is a justifiable proxy for fetal metabolic rate when other measures of fetal metabolic rate are not available; and (2) the allometric relationship between placental and birthweight is consistent with the hypothesis that the fetal–placental unit functions as a fractal supply limited system. Furthermore, our data suggest that the maternal and fetal variables we examined have at least part of their effects on the normal balance between placental weight and birth weight via effects on gross placental growth dimensions.     

Placental gene expression patterns of epidermal growth factor in intrauterine growth restriction

Objective

In this study, we compared human placental gene expression patterns of epidermal growth factor (EGF) in pregnancies with intrauterine growth restriction (IUGR) vs. normal pregnancies as control.

Study design

Gene expression of EGF was determined from human placental samples collected from all pregnancies presenting with IUGR at our institution during the study period January 1, 2010–January 1, 2011. Multiple clinical variables were also assessed including maternal age, gestational weight gain, increase of BMI during pregnancy and fetal gender.

Results

A total of 241 samples were obtained (101 in the IUGR pregnancy group, 140 in the normal pregnancy group). EGF was found to be underexpressed in the IUGR group compared to normal pregnancy (Ln2^α: −1.54; p < 0.04). Within the IUGR group no fetal gender-dependent difference was seen in EGF gene expression (Ln2^α: 0.44; p < 0.06). Similarly, no significant difference in EGF expression was noted in cases with more vs. less severe forms of IUGR (Ln2^α: −0.08; p = 0.05). IUGR pregnancies were significantly more common in the maternal age group 35–44 years compared to other age groups. Gestational weight gain and gestational BMI increase were significantly lower in IUGR pregnancies compared to controls.

Conclusions

Placental expression of EGF was found to be reduced in IUGR pregnancies vs. normal pregnancies. This may partly explain the smaller placental size and placental dysfunction commonly seen with IUGR. An increased incidence of IUGR was observed with maternal age exceeding 35 years. The probability of IUGR correlated with lower gestational weight gain and lower BMI increase during pregnancy.     

Corticotrophin-releasing factor and urocortin inhibit system A activity in term human placental villous explants

Plasma corticotrophin-releasing factor (CRF) and urocortin are elevated in preterm labour and/or fetal growth restriction (FGR). FGR is associated with reduced placental system A amino acid transporter activity and in vitro data suggest altered endocrine status could be responsible. Here we test the hypothesis that CRF and urocortin inhibit placental system A activity. Chronic (48 h) exposure of term placental villous explants to these hormones (10⁻⁷ M) significantly reduced system A activity (Na⁺-dependent ¹⁴C-methylaminoisobutyric acid uptake), whereas 1 h exposure had no effect. We propose elevated CRF and urocortin contribute to FGR through negative regulation of placental system A activity.     

Efficacy of intermittent preventive treatment with sulfadoxine-pyrimethamine on placental parasitemia in pregnant women in midwestern Nigeria

Objective

To assess the effect of intermittent preventive treatment with sulfadoxine and pyrimethamine (IPT-SP) on placental parasitemia and maternal and perinatal outcome.

Methods

We compared placental malaria parasitemia during pregnancy and pregnancy outcome in 2 groups of women receiving antenatal care at University of Benin Teaching Hospital. One group was prophylactically treated with IPT-SP and the other was not treated.

Results

The parasitemia rates for peripheral, placental, and cord blood were 11.9%, 11.4%, and 2.7% in the IPT-SP group (n = 370) and 19.1%, 22.6%, and 6.2% in the control group (n = 371) (P = 0.006, P = 0.002, and P = 0.02, respectively). The treatment reduced the odds of placental parasitemia by 37% (OR 0.63; 95% CI, 0.48-0.81). Peripheral (P = 0.002) and placental (P = 0.001) parasitemia were significantly reduced in the subgroup of women who took 2 or 3 doses of SP. Fewer women (16.2%) in the IPT-SP group than the control group (23.7%) had symptomatic malaria. Anemia at delivery was significantly lower in the IPT-SP group (10.8 vs 1.6%). The risks of abortion, preterm delivery, and low birth weight were also significantly lower in the IPT-SP group.

Conclusion

IPT-SP is effective in preventing placental parasitemia, and reduces rates of malaria, maternal anemia, abortion, preterm delivery and low birth weight among pregnant women.     

Morphological characteristics of placentas associated with idiopathic intrauterine growth retardation: a clinicopathologic study

Objectives

To investigate histopathologic findings, placental diameters and characteristics of syncytial knots in the placentas from idiopathic intrauterine growth retardation (IUGR) pregnancies, and to compare them with a normal birth weight group.

Study design

Based on strict eligibility criteria, this prospective case-control study included 52 term placentas from idiopathic IUGR pregnancies and 69 term placentas from normal birth weight pregnancies. The study was carried out at the Clinical Hospital Centre, Split, where all placentas were collected and examined. For each placenta, diameters were measured and the following histopathologic findings were recorded: infarction, intervillous thrombosis, abruption, villous branching and maturation, chorioamnionitis, decidual vasculopathy and hemorrhagic endovasculitis for each placenta. In addition we assessed quantitative (number of syncytial knots and number of syncytial nuclei per syncytial knot) and qualitative (density and surface area) characteristics of syncytial knots in each placental sample. Statistical significance was tested using χ²-test, Student's t-test and Mann-Whitney U-test. Statistical significance was set at P ≤ 0.05.

Results

There was no difference in investigated histopathologic findings between idiopathic IUGR placentas and control group placentas. Placental diameters correlated significantly with neonatal birth weight (r = 0.64; P < 0.01); with higher birth weight there is an increase in placental diameters. Syncytial knots from idiopathic IUGR had significantly smaller surface area (Z = 2.637; P = 0.008) and higher density (Z = 3.225; P = 0.001) compared with the control group, while there is no difference in number of syncytial knots per individual villus, total number of syncytial knots in each placenta sample or number of syncytial nuclei per syncytial knot.

Conclusions

The investigated histopathologic findings in idiopathic IUGR placentas are incidental, with no higher frequency than in placentas from uncomplicated pregnancies, and should not be considered as possible causative factors for idiopathic IUGR. The demonstrated qualitative changes of syncytial knots in placentas associated with IUGR could represent a compensatory mechanism.     

Maternal pro-hepcidin at term correlates with cord blood pro-hepcidin at birth

Objective

Hepcidin, a small 25 amino-acid antimicrobial peptide, has a significant role in the regulation of iron homeostasis. Pro-hepcidin, an 84 amino-acid peptide, is a precursor of the active hepcidin. The main aim of this study was to examine the association of maternal serum pro-hepcidin with cord blood pro-hepcidin levels in term pregnancies, and whether maternal and newborn iron status measurements correlate with the pro-hepcidin level.

Study design

The population consisted of 193 pregnant women admitted to the Kuopio University Hospital (Finland) for delivery, and their full-term newborn infants (cord blood). The main outcome measures were serum pro-hepcidin (ELISA), blood count including red cell indices, serum iron status markers (including iron, transferrin, transferrin saturation (TfSat), transferrin receptor (TfR) and ferritin), birth weight and placental weight and relative placental size. A Mann–Whitney U-test and Spearman's correlation were used to test the associations between the parameters.

Results

Pregnant women had higher pro-hepcidin level than their newborns (325 μg/L vs. 235 μg/L, p < 0.001). The Spearman's correlation between the maternal and cord blood serum pro-hepcidin level was highly significant (correlation coefficient 0.600, p < 0.001). Additionally, both maternal and cord blood pro-hepcidin levels correlated weakly but significantly with placental weight and relative placental size. However, pro-hepcidin level did not correlate with iron status measurements in pregnant women or in their newborns.

Conclusions

The present results suggest that pro-hepcidin is not associated with maternal or newborn iron homeostasis at term and birth, but may act in concert with the placenta, as evidenced by the correlation between maternal and fetal pro-hepcidin levels and their slight correlation with placental weight.     

Impact of obesity on surgical and oncologic outcomes in ovarian cancer

Objectives

The aim of this study is to determine the impact of obesity on surgical and oncologic outcomes after primary debulking surgery (PDS) in advanced epithelial ovarian cancer (EOC).

Methods

Women with stage IIIC/IV EOC who underwent PDS with curative intent between 1/2/2003 and 12/30/2011 were included. Patient characteristics, intraoperative and postoperative outcomes, recurrence and status were abstracted. Complications were graded according to the 4-point Accordion classification. For analyses, patients were divided into three groups according to body mass index (BMI): group 1—BMI < 25.0 kg/m²; group 2—BMI 25.0–39.9 kg/m²; and group 3—BMI ≥ 40.0 kg/m².

Results

Of the 620 patients included in the study, 36.6%, 56.9%, and 6.5% were in weight groups 1, 2, and 3, respectively.Weight group 3 was an independent predictor of severe complications after adjusting for confounders (adjusted odds ratio (95% CI): 2.93 (1.38, 6.20) for group 3 vs. group 2). Weight group was not associated with differences in residual disease (p = 0.80). The 90-day mortality rates were 11.9%, 6.7%, and 15.7%, respectively, in weight group 1, 2, and 3 (p = 0.049 unadjusted, p = 0.01 adjusted). There was no difference in OS (p = 0.52) or PFS (p = 0.23) between weight groups.

Conclusions

BMI ≥ 40.0 kg/m² is an independent predictor of severe 30-day postoperative morbidity and 90-day mortality after PDS for EOC—information useful in preoperative counseling. BMI does not appear to impact long-term oncologic outcomes including residual disease at PDS, although we had limited power at the extremes of BMI. BMI may be an important factor to consider in risk-adjustment models and reimbursement strategies.     

Factors associated with umbilical artery acidemia in term infants with low Apgar scores at 5 min

Objective

To evaluate predictors of umbilical artery acidemia in term neonates with low Apgar score.

Study design

From a cohort of term singleton deliveries over a 13-year period, we selected neonates with 5-min Apgar score <7. Acidemia was defined as umbilical artery pH < 7.00 or base excess (BE) ≤−12 mmol/L. Three pathogenic processes of neonatal acidemia were evaluated: (1) intrauterine vascular disease, defined as preeclampsia, clinical diagnosis of placental abruption, birth weight <10th centile, or histologic evidence of placental infarction or severe vascular pathology, (2) intrauterine infection, defined as clinical chorioamnionitis, histologic chorioamnionitis, or early neonatal sepsis, and (3) acute intrapartum events, which included cases of cord prolapse, amniotic fluid embolism, uterine rupture, sudden and sustained fetal bradycardia or absence of FHR variability with a previously normal pattern, shoulder dystocia or complicated breech extraction. The associations of such processes with umbilical artery evidence of acidemia were tested using χ², Fisher's exact test, Student's t-test, and logistic regression, with P < 0.05 or odds ratio (OR) with 95% confidence interval (CI) not inclusive of the unity considered significant.

Results

Among the 27,395 neonates in the cohort, an Apgar score at 5 min <7 was recorded in 94 (0.32%) and it was associated with umbilical artery acidemia in 33 cases. Logistic regression analysis showed that intrauterine vascular disease was independently associated with umbilical cord acidemia (P = 0.035, OR = 3.2, 95% CI = 1.1–9.7) whereas intrauterine infection (OR = 1.1, 95% CI 0.4–3.4) and acute intrapartum events (OR = 2.1 95% CI 0.6–7.0) were not.

Conclusions

Umbilical artery evidence of acidemia is present in 38% of term babies with low Apgar score and it is predominantly associated with chronic antepartum vascular disease. Neither intrauterine infection nor acute intrapartum events are significantly associated with umbilical artery acidemia.     

Thrombophilic risk factors for placental stillbirth

Objectives

To define the characteristics of placental stillbirth and the possible contribution of thrombophilic risk factors.

Study design

A prospective cohort study was performed. Women diagnosed with antenatal stillbirth (>20 weeks) of singleton pregnancies between 2006 and 2008 were referred postpartum for evaluation. Maternal risk factors, fetal, placental and cord abnormalities, and a detailed thrombophilia screening, including inherited and acquired thrombophilia, were evaluated. Fetal autopsy and placental pathology were encouraged.Placental stillbirth was defined as death of a normally-formed fetus with evidence of intrauterine fetal growth restriction, oligohydramnios, placental abruption and/or histological evidence of placental contribution to fetal death. Pregnancy characteristics and thrombophilia profiles were compared between placental and non-placental stillbirth cases.

Results

Sixty-seven women with stillbirth comprised the study group. Placental stillbirth was evident in 33/67 (49.3%). Significantly more women with placental stillbirth were nulliparous, when compared with non-placental stillbirth women (21/33 vs. 9/34, p = 0.002). Mean gestational age was lower for placental, compared with non-placental stillbirth (31.1 ± 6.1 weeks vs. 33.9 ± 4.8 weeks, p = 0.04), as was birth weight. Thirty-six of the 67 women (53.7%) tested positive for at least one thrombophilia. The prevalence of maternal thrombophilia was higher for placental stillbirth women (63.6%), and even higher (69.6%) for women after preterm (<37 weeks) placental stillbirth. Factor V Leiden and/or prothrombin G20210A mutation were much more prevalent in placental versus non-placental stillbirth women (OR 3.06, 95% CI 1.07-8.7).

Conclusions

Placental stillbirth comprises a unique subgroup with specific maternal characteristics. Maternal thrombophilia is highly prevalent, especially in preterm placental stillbirth. This may have implications for the management strategy in future pregnancies in this subgroup.     

A cohort study of Plasmodium falciparum malaria in pregnancy and associations with uteroplacental blood flow and fetal anthropometrics in Kenya

Objective

To use ultrasound to explore the impact of malaria in pregnancy on fetal growth and newborn outcomes among a cohort of women enrolled in an intermittent presumptive treatment in pregnancy (IPTp) with sulfadoxine/pyrimethamine (SP) program in coastal Kenya.

Methods

Enrolled women were tested for malaria at first prenatal care visit, and physical and ultrasound examinations were performed. In total, 477 women who had term, live births had malaria tested at delivery and their birth outcomes assessed, and were included in the study.

Results

Peripheral malaria was detected via polymerase chain reaction among 10.9% (n = 87) at first prenatal care visit and 8.8% (n = 36) at delivery. Insecticide-treated bed nets (ITNs) were used by 73.6% (n = 583) and were associated with decreased malaria risk. There was a trend for impaired fetal growth and placental blood flow in malaria-infected women in the second trimester, but not later in pregnancy. Among women with low body mass index (BMI), malaria was associated with reduced birth weight (P = 0.04); anthropometric measures were similar otherwise.

Conclusion

With IPTp-SP and ITNs, malaria in pregnancy was associated with transient differences in utero, and reduced birth weight was restricted to those with low BMI.     

Plasma and placental nitric oxide levels in women with and without pre-eclampsia living at different altitudes

Objective

To investigate the nitric oxide (NO) levels in the plasma and the placentas of pregnant women with pre-eclampsia and women without pre-eclampsia, and to determine the effect of high or low altitude of residence.

Methods

NO was determined by chemoluminescence and group comparisons were performed.

Results

Women with pre-eclampsia (n = 63) had higher plasma NO levels (38.6 ± 17.44 vs 30.6 ± 12.44 µmol/L, P = 0.004) and higher placental NO levels (38.5 ± 17.0 vs 24.3 ± 7.16 ng/mg protein, P < 0.05) compared with women without pre-eclampsia. A similar trend was found when comparisons were made according to altitude of residence. NO levels were significantly higher in the plasma of pre-eclamptic women living at sea level (41.11 ±18.78 vs 28.96 ± 9.57 µmol/L, P = 0.003), and in the placentas of women living at high altitude (39.51 ± 16.98 vs 21.91 ± 6.64 ng/mg protein, P < 0.0001).

Conclusion

Women with pre-eclampsia had higher plasma and placental NO levels and the differences were associated with altitude of residence.     

The lifespan of men and the shape of their placental surface at birth

Background

Tall men generally lead longer lives than short men. Within the Helsinki Birth Cohort, however, there is a group of boys among whom being tall when they entered school was associated with reduced lifespan. These boys had birthweights and maternal heights above the median for the cohort; but they tended to be lighter at birth than their mother’s body mass index (weight/height²) in pregnancy predicted. We suggested that, while they had grown rapidly in utero, their growth had faltered at some point; and their tallness at age seven was the result of a resumption during infancy of their rapid growth trajectory. We here examine the size and shape of their placentas at birth to gain further insight into their path of fetal growth.

Methods

We examined all cause mortality in the 1217 men who had birthweights and maternal heights above the median for the cohort. Their birth measurements included placental weight and the length and breadth of the placental surface.

Results

Shorter length of the placental surface was associated with increased mortality (p = 0.002). There was no similar trend with the breadth. Mortality rose as the difference between the length and breadth decreased, that is as the surface became rounder. The hazard ratio was 1.10 (1.03–1.18, p = 0.007) for every cm decrease in the difference. Among men with a round placental surface (length-breadth difference 2 cm or less) increased mortality was associated with lower birthweight (p = 0.03 or 0.005 allowing for mother’s body mass index) and shorter gestation, but not with lower head circumference or length.

Conclusion

Reduced lifespan among men is associated with a particular path of early growth. After rapid growth in early gestation, associated with tall maternal stature, soft tissue growth falters in mid-gestation. Rapid growth resumes in late gestation and continues through infancy.     

Postpartum evaluation of stress urinary incontinence among primiparas

Objective

To assess the prevalence of postpartum stress urinary incontinence (SUI); the relationship between postpartum SUI and mode of delivery; and the association between SUI and other obstetric factors.

Method

In this prospective study, 1000 primiparas with no history of UI were recruited and followed up for 4 months after delivery. The χ² and Fisher's Exact tests were used to calculate the effects of the nominal variables.

Result

The prevalence of postpartum SUI was 14.1%, and the mode of delivery was significantly associated with SUI. The prevalence rates were 15.9% after vaginal delivery, 10.7% after elective cesarean section (CS), and 25% after CS performed for obstructed labor. The prevalence of postpartum SUI was similar following spontaneous vaginal delivery and CS performed for obstructed labor (P = .21). Meanwhile, elective CS with no trial of labor was found to be associated with a significantly lower prevalence of postpartum SUI (P = .01; χ² = 12.42). A maternal body mass index greater than 30 before pregnancy and fetal weight higher than 3000 g appeared to be associated with an increased rate of SUI (P = .001; χ² = 17.6 and P = .000; χ² = 22.5, respectively).

Conclusion

Elective CS significantly reduced the rate of postpartum SUI.     

Placental share and hemoglobin level in relation to birth weight in twin anemia-polycythemia sequence

IntroductionTwin anemia-polycythemia sequence (TAPS) is a newly described form of chronic twin transfusion. Previous observational studies noted a discordance between birth weight and individual placental share in TAPS. The purpose of this study was to investigate if fetal growth in monochorionic (MC) twins with TAPS is determined by placental share or by the net inter-twin blood transfusion.MethodsAll consecutive MC twin placentas of live-born twin pairs with and without TAPS examined at our center between June 2002 and February 2014 were included in this study. Hemoglobin (Hb) levels and individual placental share were evaluated at birth and correlated with birth weight share. We excluded MC twin pregnancies with twin–twin transfusion syndrome.ResultsA total of 270 MC twin pregnancies (TAPS group, n = 20; control group without TAPS, n = 250) were included in this study. Donors with TAPS had a lower birth weight than recipients in 90% (18/20) of cases, but a larger placental share in 65% (13/20) of cases. In the TAPS group, birth weight share was positively correlated with Hb share at birth (P < 0.01) but not with placental share (P = 0.54). In the control group without TAPS, birth weight share was strongly correlated with placental share (P < 0.01) but not with Hb share (P = 0.14).DiscussionA relatively larger placental share may enable the survival of the anemic twin in TAPS.ConclusionIn contrast with uncomplicated MC twins, fetal growth in MC twins with TAPS is determined primarily by the net inter-twin blood transfusion instead of placental share.     

Association between first-trimester placental volume and birth weight

Objective

To estimate the correlation between first-trimester placental volume, birth weight, small-for-gestational-age (SGA), and preeclampsia.

Methods

A prospective study of women with singleton pregnancy at 11–13 weeks of gestation was conducted. First-trimester placental volume was measured using three-dimensional ultrasound and reported as multiple of median (MoM) for gestational age. Participants were followed until delivery where birth weight, placental weight, and occurrence of preeclampsia were collected. Non-parametric analyses were performed.

Results

We reached a complete follow-up for 543 eligible women. First-trimester placental volume was significantly correlated with birth weight (correlation coefficient: 0.18; p < 0.0001) and placental weight (cc: 0.22; p < 0.0001) adjusted for gestational age. First-trimester placental volume was smaller in women who delivered SGA neonates (median MoM: 0.79; interquartile range: 0.62–1.00; p < 0.001) and greater in women who delivered large-for-gestational-age neonates (median MoM: 1.13; 0.95–1.49; p < 0.001) when compared to women with neonates between the 10th and 90th percentile (median MoM: 1.00; 0.81–1.25). First-trimester placental volume was not associated with the risk of preeclampsia (cc: 0.01; p = 0.87).

Conclusion

First-trimester placental volume is strongly associated with fetal and placental growth. However, we did not observe a correlation between placental volume and the risk of preeclampsia.     

Maternal BMI and gestational diabetes alter placental lipid transporters and fatty acid composition

IntroductionPlacental fatty acid (FA) uptake and metabolism depend on maternal supply which may be altered when women have a high pre-pregnancy body mass index (BMI) or develop gestational diabetes (GDM). Consequently, an impaired FA transport to the fetus may negatively affect fetal development. While placental adaptation of maternal-fetal glucose transfer in mild GDM has been described, knowledge on placental FA acid metabolism and possible adaptations in response to maternal obesity or GDM is lacking.We aimed to analyze the FA composition and the expression of key genes involved in FA uptake and metabolism in placentas from women with pre-pregnancy normal weight (18.5 ≤ BMI<25 kg/m2), overweight (25 ≤ BMI<30 kg/m²), obesity (BMI ≥ 30 kg/m²), and lean pregnant women with GDM.MethodsPlacental FA content was determined by gas liquid chromatography. Placental mRNA expression of FA transport proteins (FATP1, FATP4, FATP6), FA binding proteins (FABP3, FABP4, FABP7), FA translocase (FAT/CD36) and enzymes (Endothelial lipase (EL) and lipoprotein lipase (LPL)) were quantified by qRT-PCR.ResultsHigh pre-pregnancy BMI and GDM were associated with decreased placental FATP1, FATP4, EL and increased FAT/CD36 and FATP6 expressions. LPL mRNA levels and placental total FA content were similar among groups. Specific FA, including some long-chain polyunsaturated FA, were altered.DiscussionOur results demonstrate that high pre-pregnancy BMI or GDM independently alter mRNA expression levels of genes involved in FA uptake and metabolism and the placental FA profile, which could affect fetal development and long-term health.     

Pregnancy outcomes of expectant management of stable mild to moderate chronic hypertension as compared with planned delivery

Objective

To compare outcomes between elective delivery at 37 weeks of pregnancy and expectant management among pregnant women with mild to moderate chronic hypertension.

Methods

In a two-center study, 76 women with mild to moderate chronic hypertension were randomly allocated to planned delivery at 37 completed weeks (group A) or expectant management for spontaneous onset of labor or reaching 41 weeks (group B) between April 2012 and October 2013. Differences were compared by t test, χ² test, or Fisher exact test. Odds ratios (ORs) with 95% confidence interval (CIs) were determined.

Results

There were no differences in superimposed pre-eclampsia (SPE), severe hypertension, preterm delivery, placental abruption, oligohydramnios, intrauterine growth restriction, or perinatal mortality between the groups. Group B had higher gestational age at delivery (P = 0.001) and birth weight (P = 0.01), but lower cesarean (OR 3.4; 95% CI, 1.2–10.3; P = 0.03) and neonatal care unit admission (OR 5.4; 95% CI, 1.4–21.0; P = 0.01) rates. More women with SPE were diagnosed before than after 37 weeks in group B (P = 0.01). Overall, patients who developed SPE had more adverse pregnancy outcomes than those who did not.

Conclusion

Mild to moderate chronic hypertension could be managed expectantly up to 41 weeks if SPE did not develop.     

Placental structure and inflammation in pregnancies associated with obesity

Background

Pre-gravid obesity is associated with increased morbidity and mortality for both mother and offspring. Recent studies have demonstrated a heightened inflammatory response both systemically and locally within the adipose and placental tissue in women with pre-gravid obesity, which may play a role in mediating the adverse pregnancy outcomes. The aim of this study was to characterise the maternal and placental inflammatory status and investigate associated changes in placental structure in obese women.

Methods

The pro-inflammatory status of a cohort of 47 non-obese (BMI 20-25 kg/m²) and 33 obese (≥30 kg/m²) women was characterised by measuring maternal circulating levels and placental gene expression of pro-inflammatory cytokines, and quantifying immune cell populations within the placenta. The effect of pre-gravid obesity on placental structure was investigated by examining placental maturity, vessel density, the formation of syncytial knots and sprouts, and the degree of fibrin deposition, chorangiosis and muscularisation of vessel walls.

Results

Maternal obesity was associated with significantly greater IL-1β (p < 0.05), IL-8 (p < 0.05), MCP-1 (p < 0.001) and CXCR2 (p < 0.05) mRNA expression within the placenta and higher circulating maternal levels of IL-6 (3.30 ± 0.38 vs. 1.77 ± 0.15 pg/ml) (p < 0.001) compared with non-obese women. There were no differences in the number of CD14⁺, CD68⁺ cells or neutrophils within the placental villi of non-obese and obese women. However there were significantly higher numbers of neutrophils within the interstitial space (p < 0.05). Greater muscularity of placental vessel walls was associated with maternal obesity (p = 0.03), however no other associated structural changes were observed.

Conclusions

Our findings show that although pre-gravid obesity was associated with greater expression of placental pro-inflammatory cytokines and higher circulating IL-6 in pregnancy, there were no major differences in immune cell populations within the placental villi and only a greater degree of muscularity in the vessel walls.     

Adipokines and their relation to maternal energy substrate production,insulin resistance and fetal size

Objective

The role of adipokines in the regulation of energy substrate production in non-diabetic pregnant women has not been elucidated. We hypothesize that serum concentrations of adiponectin are related to fetal growth via maternal fat mass, insulin resistance and glucose production, and further, that serum levels of leptin are associated with lipolysis and that this also influences fetal growth. Hence, we investigated the relationship between adipokines, energy substrate production, insulin resistance, body composition and fetal weight in non-diabetic pregnant women in late gestation.

Study design

Twenty pregnant women with normal glucose tolerance were investigated at 36 weeks of gestation at Uppsala University Hospital. Levels of adipokines were related to rates of glucose production and lipolysis, maternal body composition, insulin resistance, resting energy expenditure and estimated fetal weights. Rates of glucose production and lipolysis were estimated by stable isotope dilution technique.

Results

Median (range) rate of glucose production was 805 (653–1337) μmol/min and that of glycerol production, reflecting lipolysis, was 214 (110–576) μmol/min. HOMA insulin resistance averaged 1.5 ± 0.75 and estimated fetal weights ranged between 2670 and 4175 g (−0.2 to 2.7 SDS). Mean concentration of adiponectin was 7.2 ± 2.5 mg/L and median level of leptin was 47.1 (9.9–58.0) μg/L. Adiponectin concentrations (7.2 ± 2.5 mg/L) correlated inversely with maternal fat mass, insulin resistance, glucose production and fetal weight, r = −0.50, p < 0.035, r = −0.77, p < 0.001, r = −0.67, p < 0.002, and r = −0.51, p < 0.032, respectively. Leptin concentrations correlated with maternal fat mass and insulin resistance, r = 0.76, p < 0.001 and r = 0.73, p < 0.001, respectively. There was no correlation between maternal levels of leptin and rate of glucose production or fetal weight. Neither were any correlations found between levels of leptin or adiponectin and maternal lipolysis or resting energy expenditure.

Conclusion

The inverse correlations between levels of maternal adiponectin and insulin resistance as well as endogenous glucose production rates indicate that low levels of adiponectin in obese pregnant women may represent one mechanism behind increased fetal size. Maternal levels of leptin are linked to maternal fat mass and its metabolic consequences, but the data indicate that leptin lacks a regulatory role with regard to maternal lipolysis in late pregnancy.