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OBJECTIVE: To examine the association of fetal/placental DNA copy number variants (CNVs) with pathologic placental lesions (PPLs) in pregnancies complicated by stillbirth. DESIGN: A secondary analysis of stillbirth cases in the Stillbirth Collaborative Research Network case-control study. SETTING: Multicenter, 59 hospitals in 5 geographic regions in the USA. POPULATION: 387 stillbirth cases (2006–2008). METHODS: Using standard definitions, PPLs were categorized by type including maternal vascular, fetal vascular, inflammatory and immune/idiopathic lesions. Single-nucleotide polymorphism array detected CNVs of at least 500kb. CNVs were classified into two groups: normal, defined as no CNVs>500kb or benign CNVs, and abnormal, defined as pathogenic or variants of unknown clinical significance. MAIN OUTCOME MEASURES: The proportions of abnormal CNVs and normal CNVs compared between stillbirth cases with and without PPLs using the Wald Chi-squared test. RESULTS: Of 387 stillborn fetuses, 327 (84.5%) had maternal vascular PPLs and 60 (15.6%) had abnormal CNVs. Maternal vascular PPLs were more common in stillborn fetuses with abnormal CNVs compared with those with normal CNVs (81.7% vs. 64.2%; p=0.008). The proportions of fetal vascular, maternal/fetal inflammatory, and immune/idiopathic PPLs were similar among stillborn fetuses with abnormal CNVs compared to those with normal CNVs. Pathogenic CNVs in stillborn fetuses with maternal vascular PPLs spanned several known genes. CONCLUSIONS: Abnormal placental/fetal CNVs were associated with maternal vascular PPLs in stillbirth cases. Findings may provide insight on the mechanisms of specific genetic abnormalities associated with placental dysfunction and stillbirth.

To examine the performance of a model combining maternal risk factors, uterine artery pulsatility index (UtA-PI) and estimated fetal weight (EFW) at 19-24 weeks' gestation, for predicting all antepartum stillbirths and those due to impaired placentation, in a training dataset used for development of the model and in a validation dataset.The data for this study were derived from prospective screening for adverse obstetric outcome in women with singleton pregnancy attending for routine pregnancy care at 19 + 0 to 24 + 6 weeks' gestation. The study population was divided into a training dataset used to develop prediction models for placental dysfunction-related antepartum stillbirth and a validation dataset to which the models were then applied. Multivariable logistic regression analysis was used to develop a model based on a combination of maternal risk factors, EFW Z-score and UtA-PI multiples of the normal median. We examined the predictive performance of the model by, first, the ability of the model to discriminate between the stillbirth and live-birth groups, using the area under the receiver-operating-characteristics curve (AUC) and the detection rate (DR) at a fixed false-positive rate (FPR) of 10%, and, second, calibration by measurements of calibration slope and intercept.The study population of 131 514 pregnancies included 131 037 live births and 477 (0.36%) stillbirths. There are four main findings of this study. First, 92.5% (441/477) of stillbirths were antepartum and 7.5% (36/477) were intrapartum, and 59.2% (261/441) of antepartum stillbirths were observed in association with placental dysfunction and 40.8% (180/441) were unexplained or due to other causes. Second, placental dysfunction accounted for 80.1% (161/201) of antepartum stillbirths at 32 weeks' gestation, 54.2% (52/96) at 32 + 0 to 36 + 6 weeks and 33.3% (48/144) at ≥ 37 weeks. Third, the risk of placental dysfunction-related antepartum stillbirth increased with increasing maternal weight and decreasing maternal height, was 3-fold higher in black than in white women, was 5.5-fold higher in parous women with previous stillbirth than in those with previous live birth, and was increased in smokers, in women with chronic hypertension and in parous women with a previous pregnancy complicated by pre-eclampsia and/or birth of a small-for-gestational-age baby. Fourth, in screening for placental dysfunction-related antepartum stillbirth by a combination of maternal risk factors, EFW and UtA-PI in the validation dataset, the DR at a 10% FPR was 62.3% (95% CI, 57.2-67.4%) and the AUC was 0.838 (95% CI, 0.799-0.878); these results were consistent with those in the dataset used for developing the algorithm and demonstrate high discrimination between affected and unaffected pregnancies. Similarly, the calibration slope was 1.029 and the intercept was -0.009, demonstrating good agreement between the predicted risk and observed incidence of placental dysfunction-related antepartum stillbirth. The performance of screening was better for placental dysfunction-related antepartum stillbirth at 37 weeks' gestation compared to at term (DR at a 10% FPR, 69.8% vs 29.2%).Screening at mid-gestation by a combination of maternal risk factors, EFW and UtA-PI can predict a high proportion of placental dysfunction-related stillbirths and, in particular, those that occur preterm. Such screening provides poor prediction of unexplained stillbirth or stillbirth due to other causes. © 2021 International Society of Ultrasound in Obstetrics and Gynecology.

Placental inflammatory lesions are important findings that lead fetal and neonatal morbidity and mortality, and can be divided into two broad subcategories, acute inflammation caused by microorganisms and chronic inflammation caused by host immune responses. Recently, a diagnostic framework for these lesions has been established, and uniform diagnostic criteria have been recommended by the Amsterdam International Consensus Group. Chorioamnionitis is representative of the acute inflammatory lesion, and is the most frequent pathological diagnosis in placental pathology. The hallmark of chorioamnionitis is neutrophil infiltration in the membrane/chorioamnionic plate and fetal vessels. The inflammatory response can be both maternal (inflammation in the membrane or chorioamnionic plate) and fetal (inflammation in the fetal vessels-umbilical vessels or chorionic vessel). Recent studies have shown that the fetal inflammatory response is associated with neonatal mortality and morbidity. Furthermore, chronic inflammatory lesions, such as villitis of unknown etiology and chronic histiocytic intervillositis, are also important. Although their etiology remains unknown, the maternal immune response against paternal antigens has been considered a possible factor. These inflammatory lesions are associated with fetal demise and fetal growth restriction. Inflammatory lesions in the placenta are useful for understanding intrauterine conditions, guiding treatment, and predicting complications.

Background Late onset intra-uterine growth restriction (IUGR) refers to impaired growth and development of the fetus, characterized by placental morphological abnormalities that affect the fetus supply of nutrients. Human Leukocyte Antigen-G (HLA-G) is physiologically expressed during pregnancy, but in normal placenta decreased during the last weeks of gestation possibly inducing childbirth. Several viruses involved in congenital infection, such as herpesviruses, exploit HLA-G expression as an immune-escape mechanism. To date, despite different congenital herpetic infections have been associated with late IUGR, no direct implication of HHV-6 infection, has been reported. Methods We evaluated HLA-G expression and HHV-6 infection in 11 placentas from late onset IUGR newborns and 11 placentas from uncomplicated pregnancies by histopathological and immunohistochemistry analysis. Results We found higher levels of HLA-G expression and HHV-6 presence in IUGR placenta samples compared with control placenta samples. Conclusions We report HHV-6 staining in IUGR placenta samples, characterized by high HLA-G expression. These preliminary data suggest a possible involvement of HHV-6 infection in HLA-G deregulation that might affect vessel remodeling and prevent the correct pregnancy outcome in IUGR condition. This article is protected by copyright. All rights reserved.

Aim To determine which genes are important in placenta by network analysis. Methods Placenta expressing genes were screened from RNA-Seq data. Protein-protein interaction data were downloaded from STRING (v11.0) database. Google PageRank (PR) algorithm was used to identify important placental genes from protein interaction network. Six placental disease-related datasets were downloaded from NCBI GEO database, and the differential expression of the 99 genes was identified. Results We calculated PR for each placenta expressing gene and defined the top 99 genes with high PR as important genes. GAPDH has the highest PR. The 99 genes had different expression pattern in placental cell types. FN1 is up-regulated in 8 w EVT compared to 8 w CTB and 24 w EVT compared to 8 w EVT. HSPA4 is down-regulated in 8 w EVT compared to 8 w CTB and 24 w EVT compared to 8 w EVT. MIB2, TLR4, and UBB are consistently changed in preeclampsia (PE). UBB and ACTG1 were identified to be down-regulated in fetal growth restriction (FGR). SOD1 is down-regulated in preterm birth placenta. Conclusion Our findings confirmed that the importance of these genes in placenta-related diseases, and provide new candidates (MIB2, UBB, ACTG1, and SOD1) for placenta-related disease diagnosis and treatment.

Aim This study aimed to evaluate the clinical features and pregnancy outcomes of placental mesenchymal dysplasia (PMD) in Japan. Methods We requested detailed clinical information and placental tissue of PMD cases in 2000-2018 from Japanese facilities with departments of obstetrics and gynecology and analyzed the pregnancy course and neonatal outcomes. Results We collected 49 cases of PMD. Of 18 patients with measured maternal serum alpha-fetoprotein (MSAFP) levels, 15 (83.3%) had elevated levels. Maternal serum human chorionic gonadotropin (MShCG) levels were transiently elevated in five (17.8%) of 28 patients. Forty-seven patients continued their pregnancies. All pregnancies were singleton and 40 (85.1%) were associated with adverse events including fetal growth restriction (FGR), threatened premature delivery, fetal demise, and hypertensive disorder of pregnancy in 34 (72.3%), 14 (29.8%), eight (17.0%), and six (12.8%) patients, respectively. Of 47 infants, there were eight stillbirths. There were 40 (85.1%) female infants, and eight (17.0%) had Beckwith-Wiedemann syndrome. Of 39 live births, 23 (59.0%) were associated with premature induction of labor or cesarean section for obstetric indications related to FGR. Eighteen (46.2%) neonates had complications. PMD-affected placentas were pathologically heterogeneous in both grossly PMD-affected and non-affected areas. Conclusions Our study included the largest number of PMD cases with detailed clinical information. PMD is a high-risk condition for both the mother and the child. Elevated MSAFP levels with normal MShCG levels indicate PMD. Conventional perinatal management of FGR in Japan might be effective in reducing the fetal mortality rate.

From the start of the global COVID‐19 pandemic, a lot of attention has been focused on how SARS‐CoV‐2 (severe acute respiratory syndrome coronavirus type 2) impacts pregnancy. The current evidence suggests that pregnant women may be at an increased risk for more severe COVID‐19 disease and an increase in maternal death rate has been observed worldwide (1,2).

Objective To analyze all the variables in women who received fibrinogen for postpartum hemorrhage (PPH) using hierarchical cluster analysis, to provide greater insight into the risk variables involved in these women. Methods This retrospective study of women with at least 500 mL of bleeding at birth or during the postpartum period and treated with fibrinogen was conducted at the Department of Obstetrics and Gynecology, Ataturk University School of Medicine from January 2013 to January 2018. Data on the women were obtained from medical records and various risk variables were recorded and analyzed using hierarchical cluster analysis. Results A total of 114 women with PPH were included in the study. Based on a dendrogram, three main clusters of similar quality variables were created: 1) gravida, parity, age, cervical/vaginal hematoma, laparotomy, hypogastric artery ligation, uterine artery embolization, uterine artery ligation, uterine atony, distance from outer center, lowest hemoglobin, preoperative platelets, endometritis, preoperative white blood cells; 2) lowest fibrinogen, highest fibrinogen, type of birth, placenta invasion anomaly, Bakri balloon tamponade, postpartum hysterectomy, preoperative activated partial thromboplastin time (APTT), preoperative international normalized ratio (INR), placental abruption, in-utero ex fetus; 3) postoperative APTT, postoperative INR, maternal mortality, erythrocyte transfusion, plasma transfusion, hospital stay time, disseminated intravascular coagulation/HELLP syndrome, highest hemoglobin, blood group, postoperative platelets, platelet transfusion, pre-eclampsia/eclampsia, fibrinogen extract. Conclusion According to the cluster analysis, we should keep fibrinogen extract in the foreground especially in the treatment of hemorrhage in patients with variable conditions. As a result, we can determine whether fibrinogen extract, which has a high economic cost, should be kept at each center. We can also direct which patient will be referred in accordance with the referral steps.

Objective The placental development has been shown to be compromised in pregnancies affected by fetal congenital heart defects (CHD). This study aimed to investigate the frequency of complications related to utero-placental insufficiency in pregnancies with and without major CHD. Method This retrospective case-control study was conducted at a Fetal Echocardiography Center in Milan. The following outcomes were compared between the two groups: preeclampsia (PE), small for gestational age (SGA), placental disorders and preterm birth (PTB). The logistic regression analysis was adjusted for maternal age, parity, co-morbidities and mode of conception. Results The CHD group (n = 480) showed significantly increased incidence of PE (2.9% vs 0.9%; aOR, 6.50; 95% CI, 1.39-30.41; P = .017) as compared to the control group (n = 456). Placental disorders occurred more frequently in the CHD than in controls, but the increased risk showed only a borderline significance (4.5% vs 3.3%; aOR, 2.56; 95% CI, 0.99-1.02; P = .046). There was a significantly higher risk of SGA in CHD than in controls (8.7% vs 3.9%; aOR, 3.37; 95% CI, 1.51-7.51; P = .003). PTB occurred in 65/477 (13.6%) cases and in 39/447 (8.7%) controls (P = .022) (aOR, 2.17; 95% CI, 1.24-3.81; P = .007). Conclusion Major CHD are significantly associated with the risk of PE, SGA and PTB.

Background There are few publications on occurrence of nonthyroidal illness syndrome in foals and on the prognostic value of cortisol and thyroid hormone (TH) concentrations in newborn foals. Objectives To determine serum cortisol and TH concentrations (total and free thyroxine: T4 and FT4; total and free triiodothyronine: T3 and FT3) in foals born from mares with placentitis, to determine their association with survival, and their use as prognostic markers. Animals A cohort of 29 newborn foals comprising 5 Control, 14 Low‐risk, and 10 Sick foals were evaluated over the first week of life. Methods In this prospective study foals born to mares with experimentally‐induced placentitis were assigned to Low‐risk or Sick groups while foals born to control mares were classified as Control based on clinical findings. Foals were also classified as Term (n = 13), Dysmature (n = 7), or Premature (n = 9), and survival rate was recorded. Serum cortisol and TH hormone concentrations were measured at 0, 12, 24, 48, and 168 hours of life. Results Sick non‐surviving foals had lower (P

OBJECTIVES To examine the feasibility and effectiveness of a two-stage ultrasound screening strategy for detection of vasa previa and to estimate the potential impact of screening on prevention of stillbirth. METHODS This was a retrospective study of data from prospective screening for vasa previa in singleton pregnancies, undertaken at the Fetal Medicine Unit at Medway Maritime Hospital, UK, between 2012 and 2018. Women booked for prenatal care and delivery in our hospital had routine ultrasound examinations at 11-13 and 20-22 weeks' gestation. Those with velamentous cord insertion at the inferior part of the placenta at the first-trimester scan and those with low-lying placenta at the second-trimester scan were classified as high-risk for vasa previa and had transvaginal sonography searching specifically for vasa previa, at the time of the 20-22-week scan. The management and outcome of cases with suspected vasa previa is described. We excluded cases of miscarriage or termination at

INTRODUCTION Pregnancy-related medical complications are associated with a 2- to 5-fold increased risk of preterm birth (PTB), but the nature of this etiologic relation in context with maternal factors remains poorly understood. Previous studies have generally treated maternal age as a confounder but overlooked its potential as an effect modifier, whereby the magnitude of the effect of complications on PTB could differ significantly across age groups. We investigated whether advanced maternal age (≥35 years) modified the association between pregnancy complications and PTB, and compared population-attributable fractions of PTB from complications in women older vs younger than 35 years. MATERIAL AND METHODS We analyzed population-based, cross-sectional data from the Alberta Discharge Abstract Database for women aged 18-50 years with singleton live births in hospital between 2014 and 2017 (n = 152 246). Complications were preeclampsia, gestational diabetes, and placental disorders identified using diagnostic codes. Outcomes were spontaneous (sPTB) or iatrogenic (iPTB) PTB before 37 weeks of gestation. We estimated risk ratios and risk differences using modified Poisson and log binomial regression, respectively, adjusting for confounders (pregnancy history, comorbidities). Population-attributable fractions estimates were calculated from risk ratios. Age modification was tested using interaction terms and Z-tests. RESULTS Prevalence of advanced maternal age was 19.2%. Pregnancy complications and s/iPTB were more common among women aged ≥35 years. Age modified the risk of PTB from preeclampsia only, with risk differences of 9.9% (95% CI 7.2%-12.6%) in older women vs 6.1% (95% CI 4.8%-7.4%) in younger women (P-interaction = 0.012) for sPTB, and 29.5% (95% CI 26.0%-33.1%) vs 20.8% (95% CI 18.9%-22.6%, P-interaction

Background Stillbirth, defined as foetal death ≥20 weeks' gestation, is associated with poor foetal growth and is often attributed to placental abnormalities, which are also associated with poor foetal growth. Evaluating inter-relationships between placental abnormalities, poor foetal growth, and stillbirth may improve our understanding of the underlying mechanisms for some causes of stillbirth. Objective Our primary objective was to determine whether poor foetal growth, operationalised as small for gestational age (SGA), mediates the relationship between placental abnormalities and stillbirth. Methods We used data from the Stillbirth Collaborative Research Network study, a population-based case-control study conducted from 2006-2008. Our analysis included 266 stillbirths and 1135 livebirths. We evaluated associations of stillbirth with five types of placental characteristics (developmental disorders, maternal and foetal inflammatory responses, and maternal and foetal circulatory disorders) and examined mediation of these relationships by SGA. We also assessed exposure-mediator interaction. Models were adjusted for maternal age, race/ethnicity, education, body mass index, parity, and smoking status. Results All five placental abnormalities were more prevalent in cases than controls. After adjustment for potential confounders, maternal inflammatory response (odds ratio [OR] 2.58, 95% confidence interval [CI] 1.77, 3.75), maternal circulatory disorders OR 4.14, 95% CI 2.93, 5.84, and foetal circulatory disorders OR 4.58, 95% CI 3.11, 6.74 were strongly associated with stillbirth, and the relationships did not appear to be mediated by SGA status. Associations for developmental disorders and foetal inflammatory response diverged for SGA and non-SGA births, and strong associations were only observed when SGA was not present. Conclusions Foetal growth did not mediate the relationships between placental abnormalities and stillbirth. The relationships of stillbirth with maternal and foetal circulatory disorders and maternal inflammatory response appear to be independent of poor foetal growth, while developmental disorders and foetal inflammatory response likely interact with foetal growth to affect stillbirth risk.

AIM The high rate of stored preoperative autologous blood wastage is concerning. This study analyzed patients who provided preoperative autologous blood donations (PABDs) for massive bleeding during surgery for placenta previas and low-lying placentas, and investigated the optimal PABD storage volume required to avoid allogeneic transfusion. METHODS Of 386 patients who provided PABDs at our hospital from 2008 to 2013, 269 patients with placenta previas or low-lying placentas were retrospectively analyzed. The PABD storage volumes were stratified into four groups based on the amounts stored, and the allogeneic transfusion usage frequencies were compared. RESULTS A total of 124 patients (46.1%) received PABDs and 12 patients (4.5%) received allogeneic transfusions. The average PABD volume wasted was 23 940 mL/year. The allogeneic transfusion utilization rate was significantly higher in the 1- to 300-mL group (17.2%) than in the 301- to 600-mL (1.69%), 601- to 900-mL (3.82%), and 901- to 1200-mL (0%) groups (P

Even though the placenta has been known for millennia, it is still considered one of the most complex and least understood human organs. Imaging of the placenta is gaining attention due to its impact on fetal and maternal outcomes. MRI plays a vital role in evaluation of inconclusive cases by ultrasonography. It enables precise mapping of placental abnormalities for proper multidisciplinary planning and management. In this article we provide a comprehensive in-depth review of the role of antenatal MR in evaluating "The Placenta." We will describe the protocols and techniques used for MRI of the placenta, review anatomy of the placenta, describe MRI features of major placental abnormalities including those related to position, depth of implantation, hemorrhage, gestational trophoblastic neoplasia, and retained products of conception and discuss the added value of MRI in the management and preoperative planning of such abnormalities. Level of Evidence: 3 Technical Efficacy Stage: 5 J. Magn. Reson. Imaging 2019;50:1702-1717.

OBJECTIVE: To evaluate the transgenerational transmission of small-for-gestational age (SGA). METHODS: This was a cohort study of a random sample of 2043 offspring delivered between 1975 and 1993 at Hospital Sant Joan de Déu in Barcelona. Exclusion criteria were multiple pregnancy, aneuploidy or genetic syndrome, major birth defects, severe mental disease and macrosomia. Eligible individuals were contacted and those with at least one offspring were included in the study. Participants were classified according to the presence of SGA (defined as birth weight < 10(th) percentile) at birth. Multiple regression analysis was used to determine the presence of SGA or placenta-mediated disease (defined as the presence of SGA, pre-eclampsia, gestational hypertension and/or placental abruption) in the following generation. RESULTS: Of 623 individuals who agreed to participate, 152 (72 born SGA and 80 born appropriate-for-gestational age (AGA)) were reported to have at least one child. Descendants of SGA individuals presented with a lower birth-weight percentile (median, 26 (interquartile range (IQR), 7-52) vs 43 (IQR, 19-75); P < 0.001) and a higher prevalence of SGA (40.3% vs 16.3%; P = 0.001) and placenta-mediated disease (43.1% vs 17.5%; P = 0.001) than did the offspring of AGA individuals. After adjustment for confounding variables, parental SGA background was associated with an almost three-fold increased risk of subsequent SGA or any placenta-mediated disease in the following generation. This association was stronger in SGA mothers than in SGA fathers. CONCLUSIONS: Our data provide evidence suggesting a transgenerational transmission of SGA, highlighting the importance of public health strategies for preventing intrauterine growth impairment. Copyright © 2018 ISUOG. Published by John Wiley & Sons Ltd.

Prolactin family 7, subfamily d, member 1 (Prl7d1), a member of the expanding prolactin family, is mainly expressed in the placental junctional zone (including trophoblast giant cells and spongiotrophoblast cells) with peak expression observed at 12 days postcoitum (dpc) in mice. Previous studies have shown that PRL7D1 is a key mediator of angiogenesis in vitro; however, its physiological roles in placental development in vivo have not been characterized. To address this issue, we deleted Prl7d1 in mice and demonstrated that its absence results in reduced litter size and fertility. Histologically, Prl7d1 mutants exhibited striking placental abnormalities at 12.5 dpc, including a reduction in the proportion of labyrinth layers and a significant increase in decidual natural killer cells, glycogen trophoblasts, and trophoblast giant cells in the junctional zone. Moreover, placentas from Prl7d1-null mice displayed a thickened decidual spiral artery. Notably, these negative effects were more pronounced in male fetuses. Further RNA-sequencing analysis showed that Prl7d1 deletion results in significant differences in the placental transcriptome profile between the two sexes of fetuses. Together, this study demonstrates that Prl7d1 possesses antiangiogenic properties in deciduas and inhibits the development of junctional zone, which potentially alters the functional capacity of the placenta to support optimal fetal growth. Moreover, of note, the role of Prl7d1 in the placenta is regulated in a fetal sex-specific manner.

OBJECTIVE To gather additional data on pregnancy outcome when a chorionic bump is detected at the time of the 11- to 13-week scan. METHODS The presence of a chorionic bump was prospectively recorded in a database of women presenting for their first-trimester sonographic screening. Clinically relevant information was obtained by reviewing ultrasound reports and medical records or contacting the referring obstetrician or the parents themselves. RESULTS During a 4.5-year study period from June 2014 to December 2018, a chorionic bump was identified in 23 out of 3375 pregnancies, for a prevalence of 1/147 or 0.7%. All women were asymptomatic at the time of evaluation. The chorionic bump was single in 21 (91%) cases, located in the central part of the placenta in 17 (74%) cases, and the median largest diameter was 20 mm (range, 10-43). Although the placenta was low-lying in 14 (61%) cases, all but one patient had a normally located placenta at the midtrimester anatomy scan. With the exception of one pregnancy complicated with trisomy 21, the outcome was universally good. CONCLUSION Our experience suggests that a chorionic bump detected during the 11- to 13-week scan is usually a transient, is incidental finding, and probably has no clinical significance.

Background: Low-lying placentas are positioned close to the internal os of the cervix. The preferred way of delivery within this group is unclear. Objectives: To review the literature on the success of a vaginal delivery with a low-lying placenta. Search strategy: We searched OVID EMBASE and MEDLINE for studies on vaginal delivery with a low-lying placenta. Data collection and analyses: Data was extracted on successful vaginal delivery and emergency caesarean section due to haemorrhage. We distinguished between different distances between the cervical os and the placenta (internal os distance, IOD); 0–10, 11–20, and >20 mm. A meta-analysis of proportions was made for successful vaginal delivery and emergency caesarean section at every cut-off value. Maternal morbidity (i.e. antepartum blood loss, postpartum haemorrhage and blood transfusion) at different cut-off values was evaluated. Main results: Of the 999 articles retrieved, 10 articles met our inclusion criteria. A vaginal delivery was successful at an IOD of 0–10 mm in 43%, at an IOD of 11–20 mm in 85%, and at an IOD of >20 mm in 82%. A shorter IOD had a higher chance of antepartum haemorrhage, whereas a larger IOD needed postpartum blood transfusion more often. Postpartum haemorrhage did not depend on IOD. Conclusion: A low-lying placenta is not a contraindication for a trial of labour, and the morbidity in these women is not increased. However, women with a low-lying placenta have a higher chance of an emergency caesarean section compared with women with a placenta outside the lower uterine segment. Therefore, shared decision-making is mandatory in case of a trial of labour. Tweetable abstract: This systematic review demonstrates the possibility of a vaginal delivery in women with a low-lying placenta within 20 mm of the cervix.

Chronic histiocytic intervillositis (CHI) is a pregnancy disorder characterized by infiltration of maternal macrophages into the intervillous space of the human placenta, often with accompanying perivillous fibrin deposition. CHI is associated strongly with foetal growth restriction and increased risk of miscarriage and stillbirth. Although rare, affecting 6 in every 10 000 pregnancies beyond 12 weeks’ gestation, the rate of recurrence is high at 25%–100%. To date, diagnosis of CHI can only be made post‐delivery upon examination of the placenta due to a lack of diagnostic biomarkers, and criteria vary across publications. No treatment options have shown proven efficacy, and CHI remains a serious obstetric conundrum. Although its underlying aetiology is unclear, due to the presence of maternal macrophages and the reported increased incidence in women with autoimmune disease, CHI is hypothesized to be an inappropriate immune response to the semi‐allogeneic foetus. Given this lack of understanding, treatment approaches remain experimental with limited rationale. However, there is recent evidence that immunosuppression and antithrombotic therapies may be effective in preventing recurrence of associated adverse pregnancy outcomes. With similarities noted between the pathological features of CHI and acute rejection of solid organ transplants, further investigation of this hypothesis may provide a basis for tackling CHI and other immune‐related placental conditions. This review will explore parallels between CHI and allograft rejection and identify areas requiring further confirmation and exploitation of this comparison.

Background Anhydramnios results from the poor development of the placenta or problems with intrauterine development of the kidneys or urinary tract. Complete lack of amniotic fluid indicates a severe problem with the organs of the urinary system. The genes associated with anhydramnios show very diversity and are not yet well defined. Methods Whole‐exome sequencing (WES) was used for an aborted male case around the 20th week of gestation diagnosed with anhydramnios. The resulted deleterious variants were verified by Sanger sequencing. Pathogenicity of deleterious variants was explored by in silico analysis. Results A maternally inherited deleterious frameshift variant, c.1454_1455insC, p.(S486Ffs29) in exon 9 and two paternally inherited missense variants c.1037C > G, p.(Ser346Trp) in exon 7 and c.1465A > G, p.(Asn489Asp) in exon 9 of Angiotensin‐I‐Converting Enzyme (ACE) gene were found and confirmed by Sanger sequencing. c.1454_1455insC, p.(S486Ffs29) and c.1037C > G, p.(Ser346Trp) were identified as two novel compound heterozygous deleterious variants. The pathogenicity of these deleterious variants was determined by in silico analysis and both the deleterious variants disrupt the structure of the ACE protein. Conclusion Two novel compound heterozygous variants were identified in the case with anhydramnios, which may be associated with pathogenicity of anhydramnios. Our data also revealed that the WES approach may provide helpful information for genetic counseling of the families with anhydramnios., Two novel compound heterozygous deleterious variants in ACE were identified in the case with anhydramnios. Both the deleterious variants disrupt the structure of the ACE protein and in silico analysis indicates the pathogenicity of these deleterious variants. The identified novel genetic defects may be associated with the pathogenicity of anhydramnios. WES approach may provide helpful information for genetic counseling of the families with anhydramnios.

AIM The association between methylenetetrahydrofolate reductase (MTHFR) C677T polymorphism and intervillous and decidual pathology in patients with pregnancy loss was investigated. METHODS We performed a cross-sectional study on 243 patients presenting with pregnancy loss for the degree of intervillous fibrin and thrombosis (IT), and decidual fibrin and thrombosis (DT) and determined their MTHFR C677T genotypes. Overall differences in age, body mass index (BMI), gravidity, parity, number of pregnancy losses and gestational period when the pathologic samples were obtained, also were determined. RESULTS There were no significant differences in age, BMI, gravidity, parity, number of pregnancy losses and gestational period, relative to MTHFR C677T genotype (TT vs CT vs CC). There were significantly more T allele carriers and TT genotype patients among patients with severe IT (odds ratio [OR] 1.653, P = 0.033 and OR 2.246, P = 0.032, respectively) and those with severe IT and decidual thrombosis (OR 2.602, P = 0.012 and OR 3.375, P = 0.035, respectively). The CC genotype was protective against the four studied pathologic grades. CONCLUSION To our knowledge, this is the first study showing that the MTHFR C677T TT genotype and T allele are associated with severe intervillous and decidual pathologies in patients with pregnancy loss. Differences in pathologic grades of MTHFR C677T TT genotype could support the hypothesis that further periconceptional treatment for pregnancy loss could be customized depending on single nucleotide polymorphisms.

PROBLEM Vitamin D is well-known for having anti-inflammatory and immunomodulatory properties. Impaired maternal vitamin D status has been known to increase the risk of adverse pregnancy outcomes like pre-term birth. The present study aims to evaluate the impact of fetal cord serum 25-hydroxyvitamin D-mediated signaling in mediating inflammatory responses in placenta during pre-term birth. METHOD OF STUDY For the above purpose, cord serum 25 hydroxyvitamin D 25(OH)D were measured in term (n = 20) and pre-term (n = 20) born babies using ELISA. Vitamin D downstream signaling has also been checked in placenta (VDR, CYP27B1, cathelicidin LL37) along with expression of inflammatory markers (S100A8, HMGB1, TLR2, p-NF-kappaB) using Western blotting and immunohistochemistry. Pearson correlation model was used to do correlation study. RESULTS Compared with term born babies (59.31 ± 3.476), decline in cord serum 25(OH)D levels is observed in pre-term born babies (22.26 ± 1.083, P =

Until delivery, the placenta plays an important mediator role between mother and fetus. This unit is affected by peristatic conditions, such as acute or chronic maternal diseases, malnutrition, drugs, and others. But also genetic factors and fetal malformations due to embryonic developmental disorders may contribute to macroscopically visible changes and functional disorders of the placenta. In a constantly ongoing progress of maturation, the placenta records and saves changes due to fetal distress partly as maturation disorders. Understanding of maturation disorders might, therefore, be an important contribution to a better understanding of influences on villous differentiation and might improve follow up and fetal outcome to reduce recurrence risk. However, an internationally unified classification system of maturation disorders does not exist. In this review, terminology, trials, and classifications of villous maturation disorders are summed up and compared, to pinpoint the need of agreement on an international unified and reproducible classification of maturation disorders.

Implantation abnormalities are a group of disorders encompassing several entities with different degree of severity. This section will cover the etiopathogenesis, imaging findings, definition, risk factors, and pathology of the abnormally located and morbidly adherent placenta.

The placenta is one of the most exciting organs. It is dynamic; its morphology and function continuously develop and adjust over its brief life span. It mediates the physiology of two distinct yet highly interconnected individuals. The pathology that develops in the placenta, and the adaptations the placenta undergoes to mitigate this pathology, may influence the later life health of the mother and baby (Circ Res, 116, 2015, 715; Hum Reprod Update, 17, 2011, 397; Nutr Rev 71, 2013, S88; Placenta, 36, 2015, S20). Pathological placenta examination may reveal macroscopic and microscopic patterns that provide valuable information to the obstetricians, neonatologists, and pediatricians caring for the family. The placenta often plays a key role in understanding adverse fetal outcomes such as hypoxic brain injury, cerebral palsy, fetal growth restriction, stillbirth, and neonatal death (Placenta, 35, 2014, 552; Placenta, 52, 2017, 58; Placenta, 30, 2009, 700; Obstet Gynecol, 114, 2009, 809; Clin Perinatol, 33, 2006, 503; Pediatr Dev Pathol, 11, 2008, 456; Arch Pathol Lab Med, 124, 2000, 1785). Moreover, it may help to understand the pathophysiology of pregnancy, improve management of subsequent pregnancies, and assist in medicolegal assessment. Placental pathologic examination may even provide evidence of susceptibility to adult-onset diseases such as diabetes (Pediatr Dev Pathol, 6, 2003, 54; Diabetes Metab, 36, 2010, 682; BJOG, 113, 2006, 1126; Int J Gynaecol Obstet, 104, 2009, S25; Zentralbl Gynakol, 97, 1975, 875). Pathologic examination of the placenta may thus be of tremendous value, particularly for those women experiencing an adverse pregnancy outcome. However, this potential utility may be entirely wasted, if the findings are not communicated in an effective manner to the appropriate clinicians. An optimized, readily understandable report of pathological findings is essential for clinical utility.

The placenta is a fetal organ, composed of fetal DNA and as such reflects the fetal phenotype. The placenta consists of an umbilical cord, fetal membranes (amnion and chorion), and the placental disc which in turn is comprised of villous tissue. Both maternal and fetal disorders have placental sequelae and placental abnormalities can affect both maternal and fetal well-being. As such, placentas are often helpful in future maternal and neonatal healthcare. Thus, examination of the placenta is important for both mother and infant. On this basis, a list of indications for placental examinations has been created by a multidisciplinary group of pathologists, maternal-fetal-medicine specialists, and neonatologists that, if followed, will ensure that the vast majority of placentas that ultimately show any significant pathology will be examined (Arch Pathol Lab Med, 121, 1997, 449-76). This list include fetal, maternal, and placental indications. This chapter will discuss those indications as well as give a brief overview of macroscopic placental examination and procedure.

Fetal vascular malperfusion is the most recent term applied to a group of placental lesions indicating reduced or absent perfusion of the villous parenchyma by the fetus. The most common etiology of malperfusion is umbilical cord obstruction leading to stasis, ischemia, and in some cases thrombosis. Other contributing factors may include maternal diabetes, fetal cardiac insufficiency or hyperviscosity, and inherited or acquired thrombophilias. Severe or high grade fetal vascular malperfusion is an important risk factor for adverse pregnancy outcomes including fetal growth restriction, fetal CNS injury, and stillbirth. Overall recurrence risk for subsequent pregnancies is low.

The placenta functions as a shield against infection of the fetus. The innate and adaptive immune defenses of the developing fetus are poorly equipped to fight infections. Infection by bacteria, viruses, and protozoa may cause infertility, spontaneous abortion, stillbirth, growth retardation, anomalies of development, premature delivery, neonatal morbidity, and mortality. However, appreciation of the human microbiome and host cell-microbe interactions must be taken into consideration as we try to determine what interactions are pathologic. Infection is typically recognized histologically by the presence of inflammation. Yet, several factors make comparison of the placenta to other human organs difficult. The placenta comprises tissues from two persons, complicating the role of the immune system. The placenta is a temporary organ. It must be eventually expelled; the processes leading to partuition involve maternal inflammation. What is normal or pathologic may be a function of timing or extent of the process. We now must consider whether bacteria, and even some viruses, are useful commensals or pathogens. Still, recognizing infection of the placenta is one of the most important contributions placental pathologic examination can give to care of the mother and neonate. This review provides a brief overview of placental defense against infection, consideration of the placental microbiome, routes of infection, and the histopathology of amniotic fluid infection and TORCH infections.

Twin placentas are frequently received in pathology laboratories for evaluation of chorionicity and because twin pregnancies have higher rates of pregnancy complications. In addition to pathologies common in singleton pregnancies, twin pregnancies have increased frequencies of complications such as preterm birth and velamentous cord insertions and also are affected by complications unique to multiple pregnancies that are mediated by vascular connections between the placental territories of certain types of twins. This article aims to provide an approach to examination of the twin placenta for practicing pathologists or those interested in placental pathology while outlining the key characteristics of twin complications as seen in the placenta.

Here, we review three important placental pathologies with significant clinical implications and recurrence risks. They are, in order of most to least frequently seen, villitis of unknown etiology, chronic histiocytic intervillositis, and massive perivillous fibrin deposition (also known as maternal floor infarction). These entities occur in both preterm and term gestations and are observed more frequently with maternal and obstetric disorders including prior pregnancy loss, hypertension/preeclampsia, and autoimmune disease. They are associated with, and probably the cause of, significant perinatal morbidity and mortality including intrauterine growth restriction, fetal and neonatal demise, and fetal/neonatal neurocompromise (seizures and cerebral palsy). All three entities have high recurrence risks, with recurrence rates ranging from 34 to 100%. The histologic features of villitis of unknown etiology, chronic histiocytic intervillositis, and massive perivillous fibrin deposition are described herein. We discuss the clinical associations and suggest the subsequent clinical and pathological evaluation. Hypotheses as to the biology of these lesions are reviewed.

_Introduction:_ Women with a history of placenta-related pregnancy complications, such as preeclampsia, intrauterine growth restriction or preterm delivery, have an increased risk for recurrence of such complications. This recurrence is likely the result of underlying endothelial dysfunction that leads to abnormal placentation, especially in complications with an early onset. This study provides an overview of biomarkers of placental development and function in pregnancies from women with a history of placenta-related complications. _Material and methods:_ A systematic literature search was conducted limited to human studies and including keywords related to a history of placenta-related complications and markers of placental development and function. Two independent reviewers assessed eligibility and quality of 1553 retrieved unique articles. _Results:_ Five articles reporting on placental development and function in women with an obstetric history of preeclampsia (n = 3), intrauterine growth restriction (n = 1) and preterm delivery (n = 2) were eligible for quality assessment. We identified associations between a history of preeclampsia and abnormal placental histological findings at term in the current pregnancy, but found contradictory results regarding presence of uterine artery notching. In women with a history of very preterm delivery (

Introduction Mothers at risk of preterm birth are treated with antenatal corticosteroids, which have advantageous effects for prematurely born infants. Accelerated villous maturation in the placenta is also associated with improved perinatal outcome. The primary aim of this study was to examine the association between antenatal corticosteroids and accelerated villous maturation. The secondary aim was to study associations with other placental pathologies. Material and methods A retrospective cohort study including 105 women who had (n = 75) or had not (n = 30) been treated with antenatal corticosteroids. The women gave birth between 22+0 and 26+6 weeks of gestation in Stockholm County between 1 April 2004 and 31 March 2007. A pathologist blinded to all clinical data except gestational age examined the placental slides to identify pathology parameters. The outcomes were correlated with antenatal corticosteroid treatment, and confounding factors were adjusted using logistic regression. Results Accelerated villous maturation was significantly higher in the group treated with corticosteroids (odds ratio 16, 95% CI 2.4–690, p = 0.0005). After adjustment for gestational age and preeclampsia, the difference remained significant (odds ratio 8.9, 95% CI 1.2–389, p = 0.021). No significant associations were found regarding the secondary outcome variables, after adjusting for possible confounders. Conclusions Antenatal corticosteroid treatment before preterm birth is associated with accelerated villous maturation. This could be one of the pathways by which corticosteroids are beneficial for preterm infants.

Objective To demonstrate the feasibility and efficacy of high-intensity focused ultrasound (HIFU) to non-invasively treat placental tissues in a monkey model of pregnancy. Materials and methods A toroidal HIFU transducer working at 2.5 MHz with an integrated ultrasound-imaging probe was used. Eight pregnant monkeys were exposed to HIFU treatment after anesthesia. Lesions on placental tissues were performed non-invasively by placing the HIFU probe on the skin. Fetal and maternal parameters, such as maternal heart rate, fetal heart rate, and subcutaneous and intra-amniotic fluid temperature, were recorded during HIFU exposure. A C-section was performed immediately after insonification to extract the placenta, inspect the fetus and inspect the maternal abdominal cavity. Placental HIFU lesions were studied using ultrasound images, gross pathology and histology. Results The average gestational age of the animals was 72 ± 4 days. Thirteen HIFU exposures were performed on placentas. The parameters used in this study were acoustic powers of 65, 80, 110 and 120 W applied for 30, 15, 20 and 20 seconds, respectively. This gradual increase in the total energy delivered was used to determine a set of parameters to create reproducible lesions in the placentas without any complications. Six placental lesions were observed with average diameters of 6.4 ± 0.5 mm and 7.8 ± 0.7 mm and an average depth of 3.8 ± 1.5 mm. Ultrasound images revealed a hyperechoic region that was well correlated with the macroscopic analyses of the HIFU lesions. Necrosis of placental tissues exposed to HIFU was confirmed with macroscopic and microscopic analyses. No significant variation in maternal and fetal parameters was observed during HIFU exposure. Conclusion This study demonstrates the feasibility of HIFU applied non-invasively to the placental unit within an in vivo pregnant monkey model. The technique is safe in the very short term and is potentially translatable to human pregnancy.

Background Pregnancies have been reported after endometrial ablation but there is little data regarding subsequent pregnancy outcomes. Objective To review systematically the available evidence regarding pregnancy outcomes after endometrial ablation, in order to equip physicians effectively to counsel women considering endometrial ablation. Search strategy MEDLINE, Embase, Cochrane, and ClinicalTrials.gov were searched through January 2017. Selection criteria Published and unpublished literature in any language describing pregnancy after endometrial ablation or resection was eligible. Data collection and analysis Data about preconception characteristics and pregnancy outcomes were extracted and analysed according to study design of source and pregnancy viability. Main results We identified 274 pregnancies from 99 sources; 78 sources were case reports. Women aged 26–50 years (mean 37.5 ± 5 years) conceived a median of 1.5 years after ablation (range: 3 weeks prior to 13 years after). When reported, 80–90% had not used contraception. In all, 85% of pregnancies from trial/observational studies ended in termination, miscarriage or ectopic pregnancy. Pregnancies that continued (case report and non-case report sources) had high rates of preterm delivery, caesarean delivery, caesarean hysterectomy, and morbidly adherent placenta. Case reports also frequently described preterm premature rupture of membranes, intrauterine growth restriction, intrauterine fetal demise, uterine rupture, and neonatal demise. Conclusions An unexpectedly high rate of pregnancy complications is reported in the available literature (which may reflect publication bias) and high-quality evidence is lacking. However, based on the existing evidence, women undergoing endometrial ablation should be informed that subsequent pregnancy may have serious complications and should be counselled to use reliable contraception after the procedure. Tweetable abstract Systematic review – pregnancies reported after endometrial ablation have an increased risk of adverse outcomes.

Objective The objectives of the study are to describe the obstetric outcomes associated with massive perivillous fibrin deposition (MFD) compared with a control series and to determine if outcome differs according to the extent of fibrin deposition. Method Retrospective case–control study based on placentas analyzed over a consecutive 12-year period. MFD was considered severe if it extended over more than 50% of the placenta and moderate between 25% and 50%. Results During the study period, MFD was observed on 71 placentas, 39 severe and 32 moderate. Compared with the 142 control women, the 39 women with severe MFD more often had histories of autoimmune disease and intrauterine fetal death. The case women with MFD were associated with elevated levels of maternal alpha-fetoprotein and with a high risk of severe growth restriction and/or intrauterine death. Compared with the infants with moderate MFD, those with severe MFD had also more abnormal umbilical artery Doppler velocimetry findings and more often intrauterine deaths and lower birthweights. Conclusion Regardless of their extent, MFD that covered at least 25% of the placenta was almost always accompanied by severe growth restriction and by a high risk of intrauterine fetal death. Moreover, severe MFD tend to be associated with autoimmune diseases of the mothers, and pregnancies show more often a pathologic Doppler of the umbilical arteries and more often intrauterine fetal death that the moderate form. © 2017 John Wiley & Sons, Ltd.

A partial molar pregnancy almost always ends in miscarriage due to a triploid fetus. We describe a rare case of a singleton, partial molar pregnancy with a seemingly huge placenta, which continued to delivery of a live-born diploid baby. A 27-year-old primigravida suffered from severe pre-eclampsia and progressive anemia. The uterus was enormously enlarged for the gestational age. A cesarean section was performed because of deterioration of maternal status at 25 weeks' gestation, when more than 3000 mL blood spouted concurrently with the delivery of the placenta. The histological examination showed congestion in the decidua, which indicated disturbance of maternal venous return from the intervillous space. The chromosome complement of the placenta and the neonate were 69,XXX and 46,XX, respectively. We also reviewed all published cases of a singleton, partial molar pregnancy. A literature search yielded 18 cases of a singleton, diploid fetus with partial molar pregnancy. The mean gestational age at delivery was 24.5 ± 6.2 weeks, and fetuses survived outside the uterus in only four cases (22.2%). Intriguingly, previous reports numbered 10 cases with diploid placenta as well as five cases with no karyotyping of the placenta, indicating that they may have included a complete mole in a twin pregnancy or placental mesenchymal dysplasia. In conclusion, this was the first case of placentomegaly that presented manifestations of excessive abdominal distension and maternal severe anemia, and the second case of a singleton, partial molar pregnancy confirmed by chromosome analysis resulting in a diploid living baby.

Introduction Neonatal outcomes after the maternal obstetric near-miss complications of uterine rupture, abnormally invasive placenta, and emergency peripartum hysterectomy were assessed. Material and methods This case-control study was conducted as part of the Nordic Obstetric Surveillance Study (NOSS). Data on 211 newborns from 197 deliveries in which an obstetric near-miss complication was involved, were collected prospectively from April 2009 to August 2011 from all Finnish delivery units via questionnaires. Missing cases were obtained from national health registers and confirmed by the clinics. Control populations consisted of all other children born during the same period of time in the Finnish Medical Birth Register (n = 147 551). Results The number of stillbirths in this cohort was high [n = 8, 3.8% vs. 0.3% among controls, odds ratio (OR) 12.5, 95% confidence interval (CI) 6.32–24.9]. In addition, there were two neonatal deaths. The majority of cases (n = 8, 80%) were connected to uterine rupture. The risk of severe birth asphyxia diagnosis was increased compared with controls (n = 17, 8.1% vs. 0.1%, OR 137, 95% CI 82.7–226). A low umbilical artery pH (

Introduction. Abnormally invasive placenta is a major cause of maternal morbidity and mortality. The aim of this study was to assess the effectiveness of a standardized operative approach performed by gynecological oncologists in the surgical management of abnormally invasive placenta. Materials and methods. We performed a retrospective analysis of all cases of morbid placental adherence managed at the Mater Mothers' Hospitals, Brisbane, Australia between January 2000 and June 2013. A standard operative approach involving extensive retro-peritoneal and bladder dissection before delivery of the fetus, was undertaken when a gynecological oncologist was present at the start of the procedure. Main outcome measures were estimated blood loss, transfusion requirements, and maternal and neonatal morbidity. Results. The study includes 98 cases of histologically confirmed abnormally invasive placenta. Median estimated blood loss for the entire cohort was 2150 mL (range 300-11 500 mL). Women were divided into three groups, (1) those who had a gynecological oncologist present at the start of the procedure (group 1; n = 43), (2) those who had a gynecological oncologist called in during the procedure (group 2; n = 23), and (3) those who had no gynecological oncologist involved (group 3; n = 32). Group 2 had a significantly higher blood loss than the other groups (p = 0.001) (median 4400 mL). Transfusion requirements were higher in groups 2 and 3 compared with group 1 (p = 0.004). Other maternal and neonatal morbidity was similar across all three groups. Conclusion. This study supports the early presence of a gynecological oncologist at delivery when abnormally invasive placenta is suspected and demonstrates that a "call if needed" approach is not acceptable for these complex cases.

Diagnosis of Placental Mesenchymal Dysplasia with a focus on magnetic resonance imaging (MRI)

Neonatal sepsis is a leading cause of neonatal death during the first-week postfoaling. Despite recent advancements in the diagnosis and treatment of sepsis in the newborn foal, the non-specific clinical signs and subtle nature of this disease may result in delayed diagnosis until severe progression of the disease; thus, early detection of sepsis remains critical for a favourable outcome. This study aimed to identify early blood markers as predictive of sepsis on foals.Thirty-five foals were allocated into three groups: healthy control foals (n=7) and foals born from mares with placentitis: septic foals (n=9) and non-septic foals (n=19). Blood samples were obtained immediately after foaling and at 12, 24 and 48 hours. All samples were assessed for glucose, lactate, triglycerides, total cholesterol, urea, creatinine, total solids, fibrinogen, gamma-glutamyl transferase (GGT), serum amyloid A (SAA) and alpha-fetoprotein (AFP) concentrations.At foaling, glucose and GGT concentrations were lower in septic foals (P0.001). Of interest, SAA, AFP, creatinine and total cholesterol were higher in septic foals at parturition (P0.05). At 12 hours, lactate, triglycerides and total cholesterol concentrations were higher in septic foals. When evaluated at 24 and 48 hours, higher concentrations of SAA and AFP were found in placentitis foals than in the control group.Total cholesterol and lactate appear to be suitable markers for sepsis during the first 24 hours postpartum. Septic foals displayed altered energy metabolisms as determined by increased triglycerides and cholesterol concentrations, hypoglycaemia at birth and reduced activity of the GGT and increased lactate and urea concentrations. Sepsis was associated with high concentrations of SAA and AFP.

Objective Our objectives were: (1) to examine the association between maternal, fetal, and placental phenotypes of preterm delivery and medically indicated early delivery of singletons during the late preterm and early term periods; and (2) to identify the specific maternal, fetal, and placental conditions associated with these early deliveries. Design Retrospective study. Setting City of London and Middlesex County, Ontario, Canada. Sample Singleton live deliveries, at 34–41 weeks of gestation to women in London and Middlesex. Methods We obtained data from a city-wide perinatal database (2002–2011; n = 25 699). We used multinomial logistic regression for multivariable analyses. Main outcome measure The outcome was the occurrence of medically indicated late preterm (34–36 weeks of gestation) and early term (37–38 weeks of gestation) delivery, versus delivery at full term (39–41 weeks of gestation). Results After controlling for confounding factors, all phenotypes were associated with increased odds of medically indicated late preterm and early term delivery. Within the maternal phenotype, chronic maternal medical conditions were associated with increased odds of medically indicated early term delivery (e.g. for gastrointestinal disease, adjusted odds ratio, aOR 1.72, 95% CI 1.47–2.00; for anaemia, aOR 1.40, 95% CI 1.20–1.63), but not late preterm delivery. Conclusions The aetiology of medically indicated early delivery close to full term is heterogeneous. Patterns of associations suggest slightly different conditions underlying the late preterm and early term phenotypes, with chronic maternal medical conditions being associated with early term delivery but not with late preterm delivery. These results have implications for the prevention of early delivery as well as the identification of high-risk groups among those born early. Tweetable Abstract The aetiology of medically indicated late preterm and early term delivery is heterogeneous.