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OBJECTIVE:  The aim of Placental Assessment in Response to Environmental Pollution Study (PARENTs) was to determine whether imaging of the placenta by novel multiparametric magnetic resonance imaging (MRI) techniques in early pregnancy could help predict adverse pregnancy outcomes (APOs) due to ischemic placental disease (IPD). Additionally, we sought to determine maternal characteristics and environmental risk factors that contribute to IPD and secondary APOs. STUDY DESIGN:  Potential patients in their first trimester of pregnancy, who agreed to MRI of the placenta and measures of assessment of environmental pollution, were recruited into PARENTs, a prospective population-based cohort study. Participants were seen at three study visits during pregnancy and again at their delivery from 2015 to 2019. We collected data from interviews, chart abstractions, and imaging. Maternal biospecimens (serum, plasma, and urine) at antepartum study visits and delivery specimens (placenta, cord, and maternal blood) were collected, processed, and stored. The primary outcome was a composite of IPD, which included any of the following: placental abruption, hypertensive disease of pregnancy, fetal growth restriction, or a newborn of small for gestational age. RESULTS:  In this pilot cohort, of the 190 patients who completed pregnancy to viable delivery, 50 (26%) developed IPD. Among demographic characteristics, having a history of prior IPD in multiparous women was associated with the development of IPD. In the multiple novel perfusion measurements taken of the in vivo placenta using MRI, decreased high placental blood flow (mL/100 g/min) in early pregnancy (between 14 and 16 weeks) was found to be significantly associated with the later development of IPD. CONCLUSION:  Successful recruitment of the PARENTs prospective cohort demonstrated the feasibility and acceptability of the use of MRI in human pregnancy to study the placenta in vivo and at the same time collect environmental exposure data. Analysis is ongoing and we hope these methods will assist researchers in the design of prospective imaging studies of pregnancy. KEY POINTS: · MRI was acceptable and feasible for the study of the human placenta in vivo.. · Functional imaging of the placenta by MRI showed a significant decrease in high placental blood flow.. · Measures of environmental exposures are further being analyzed to predict IPD..

Objective: To identify which components of maternal vascular malperfusion (MVM) pathology are associated with adverse pregnancy outcomes and to investigate the morphological phenotypes of MVM placental pathology and their relationship with distinct clinical presentations of pre‐eclampsia and/or fetal growth restriction (FGR). Design: Retrospective cohort study. Setting: Tertiary care hospital in Toronto, Canada. Population: Pregnant individuals with low circulating maternal placental growth factor (PlGF) levels (<100 pg/mL) and placental pathology analysis between March 2017 and December 2019. Methods: Association between each pathological finding and the outcomes of interest were calculated using the chi‐square test. Cluster analysis and logistic regression was used to identify phenotypic clusters, and their association with adverse pregnancy outcomes. Cluster analysis was performed using the K‐modes unsupervised clustering algorithm. Main outcome measures: Preterm delivery <34+0 weeks of gestation, early onset pre‐eclampsia with delivery <34+0 weeks of gestation, birthweight <10th percentile (small for gestational age, SGA) and stillbirth. Results: The diagnostic features of MVM most strongly associated with delivery <34+0 weeks of gestation were: infarction, accelerated villous maturation, distal villous hypoplasia and decidual vasculopathy. Two dominant phenotypic clusters of MVM pathology were identified. The largest cluster (n = 104) was characterised by both reduced placental mass and hypoxic ischaemic injury (infarction and accelerated villous maturation), and was associated with combined pre‐eclampsia and SGA. The second dominant cluster (n = 59) was characterised by infarction and accelerated villous maturation alone, and was associated with pre‐eclampsia and average birthweight for gestational age. Conclusions: Patients with placental MVM disease are at high risk of pre‐eclampsia and FGR, and distinct pathological findings correlate with different clinical phenotypes, suggestive of distinct subtypes of MVM disease. [ABSTRACT FROM AUTHOR]

Aim: To document the outcomes of second‐trimester induction of labor with laminaria cervical dilation followed by gemeprost vaginal tablets, with a particular emphasis on its complications. Methods: This was a single‐center retrospective cohort study of women who experienced medical abortions between 12 and 21 weeks of gestation from January 2016 to July 2021. Procedures were performed with three laminaria cervical dilation for 2 days followed by the administration of gemeprost (1 mg, vaginal tablet) every 3 h with a maximum of five tablets per day. Epidural anesthesia was provided upon request. The primary outcome was successful labor induction, which was defined as fetal expulsion without assisted surgical procedures. Other maternal outcomes, complications and related interventions during and after the procedure were assessed. Results: Among 319 women, 313 (98.1%) experienced successful labor induction with a median of one gemeprost tablet. The median blood loss during the abortion was 145 mL, and three women (0.9%) required blood transfusion. Fever was observed in 19 women (6.0%) during hospitalization, although most cases were drug fever. Thirteen women (4.1%) had abnormal uterine bleeding ~24 days after the abortion. Eleven cases (3.4%) were associated with retained products of conception, of which three cases required uterine artery embolization and three needed surgical curettage. Conclusions: Second‐trimester induction of labor with laminaria cervical dilation and subsequent gemeprost vaginal tablets is a reliable method for completing medical abortions. Abnormal uterine bleeding several weeks after abortion is suspected to be a retained product of conception that could require invasive treatment. [ABSTRACT FROM AUTHOR]

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Purpose: New-onset proteinuria, as a pivotal sign of representative renal lesions in preeclampsia, is still the most common diagnostic tool for this condition and has been proven to be related to a significantly abnormal sFlt-1/VEGF ratio in circulation. At the same time, blood pressure control plays a vital role in the occurrence and evolution of proteinuria. Therefore, it is particularly helpful to investigate their interval, not only for performing urinalysis for protein more accurately but also for evaluating blood pressure as well as the aggravation of illness, as the related research is limited. Methods: This retrospective study included 515 preeclampsia patients and 358 normotensive pregnant women who labored in the Second Hospital of Tianjin Medical University from January 2016 to January 2020. First, we described the onset circumstance of high blood pressure and proteinuria as well as the interval among the case group and the subgroups. Then, we determined whether there were significant differences in the basic information, laboratory test results, and newborns between the case and normal groups. Finally, multifactor ANOVA was used to determine the factors influencing the interval. Results: 1. The two most common complications in preeclampsia were proteinuria (88.35%) and placental dysfunction (5.05%). Moreover, 72.04% of preeclampsia cases were diagnosed by abnormal blood pressure together with new-onset proteinuria. 2. The average interval between high blood pressure and proteinuria was 22 gestational days (from 0 to 106 days), and this interval was not significantly different between mild and severe PE (26 days vs. 21 days, P > 0.05) but significantly differed between early-onset and late-onset PE (9 days vs. 28 days, P < 0.05). 3. The number of prenatal visits, serum creatinine in the early trimester, gestational time and diastolic blood pressure value when increased blood pressure was initially detected may influence the interval between the onset of increased blood pressure and proteinuria. Conclusion: New-onset proteinuria was still the main parameter for identifying preeclampsia. The interval between increased blood pressure and proteinuria was probably related to the imbalance in the sFlt-1/VEGF ratio; therefore, we should pay attention to monitor proteinuria during the prenatal visits, especially for patients with a lower frequency of prenatal visits, higher serum creatinine in the early trimester, earlier onset and higher diastolic blood pressure at the initial onset of increased blood pressure. [ABSTRACT FROM AUTHOR]

IntroductionTo characterize early-gestation changes in placental structure, perfusion, and oxygenation in the context of ischemic placental disease (IPD) as a composite outcome and in individual sub-groups.MethodsIn a single-center prospective cohort study, 199 women were recruited from antenatal clinics between February 2017 and February 2019. Maternal magnetic resonance imaging (MRI) studies of the placenta were temporally conducted at two timepoints: 14-16 weeks gestational age (GA) and 19-24 weeks GA. The pregnancy was monitored via four additional study visits, including at delivery. Placental volume, perfusion, and oxygenation were assessed at both MRI timepoints. The primary outcome was defined as pregnancy complicated by IPD, with group assignment confirmed after delivery.ResultsIn early gestation, mothers with IPD who subsequently developed fetal growth restriction (FGR) and/or delivered small-for gestational age (SGA) infants showed significantly decreased MRI indices of placental volume, perfusion, and oxygenation compared to controls. The prediction of FGR or SGA by multiple logistic regression using placental volume, perfusion, and oxygenation revealed receiver operator characteristic curves with areas under the curve of 0.81 (Positive predictive value (PPV) = 0.84, negative predictive value (NPV) = 0.75) at 14-16 weeks GA and 0.66 (PPV = 0.78, NPV = 0.60) at 19-24 weeks GA.DiscussionMRI indices showing decreased placental volume, perfusion and oxygenation in early pregnancy were associated with subsequent onset of IPD, with the greatest deviation evident in subjects with FGR and/or SGA. These early-gestation MRI changes may be predictive of the subsequent development of FGR and/or SGA.

We report an uncommon clinical presentation of a placental site trophoblastic tumor. The patient presented initially with abdominal pain with, fever, bleeding and pelvic mass on ultrasonography leading to the wrong diagnosis of a pelvic abscess. Dilation and curettage were performed and pathological examination confirmed the diagnosis of placental site trophoblastic tumor. Therefore, she underwent abdominal hysterectomy. Four years after surgery, the patient is still disease free. Gestational trophoblastic diseases should be considered in every patient presenting abnormal uterine bleeding after delivery or pregnancy loss despite the associated symptoms being very unusual.

Placenta accreta spectrum (PAS) is a relatively new obstetric condition which, until recently, was poorly understood. The true incidence is unknown because of the poor quality and heterogeneous diagnostic criteria. Classification systems have attempted to provide clarity on how to grade and diagnose PAS, but these are no longer reflective of our current understanding of PAS. This is particularly true for placenta percreta, which referred to extrauterine disease, as recent studies have demonstrated that placental villi associated with PAS have minimal potential to invade beyond the uterine serosa. It is accepted that PAS is a direct consequence of previous iatrogenic uterine injury, most commonly a previous cesarean section. Here, we “look back to look forwards”—starting with the primary predisposing factor for PAS, an iatrogenic uterine injury and subsequent wound healing. We then consider the evolution of definitions and diagnostic criteria of PAS from its first description over a century ago to current classifications. Finally, we discuss why modifications to the current classifications are needed to allow accurate diagnosis of this rare but life‐threatening complication, while avoiding overdiagnosis and potential patient harm. [ABSTRACT FROM AUTHOR]

Background: The 10th revision of the International Classification of Diseases, Clinical Modification (ICD‐10) includes diagnosis codes for placenta accreta spectrum for the first time. These codes could enable valuable research and surveillance of placenta accreta spectrum, a life‐threatening pregnancy complication that is increasing in incidence. Objective: We sought to evaluate the validity of placenta accreta spectrum diagnosis codes that were introduced in ICD‐10 and assess contributing factors to incorrect code assignments. Methods: We calculated sensitivity, specificity, positive predictive value and negative predictive value of the ICD‐10 placenta accreta spectrum code assignments after reviewing medical records from October 2015 to March 2020 at a quaternary obstetric centre. Histopathologic diagnosis was considered the gold standard. Results: Among 22,345 patients, 104 (0.46%) had an ICD‐10 code for placenta accreta spectrum and 51 (0.23%) had a histopathologic diagnosis. ICD‐10 codes had a sensitivity of 0.71 (95% CI 0.56, 0.83), specificity of 0.98 (95% CI 0.93, 1.00), positive predictive value of 0.61 (95% CI 0.48, 0.72) and negative predictive value of 1.00 (95% CI 0.96, 1.00). The sensitivities of the ICD‐10 codes for placenta accreta spectrum subtypes— accreta, increta and percreta—were 0.55 (95% CI 0.31, 0.78), 0.33 (95% CI 0.12, 0.62) and 0.56 (95% CI 0.31, 0.78), respectively. Cases with incorrect code assignment were less morbid than cases with correct code assignment, with a lower incidence of hysterectomy at delivery (17% vs 100%), blood transfusion (26% vs 75%) and admission to the intensive care unit (0% vs 53%). Primary reasons for code misassignment included code assigned to cases of occult placenta accreta (35%) or to cases with clinical evidence of placental adherence without histopatholic diagnostic (35%) features. Conclusion: These findings from a quaternary obstetric centre suggest that ICD‐10 codes may be useful for research and surveillance of placenta accreta spectrum, but researchers should be aware of likely substantial false positive cases. [ABSTRACT FROM AUTHOR]

Objective: We aimed to examine the association of clinical risk factors and placental lesions, in gestations complicated with preeclampsia, with the need for antihypertensive treatment in the early postpartum period. Methods: The computerized files and placental reports of all singleton deliveries at 24.0–42.0 weeks complicated by preeclampsia were reviewed between January 2013 and October 2020. Obstetric characteristics and placental lesions were compared between patients who required antihypertensive treatment in the early postpartum period and those who did not (control group). Placentas were classified into maternal and fetal malperfusion lesions and inflammatory responses. Results: As compared to controls (n = 200), the anti-hypertensive treatment group (n = 95) was characterized by increased rates of preterm birth, preeclampsia with severe features, and cesarean delivery (p < 0.001 for all). More placental hematomas (p = 0.01) and placental maternal vascular lesions (p = 0.03) were observed in the antihypertensive treatment group as compared to controls. In adjusted logistic regression analysis, gestational age (OR 0.86, 95% CI 0.79–0.93, p = 0.001) and preeclampsia with severe features (OR 8.89, 95% CI 3.18–14.93 p < 0.001) were found to be independently associated with the need for postpartum antihypertensive treatment. Conclusion: Placental vascular lesions are more common in preeclamptic patients who need postpartum antihypertensive treatment, yet only early onset of preeclampsia with severe features was found to be independently associated with antihypertensive treatment in the early postpartum period. [ABSTRACT FROM AUTHOR]

Abnormal fetal growth, i.e., intrauterine growth restriction (IUGR) or fetal growth restriction (FGR) and fetal overgrowth, is associated with increased perinatal morbidity and mortality and is strongly linked to the development of metabolic and cardiovascular disease in childhood and later in life. Emerging evidence suggests that changes in placental amino acid transport may contribute to abnormal fetal growth. This review is focused on amino acid transport in the human placenta, however, relevant animal models will be discussed to add mechanistic insights. At least 25 distinct amino acid transporters with different characteristics and substrate preferences have been identified in the human placenta. Of these, System A, transporting neutral nonessential amino acids, and System L, mediating the transport of essential amino acids, have been studied in some detail. Importantly, decreased placental Systems A and L transporter activity is strongly associated with IUGR and increased placental activity of these two amino acid transporters has been linked to fetal overgrowth in human pregnancy. An array of factors in the maternal circulation, including insulin, IGF‐1, and adiponectin, and placental signaling pathways such as mTOR, have been identified as key regulators of placental Systems A and L. Studies using trophoblast‐specific gene targeting in mice have provided compelling evidence that changes in placental Systems A and L are mechanistically linked to altered fetal growth. It is possible that targeting specific placental amino acid transporters or their upstream regulators represents a novel intervention to alleviate the short‐ and long‐term consequences of abnormal fetal growth in the future. [ABSTRACT FROM AUTHOR]

BACKGROUND The placenta is a unique and pivotal organ in reproduction, controlling crucial growth and cell differentiation processes that ensure a successful pregnancy. Placental development is a tightly regulated and dynamic process, in which the transforming growth factor beta (TGFβ) superfamily plays a central role. This family of pleiotropic growth factors is heavily involved in regulating various aspects of reproductive biology, particularly in trophoblast differentiation during the first trimester of pregnancy. TGFβ signalling precisely regulates trophoblast invasion and the cell transition from cytotrophoblasts to extravillous trophoblasts, which is an epithelial-to-mesenchymal transition-like process. Later in pregnancy, TGFβ signalling ensures proper vascularization and angiogenesis in placental endothelial cells. Beyond its role in trophoblasts and endothelial cells, TGFβ signalling contributes to the polarization and function of placental and decidual macrophages by promoting maternal tolerance of the semi-allogeneic foetus. Disturbances in early placental development have been associated with several pregnancy complications, including preeclampsia (PE) which is one of the severe complications. Emerging evidence suggests that TGFβ is involved in the pathogenesis of PE, thereby offering a potential target for intervention in the human placenta. OBJECTIVE AND RATIONALE This comprehensive review aims to explore and elucidate the roles of the major members of the TGFβ superfamily, including TGFβs, bone morphogenetic proteins (BMPs), activins, inhibins, nodals, and growth differentiation factors (GDFs), in the context of placental development and function. The review focusses on their interactions within the major cell types of the placenta, namely trophoblasts, endothelial cells, and immune cells, in both normal pregnancies and pregnancies complicated by PE throughout pregnancy. SEARCH METHODS A literature search was carried out using PubMed and Google Scholar, searching terms: 'TGF signalling preeclampsia', 'pregnancy TGF signalling', 'preeclampsia tgfβ', 'preeclampsia bmp', 'preeclampsia gdf', 'preeclampsia activin', 'endoglin preeclampsia', 'endoglin pregnancy', 'tgfβ signalling pregnancy', 'bmp signalling pregnancy', 'gdf signalling pregnancy', 'activin signalling pregnancy', 'Hofbauer cell tgfβ signalling', 'placental macrophages tgfβ', 'endothelial cells tgfβ', 'endothelium tgfβ signalling', 'trophoblast invasion tgfβ signalling', 'trophoblast invasion Smad', 'trophoblast invasion bmp', 'trophoblast invasion tgfβ', 'tgfβ preeclampsia', 'tgfβ placental development', 'TGFβ placental function', 'endothelial dysfunction preeclampsia tgfβ signalling', 'vascular remodelling placenta TGFβ', 'inflammation pregnancy tgfβ', 'immune response pregnancy tgfβ', 'immune tolerance pregnancy tgfβ', 'TGFβ pregnancy NK cells', 'bmp pregnancy NK cells', 'bmp pregnancy tregs', 'tgfβ pregnancy tregs', 'TGFβ placenta NK cells', 'TGFβ placenta tregs', 'NK cells preeclampsia', 'Tregs preeclampsia'. Only articles published in English until 2023 were used. OUTCOMES A comprehensive understanding of TGFβ signalling and its role in regulating interconnected cell functions of the main placental cell types provides valuable insights into the processes essential for successful placental development and growth of the foetus during pregnancy. By orchestrating trophoblast invasion, vascularization, immune tolerance, and tissue remodelling, TGFβ ligands contribute to the proper functioning of a healthy maternal–foetal interface. However, dysregulation of TGFβ signalling has been implicated in the pathogenesis of PE, where the shallow trophoblast invasion, defective vascular remodelling, decreased uteroplacental perfusion, and endothelial cell and immune dysfunction observed in PE, are all affected by an altered TGFβ signalling. WIDER IMPLICATIONS The dysregulation of TGFβ signalling in PE has important implications for research and clinical practice. Further investigation is required to understand the underlying mechanisms, including the role of different ligands and their regulation under pathophysiological conditions, in order to discover new therapeutic targets. Distinguishing between clinically manifested subtypes of PE and studying TGFβ signalling in different placental cell types holistically is an important first step. To put this knowledge into practice, pre-clinical animal models combined with new technologies are needed. This may also lead to improved human research models and identify potential therapeutic targets, ultimately improving outcomes for affected pregnancies and reducing the burden of PE. [ABSTRACT FROM AUTHOR]

BACKGROUND With increasing significance of developmental programming effects associated with placental dysfunction, more investigations are devoted to improving the characterization and understanding of placental signatures in health and disease. The placenta is a transitory but dynamic organ adapting to the shifting demands of fetal development and available resources of the maternal supply throughout pregnancy. Trophoblasts (cytotrophoblasts, syncytiotrophoblasts, and extravillous trophoblasts) are placental-specific cell types responsible for the main placental exchanges and adaptations. Transcriptomic studies with single-cell resolution have led to advances in understanding the placenta's role in health and disease. These studies, however, often show discrepancies in characterization of the different placental cell types. OBJECTIVE AND RATIONALE We aim to review the knowledge regarding placental structure and function gained from the use of single-cell RNA sequencing (scRNAseq), followed by comparing cell-type-specific genes, highlighting their similarities and differences. Moreover, we intend to identify consensus marker genes for the various trophoblast cell types across studies. Finally, we will discuss the contributions and potential applications of scRNAseq in studying pregnancy-related diseases. SEARCH METHODS We conducted a comprehensive systematic literature review to identify different cell types and their functions at the human maternal–fetal interface, focusing on all original scRNAseq studies on placentas published before March 2023 and published reviews (total of 28 studies identified) using PubMed search. Our approach involved curating cell types and subtypes that had previously been defined using scRNAseq and comparing the genes used as markers or identified as potential new markers. Next, we reanalyzed expression matrices from the six available scRNAseq raw datasets with cell annotations (four from first trimester and two at term), using Wilcoxon rank-sum tests to compare gene expression among studies and annotate trophoblast cell markers in both first trimester and term placentas. Furthermore, we integrated scRNAseq raw data available from 18 healthy first trimester and nine term placentas, and performed clustering and differential gene expression analysis. We further compared markers obtained with the analysis of annotated and raw datasets with the literature to obtain a common signature gene list for major placental cell types. OUTCOMES Variations in the sampling site, gestational age, fetal sex, and subsequent sequencing and analysis methods were observed between the studies. Although their proportions varied, the three trophoblast types were consistently identified across all scRNAseq studies, unlike other non-trophoblast cell types. Notably, no marker genes were shared by all studies for any of the investigated cell types. Moreover, most of the newly defined markers in one study were not observed in other studies. These discrepancies were confirmed by our analysis on trophoblast cell types, where hundreds of potential marker genes were identified in each study but with little overlap across studies. From 35 461 and 23 378 cells of high quality in the first trimester and term placentas, respectively, we obtained major placental cell types, including perivascular cells that previously had not been identified in the first trimester. Importantly, our meta-analysis provides marker genes for major placental cell types based on our extensive curation. WIDER IMPLICATIONS This review and meta-analysis emphasizes the need for establishing a consensus for annotating placental cell types from scRNAseq data. The marker genes identified here can be deployed for defining human placental cell types, thereby facilitating and improving the reproducibility of trophoblast cell annotation. [ABSTRACT FROM AUTHOR]

Background and Objectives: Preeclampsia has been linked to an inflammatory response that may be brought on by endothelial cell dysfunction. This paper investigates the pathomechanism of syncytiotrophoblast basement membrane (STBM) damage and Placental Protein 13 (PP13) release, which may have a role in systemic endothelial dysfunction in preeclampsia. Materials and Methods: This comparative cross-sectional study involves 54 preeclampsia patients (27 early-onset preeclampsia and 27 late-onset preeclampsia) and 27 pregnant women with normal blood pressure. An enzyme-linked immunosorbent assay was performed to evaluate maternal blood levels of PP13. Following birth, a portion of the placenta was collected for transmission electron microscope (TEM) and immunohistochemical (IHC) analysis. The data were analyzed using STATA version 15. Results: PP13 expression in the placental syncytiotrophoblast was significantly lower in the early-onset preeclampsia, compared to late-onset preeclampsia and normotensive pregnancy, group (p < 0.001). In contrast, serum PP13 levels were found to be the highest in the early-onset preeclampsia group, although no significant difference were found in mean maternal serum levels of PP13 between the three groups. The decreased PP13 expression in placental syncytiotrophoblast can be attributed to the greater extent of damage in the STBM in early-onset preeclampsia that leads to the release of a larger amount of PP13 into maternal circulation. The hypothesis aligns with the TEM analysis results. Preeclamptic pregnancies showed placental syncytiotrophoblast aponeurosis, whereas normotensive pregnancies did not. Placental lesions and STBM shedding were found to be more pronounced in early-onset preeclampsia compared to late-onset preeclampsia. Conclusions: PP13 and STBM damage may play a role in systemic endothelial dysfunction in preeclampsia. [ABSTRACT FROM AUTHOR]

Purpose: Obesity and preeclampsia share similar patho-mechanisms and can both affect placental pathology. We aimed to investigate pregnancy outcomes in correlation with placental pathology among pregnancies complicated by preeclampsia in three different maternal body mass index (BMI, kg/m2) groups. Methods: In this retrospective cohort study, medical and pathological records of patients with preeclampsia and a singleton pregnancy delivered between 2008 and 2021 at a single tertiary medical center were reviewed. Study population was divided into three BMI groups: BMI < 22.6 kg/m2 (low BMI group), 22.7 ≤ BMI ≤ 28.0 kg/m2 (middle-range BMI group), and BMI > 28.0 kg/m2 (high BMI group). Data regarding maternal characteristics, neonatal outcomes, and placental histopathological lesions were compared. Results: The study groups included a total of 295 patients diagnosed with preeclampsia—98, 99, and 98 in the low, middle-range, and high BMI groups respectively. Neonatal birth weight was significantly decreased in the low maternal BMI group compared to both middle and high BMI groups (p = 0.04) with a similar trend seen in placental weight (p = 0.03). Villous changes related to maternal malperfusion were more prevalent in the low and high BMI groups compared to middle-range BMI group (p < 0.01) and composite maternal vascular malperfusion lesions were also more prevalent in the groups of BMI extremities compared to the middle-range BMI group (p < 0.01). Conclusion: Maternal BMI might influence neonatal outcomes and placental pathology in pregnancies complicated by preeclampsia. Both extremes of BMI were associated with higher rates of placental maternal vascular malperfusion. Balanced BMI in women at risk for preeclampsia may reduce the incidence of placental lesions. [ABSTRACT FROM AUTHOR]

Problem: Early‐onset preeclampsia (EOPE) is a severe gestational hypertensive disorder with significant feto‐maternal morbidity and mortality due to uteroplacental insufficiency. Circulating extracellular vesicles of placental origin (EV‐P) are known to be involved in the pathophysiology of EOPE and might serve as an ideal reservoir for its specific biomarkers. Therefore, we aimed to characterize and perform comparative proteomics of circulating EV‐P from healthy pregnant and EOPE women before delivery. Method of Study: The EV‐P from both groups were isolated using immunoaffinity and were characterized using transmission electron microscopy, dynamic light scattering, nanoparticle tracking analysis, and immunoblotting. Following IgG albumin depletion, the pooled proteins that were isolated from EV‐P of both groups were subjected to quantitative TMT proteomics. Results: Circulating term EV‐P isolated from both groups revealed ∼150 nm spherical vesicles containing CD9 and CD63 along with placental PLAP and HLA‐G proteins. Additionally, the concentration of EOPE‐derived EV‐P was significantly increased. A total of 208 proteins were identified, with 26 among them being differentially abundant in EV‐P of EOPE women. This study linked the pathophysiology of EOPE to 19 known and seven novel proteins associated with innate immune responses such as complement and TLR signaling along with hemostasis and oxygen homeostasis. Conclusion: The theory suggesting circulating EVs of placental origin could mimic molecular information from the parent organ—"the placenta"—is strengthened by this study. The findings pave the way for possible discovery of novel prognostic and predictive biomarkers as well as provide insight into the mechanisms driving the pathogenesis of EOPE. [ABSTRACT FROM AUTHOR]

Fetal growth restriction is a common complication of pregnancy with a complex etiology and limited possibilities of di)agnosis and treatment. The relevance of this difficult obstetric problem is determined by various published diagnostic criteria, relatively low detection rates, and limited options for prevention and treatment. Fetal growth restriction is defined as the inability of the fetus to reach its genetically determined growth potential, most often due to abnormal placentation. Forms of fetal growth restriction with early or late onset are distinguished based on the gestational age determined during prenatal ultrasound diagnosis. According to most recommendations, the 32nd week of pregnancy is set as the cut-off point for distinguishing between early and late onset fetal growth restriction. The definition underlying this classification is based on differences between these two phenotypes of fetal growth restric)tion in severity, natural history, Doppler findings, association with hypertensive complications, placental features, and management. It is important to distinguish two separate conditions: fetal growth restriction and small-for-gestational fetus, which differ in short-term and long-term perinatal outcomes. A fetus is defined as small for gestational age if the estimated weight or weight of the fetus at birth is below the 10th percentile. Fetal growth restriction is diagnosed if the estimated fetal weight is below the 3rd percentile or a combination of pathological blood flow in the umbilical arteries and/or uterine arteries in fetuses with an estimated weight below the 10th percentile. It can also occur in fetuses and newborns with a body weight above the 10th percentile. The need to distinguish between fetal growth restriction and small-for-gestational-age fetus is related to the fact that fetal growth restriction is the main cause of stillbirth, neonatal death, higher perinatal morbidity, as well as increased risk of diseases in adulthood. The article analyzes the approaches to differentiating fetal growth restriction from small growth retardation in terms of fetal gestation period and further increasing the accuracy of diagnosis, as well as the modern concept of pathogenesis, with an emphasis on oxidant stress as a key molecular mechanism of adverse outcomes. Appropriate interventions during pregnancy to reduce perinatal complications should include antenatal monitoring and drug therapy. [ABSTRACT FROM AUTHOR]

We examined 164 pregnant women who were divided into three groups. Group I included 76 pregnant women (46.4 %) with euthyroid goiter of I–II degree. Group II consisted of 63 pregnant women (38.4 %) with subclinical hypothyroidism and diffuse thyroid goiter of I–II degree. Group III was the controls and consisted of 25 (15.2 %) pregnant women without thyroid pathology. The placenta was studied with the characteristics of ultrasound placentography, placental maturation disorders, the area and localization were determined, and pathological changes in the placental tissue were detected. Changes in the systolic-diastolic ratio in the uterine arteries and umbilical cord arteries were assessed, the resistance index in the uterine arteries, the pulsatile index in the fetal aorta and middle cerebral artery were determined using the method of color Doppler mapping of blood flow in the mother-placenta-fetus system. Study of the echographic picture of structural changes in the placenta revealed a significant impairment of its maturation, especially in the group with euthyroidism. Ultrasound screening revealed that in every second pregnant woman with thyroid disease, the condition of the placenta did not correspond to the gestational age, there were swelling, cysts and placental infarctions, a high frequency of diffuse changes in placental tissue, and hyperechogenic inclusions in the amniotic fluid. An increase in the resistance index in the uterine arteries of pregnant women, especially those with subclinical hypothyroidism, is noteworthy. With increasing gestational age, the peripheral resistance of the placental microvasculature increases due to involutional-dystrophic changes and circulatory disorders, which allows us to develop criteria for the prognosis and diagnosis of placental dysfunction, and to prevent perinatal disorders in pregnant women with thyroid disease. [ABSTRACT FROM AUTHOR]

Chronic venous disease (CVD) comprises a spectrum of morphofunctional disorders affecting the venous system, affecting approximately 1 in 3 women during gestation. Emerging evidence highlights diverse maternofetal implications stemming from CVD, particularly impacting the placenta. While systemic inflammation has been associated with pregnancy-related CVD, preliminary findings suggest a potential link between this condition and exacerbated inflammation in the placental tissue. Inflammasomes are major orchestrators of immune responses and inflammation in different organs and systems. Notwithstanding the relevance of inflammasomes, specifically the NLRP3 (nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing-3)- which has been demonstrated in the placentas of women with different obstetric complications, the precise involvement of this component in the placentas of women with CVD remains to be explored. This study employs immunohistochemistry and real-time PCR (RT-qPCR) to examine the gene and protein expression of key components in both canonical and non-canonical pathways of the NLRP3 inflammasome (NLRP3, ASC—apoptosis-associated speck-like protein containing a C-terminal caspase recruitment domain—caspase 1, caspase 5, caspase 8, and interleukin 1β) within the placental tissue of women affected by CVD. Our findings reveal a substantial upregulation of these components in CVD-affected placentas, indicating a potential pathophysiological role of the NLRP3 inflammasome in the development of this condition. Subsequent investigations should focus on assessing translational interventions addressing this dysregulation in affected patient populations. [ABSTRACT FROM AUTHOR]

Preeclampsia (PE) is a hypertensive condition that occurs during pregnancy and accounts for 2% to 8% of complications related to pregnancy globally. The diagnosis of preeclampsia is made when the blood pressure exceeds 140/90 mmHg after 20 weeks of pregnancy, occurring on two separate occasions with a minimum time gap of 4 hours, or exceeds 160/100 mmHg within a short period of time. Several biomarkers have been identified for prediction and diagnosis of preeclampsia. One of these biomarkers is Placental induced growth factor (PlGF), a factor that promotes angiogenesis, which belongs to the vascular endothelial growth factor family. Significantly reduced serum levels of placental growth factor (PIGF) have been observed in women diagnosed with preeclampsia compared to normotensive pregnancies. This study was designed to answer the question whether the measurement of PIGF at third trimester might be a predictive factor for the appearance of preeclampsia. Method: A comparative study was made on 40 women with PE and 40 age-gestational-age matched women without preeclampsia, as case and control, respectively. Levels of serum PIGF were measured, compared and its role in prediction of preeclampsia was studied. Results: The mean serum level of PIGF in cases was significantly lower (78.54±152.63pg/ml) than mean serum PIGF level of controls (553.73±263.27 pg./ml). When ROC analysis was done, PIGF =121.9pg/ml was found giving highest Youden index with sensitivity of 97.50%(95%CI-86.8 - 99.9), specificity of 100% (95%CI-91.2-100) and AUC of 0.97 (95% CI =0.91-0.99). Conclusion: Along with the hallmark symptoms of preeclampsia like high blood pressure and proteinuria, measurement of PIGF levels in late pregnant stage may be helpful in prediction of preeclampsia before actual onset of clinical symptoms which further assist in better diagnosis and management of disease. [ABSTRACT FROM AUTHOR]

Aim: Placenta accreta spectrum disorders (PAS) are a global threat to maternal well-being. The aim of this study was to assess differences in clinical characteristics and maternal outcomes between Turkish natives and Syrian refugees giving birth with a diagnosis of PAS at a tertiary centre, and to experience the management of this condition in the unique context of Türkiye, home to one of the world's largest refugee populations. Material and Method: A retrospective study was conducted using the medical records of 228 singleton pregnancies at high risk of PAS, between January 2019 and October 2022. PAS risk assessment was initially performed by ultrasound at mid-trimester, with diagnosis confirmed histologically or clinically, indicating the presence of placental retention following attempted manual removal. The study population was divided into two groups: native and refugee. We investigated disparities in demographic and medical characteristics and primary maternal and neonatal outcomes. Results: The study found an increased prevalence of previous cesarean delivery (p=0.005), anterior placenta (p<0.000), placenta previa (p=0.047), and deeper placental invasion (increta/percreta) (p<0.000) in the native group (n=161). The native group had a significantly higher rate of estimated blood loss (2093.5±1516.4 mL vs. 714.1±731.6 mL, p<0.000) and peripartum hysterectomy (p=0.005) compared to the refugee group (n=67). The refugee group had a notably higher incidence of delayed diagnosis (p<0.000) and a shorter surgery duration (p=0.027) compared to the native group. Conclusion: The current study highlights significant differences in patient characteristics and outcomes between native and refugee pregnant women with PAS. Despite facing challenges, these women did not encounter adverse perinatal outcomes, indicating the efficacy of healthcare interventions. [ABSTRACT FROM AUTHOR]

We report an uncommon clinical presentation of a placental site trophoblastic tumor. The patient presented initially with abdominal pain with, fever, bleeding and pelvic mass on ultrasonography leading to the wrong diagnosis of a pelvic abscess. Dilation and curettage were performed and pathological examination confirmed the diagnosis of placental site trophoblastic tumor. Therefore, she underwent abdominal hysterectomy. Four years after surgery, the patient is still disease free. Gestational trophoblastic diseases should be considered in every patient presenting abnormal uterine bleeding after delivery or pregnancy loss despite the associated symptoms being very unusual.

Although frequently employed in the delivery room, current guidelines do not recommend the use of ultrasound in the setting of postpartum hemorrhage (PPH). The aim of this survey was to evaluate the routine use of ultrasonography during PPH. A questionnaire, composed by a series of questions that assess participant characteristics and ultrasound use during PPH, was sent to members of the Italian Society of Ultrasound in Obstetrics and Gynecology currently employed in obstetrical units. Answers were subsequently grouped based on participant characteristics. Based on the responses of 200 participants it was found that ultrasound was routinely employed by 67 % of participants during PPH, by 85 % if Retained Products of Conception (RPOC) was suspected, by 67 % during Bakri balloon placement and by 69 % during curettage procedures. Routine ultrasound use was higher amongst participants working in hospitals with a higher number of deliveries, by those with more years of experience using ultrasound in labor, and by those that had attended specific postgraduate training courses. Despite the lack of recommendations in the current guidelines, the results of this survey show that ultrasound seems to be commonly employed by maternal fetal medicine practitioners in the management of PPH. [ABSTRACT FROM AUTHOR]

Background: Despite pregnancy's hypercoagulable state, the correlation between inherited thrombophilia and thrombotic adverse pregnancy outcomes remains uncertain. The objective of this study was to determine the prevalence of inherited thrombophilic polymorphisms among asymptomatic pregnant individuals and to examine their potential correlation with adverse perinatal outcomes. Methods: in this single-center prospective study, 105 healthy pregnant women were included. Genotyping was conducted for factor V Leiden (FVL), prothrombin gene mutation, methylenetetrahydrofolate reductase enzyme (MTHFR) C677T, MTHFR A1298C, and plasminogen activator inhibitor-1 (PAI-1), alongside the assessment of protein C (PC), protein S (PS), and antithrombin (AT) levels. The study analyzed the association between inherited thrombophilic polymorphisms and pregnancy complications linked to placental insufficiency, such as gestational hypertension (GH), preeclampsia (PE), intrauterine death (IUD), fetal growth restriction (FGR), and placental abruption. Results: The prevalence of identifiable thrombophilic polymorphism mutations was 61.9% (95% confidence interval—CI 52.4–70.8%), with the most common single mutation being PAI-1 4G/5G (12/105, 11.4%, 95% CI 6.4–18.5). The most frequent combined mutation was heterozygosity for MTHFR C677T and PAI-1 (12/105, 11.4%, 95% CI 6.4–18.5). Notably, no FVL homozygous carriers or single homozygous and heterozygous carriers for prothrombin polymorphisms were found. Additionally, no deficiencies in PC and AT were detected among participants. Except for homozygosity for PAI-1, none of the studied polymorphisms demonstrated a significant association with pregnancy complications linked to placental insufficiency. Conclusions: The asymptomatic carriers of inherited thrombophilic polymorphisms do not have an increased risk of adverse perinatal outcomes. [ABSTRACT FROM AUTHOR]

Pregnancy-related complications (PRC) impact maternal and fetal morbidity and mortality and place a huge burden on healthcare systems. Thus, effective diagnostic screening strategies are crucial. Currently, national and international guidelines define patients at low risk of PRC exclusively based on their history, thus excluding the possibility of identifying patients with de novo risk (patients without a history of disease), which represents most women. In this setting, previous studies have underlined the potential contribution of non-coding RNAs (ncRNAs) to detect patients at risk of PRC. However, placenta biopsies or cord blood samples are required, which are not simple procedures. Our review explores the potential of ncRNAs in biofluids (fluids that are excreted, secreted, or developed because of a physiological or pathological process) as biomarkers for identifying patients with low-risk pregnancies. Beyond the regulatory roles of ncRNAs in placental development and vascular remodeling, we investigated their specific expressions in biofluids to determine favorable pregnancy outcomes as well as the most frequent pathologies of pregnant women. We report distinct ncRNA panels associated with PRC based on omics technologies and subsequently define patients at low risk. We present a comprehensive analysis of ncRNA expression in biofluids, including those using next-generation sequencing, shedding light on their predictive value in clinical practice. In conclusion, this paper underscores the emerging significance of ncRNAs in biofluids as promising biomarkers for risk stratification in PRC. The investigation of ncRNA expression patterns and their potential clinical applications is of diagnostic, prognostic, and theragnostic value and paves the way for innovative approaches to improve prenatal care and maternal and fetal outcomes. [ABSTRACT FROM AUTHOR]

Maternal vascular hypoperfusion is the most common cause of fetal growth restrict ion. Maternal oxidative status features are identifiable on placental pathology, and antepartum diagnostic methods are rapidly evolving. The current study was constructed to determine the maternal oxidative status by measuring serum ischemia modified albumin (IMA) levels in pregnancies complicated with idiopathic intrauterine growth restriction (IUGR). The current study was designed as a descriptive and cohort trial. A total of 87 pregnant women; 45 healthy controls and 42 pregnancies complicated with idiopathic IUGR were included to the study population. Maternal serum IMA concentration was measured prior to the administration of any medication. The perinatal outcomes of patie nts were also recorded. Maternal serum IMA concentration in pregnancies complicated by idiopathic IUGR was higher than in healthy controls. There was no significant difference between the groups (0.54±0.04 versus 0.55±0.06 ABSU, p: 0.314). IUGR is a significant pregnancy complication. Elevated oxidative stress which leads to an ischemic microenvironment is associated with IUGR. Maternal serum IMA which is a possible marker for oxidative stress is not increase in pregnancies complicated with idiopathic IUGR. [ABSTRACT FROM AUTHOR]

* Context.--Case studies reporting intraplacental choriocarcinoma (IPC) and intraplacental "chorangiocarcinoma" have recently increased, with IPC also represented in molecular analyses of gestational trophoblastic neoplasms. Objective.--To provide an overview of 2 intraplacental neoplastic lesions that can have a significant impact on both mother and fetus/infant, focusing on diagnostic characteristics, and ancillary and molecular tools that support diagnosis, determine prognosis, and further elucidate the nature of these lesions. Data Sources.--Data were compiled from a PubMed literature review that included diagnostic and additional keywords within the scope of study for gestational choriocarcinoma in general. Illustrative cases were retrieved from the pathology archives at Michigan Medicine, including the consultation files of the author. Conclusions.--Intraplacental gestational tumors exist along the spectrum of benign (chorangioma) to aggressive malignant (choriocarcinoma) neoplasms with a high potential for metastasis. Although most gestational choriocarcinomas follow complete hydatidiform mole, 20% to 25% occur in association with normal intrauterine gestations, including rare cases in which they are detected within the placenta (IPC). IPCs range from asymptomatic to widely metastatic, with metastases possible even when only microscopic IPCs are present. A second, even less common lesion, variably called "chorangiocarcinoma" and chorangioma with atypical trophoblast proliferation, is also reviewed. The incidence of these lesions is likely to be underestimated. Heightened suspicion and more liberal placental sampling, particularly when specific clinical features are present, may result in higher detection. Enhanced detection to provide the earliest intervention for both mother and infant may improve prognosis, particularly for asymptomatic disease that may later present with metastasis. [ABSTRACT FROM AUTHOR]

* Context.--Chronic histiocytic intervillositis (CHI) is a rare condition characterized by maternal immune cell infiltration into the human placenta. CHI is strongly associated with fetal growth restriction, miscarriage, and stillbirth, and knowledge of its etiology, and consequently effective treatment, is limited. Currently, diagnosis is largely subjective and varies between centers, making comparison between studies challenging. Objective.--To objectively quantify and interrelate inflammatory cells and fibrin in placentas with CHI compared with controls and determine how pathology may be altered in subsequent pregnancies following diagnosis. Macrophage phenotype was also investigated in untreated cases of CHI. Design.--Computerized analysis was applied to immunohistochemically stained untreated (index) cases of CHI, subsequent pregnancies, and controls. Index placentas were additionally stained by immunofluorescence for M1 (CD80 and CD86) and M2 macrophage markers (CD163 and CD206). Results.--Quantification revealed a median 32-fold increase in macrophage infiltration in index cases versus controls, with CHI recurring in 2 of 11 (18.2%) subsequent pregnancies. A total of 4 of 14 placentas (28.6%) with a diagnosis of CHI did not exhibit infiltration above controls. Macrophages in index pregnancies strongly expressed CD163. There was no significant difference in fibrin deposition between index cases and controls, although subsequent pregnancies displayed a 2-fold decrease compared with index pregnancies. CD31 T cells were significantly elevated in index pregnancies; however, they returned to normal levels in subsequent pregnancies. Conclusions.--In CHI, intervillous macrophages expressed CD163, possibly representing an attempt to resolve inflammation. Computerized analysis of inflammation in CHI may be useful in determining how treatment affects recurrence, and alongside pathologist expertise in grading lesion severity. [ABSTRACT FROM AUTHOR]

This study aims to report the treatment of retained placenta in a doe by administration of intrauterine antibiotics, accompanied by intramuscular injection of antibiotics, anti-inflammatory, and injection of vitamins A, D, and E as supportive treatment. The Saanen doe was brown, approximately two years old with a BCS of 3/5 and kidding for the first time on January 11, 2023. The following day, it was reported that the doe's placenta had not been expelled until 24 hours after kidding. Physically the doe was weak, unable to stand, and reddish-brown discharge was seen came out of the vulva. Based on these conditions the doe was diagnosed as having retained placenta with a fausta prognosis. The doe was treated with a bolus of antibiotics contained 250 mg sulphadiazine and 50 mg trimethoprim which was diluted with 5 mL of 0.9% NaCl for uterine lavage. Systemic treatment consisted of intramuscular injection of ceftiofur at 1.1 mg/kg bw, flunixin meglumine at 1.1 mg/kg bw, as well as a combination of 300,000 IU of vitamin A palmitate, 100,000 IU of vitamin D3, and 50 mg of vitamin E acetate as supportive treatment. The treatment was successful, the doe was able to stand and eat when examined the next day after treatment. The doe returned to estrus 42 days after treatment. It could be concluded that treatment of retained placenta in a doe with intrauterine broad-spectrum antibiotics, beta-lactamase antibiotics and intramuscular antiinflammatory, with vitamins A, D and E as supportive therapy was effective and the doe returned to estrus 42 days after treatment. [ABSTRACT FROM AUTHOR]

Aim: To evaluate placental pathology in term and post-term births, investigate differences in clinical characteristics, and assess the risk of adverse neonatal outcome. Methods: This prospective observational study included 315 singleton births with gestational age (GA) > 36 weeks + 6 days meeting the local criteria for referral to placental histopathologic examination. We applied the Amsterdam criteria to classify the placentas. Births were categorized according to GA; early-term (37 weeks + 0 days to 38 weeks + 6 days), term (39 weeks + 0 days to 40 weeks + 6 days), late-term (41 weeks + 0 days to 41 weeks + 6 days), and post-term births (≥ 42 weeks + 0 days). The groups were compared regarding placental pathology findings and clinical characteristics. Adverse neonatal outcomes were defined as 5-minute Apgar score < 7, umbilical cord artery pH < 7.0, admission to the neonatal intensive care unit or intrauterine death. A composite adverse outcome included one or more adverse outcomes. The associations between placental pathology, adverse neonatal outcomes, maternal and pregnancy characteristics were evaluated by logistic regression analysis. Results: Late-term and post-term births exhibited significantly higher rates of histologic chorioamnionitis (HCA), fetal inflammatory response, clinical chorioamnionitis (CCA) and transfer to neonatal intensive care unit (NICU) compared to early-term and term births. HCA and maternal smoking in pregnancy were associated with adverse outcomes in an adjusted analysis. Nulliparity, CCA, emergency section and increasing GA were all significantly associated with HCA. Conclusions: HCA was more prevalent in late and post-term births and was the only factor, along with maternal smoking, that was associated with adverse neonatal outcomes. Since nulliparity, CCA and GA beyond term are associated with HCA, this should alert the clinician and elicit continuous intrapartum monitoring for timely intervention. [ABSTRACT FROM AUTHOR]

Background: Because the cause of increasing rates of postpartum hemorrhage (PPH) and manual placental removal (MROP) is still unknown, we described trends in PPH, MROP, and childbirth interventions and examined factors associated with changes in rates of PPH and MROP. Methods: This nationwide cohort study used national perinatal registry data from 2000 to 2014 (n = 2,332,005). We included births of women who gave birth to a term singleton child in obstetrician‐led care or midwife‐led care. Multivariable logistic regression analyses were used to examine associations between characteristics and interventions, and PPH ≥ 1000 mL and MROP. Results: PPH rates increased from 4.3% to 6.6% in obstetrician‐led care and from 2.5% to 4.8% in midwife‐led care. MROP rates increased from 2.4% to 3.4% and from 1.0% to 1.4%, respectively. A rising trend was found for rates of induction and augmentation of labor, pain medication, and cesarean section, while rates of episiotomy and assisted vaginal birth declined. Adjustments for characteristics and childbirth interventions did not result in large changes in the trends of PPH and MROP. After adjustments for childbirth interventions, in obstetrician‐led care, the odds ratio (OR) of PPH in 2014 compared with the reference year 2000 changed from 1.66 (95% CI 1.57–1.76) to 1.64 (1.55–1.73) among nulliparous women and from 1.56 (1.47–1.66) to 1.52 (1.44–1.62) among multiparous women. For MROP, the ORs changed from 1.51 (1.38–1.64) to 1.36 (1.25–1.49) and from 1.56 (1.42–1.71) to 1.45 (1.33–1.59), respectively. Conclusions: Rising PPH trends were not associated with changes in population characteristics and rising childbirth intervention rates. The rising MROP was to some extent associated with rising intervention rates. [ABSTRACT FROM AUTHOR]

Background: Placental infarction refers to a localized area of ischemic villous necrosis resulting from the interruption of maternal blood flow to the intervillous space, which can be attributed to spasm, stenosis, or occlusion of the decidual spiral artery caused by systemic or localized maternal vascular disease. The presence of large placental infarcts may pose significant risks to fetal well-being, including intrauterine growth retardation, fetal distress, and even fetal demise. Although placental infarction is commonly identified during postnatal pathological examinations, its prenatal diagnosis through ultrasound remains challenging and has been rarely reported. Case Presentation: This report presents a case of acute placental infarction diagnosed by prenatal ultrasound using Superb Micro-vascular Imaging (SMI) technology. At 23 weeks' gestation, the ultrasound revealed that the placenta was attached to the left lateral and posterior walls of the uterus, showing localized thickening. Within this area of thickening, there were observed inhomogeneous hypoechoic regions. Superb Micro-vascular Imaging (SMI) revealed an abnormal echogenic region within the thickened placental tissue that lacked microvascular blood flow signals, but showed surrounding vascularity. Visually, this elliptical-shaped echogenic region enveloped by microvascular blood flow. From the 29th weeks of gestation onward, ultrasound suggested that the fetus was small for gestational age. A live baby weighing 2360g was delivered by cesarean section at 37 weeks' gestation. The placenta was approximately 20× 18 × 3 cm with large grayish-yellow infarcts. Conclusion: SMI allows rapid screening of large placental infarcts and easy detection of regions without normal vessel trees, thereby reducing missed diagnoses. Infarct area is easily measured by measuring the area surrounded by small blood vessels, especially in acute placental infarction, which is very helpful in accurately determining infarct size. [ABSTRACT FROM AUTHOR]

Pre-eclampsia (PE) is a placenta-mediated disease and remains a major cause of maternal and neonatal mortality and morbidity. As PE develops, normal pregnancy's hypercoagulable balance is disrupted, leading to platelet hyperactivation, excessive pathological hypercoagulability, and perturbed fibrinolysis. This narrative review aims to summarize the current knowledge regarding hemostasis in PE compared with healthy gestation and the potential effects of maternal PE on neonatal hemostasis. Finally, it aims to discuss hemostasis assessments for normal pregnancies and PE, emphasizing the role of viscoelastic tests, namely, thromboelastography (TEG) and thromboelastometry (ROTEM), for monitoring PE-associated hemostatic alterations. The use of TEG/ROTEM for assessing the hemostatic profile of PE women has been little considered, even though conventional coagulation tests (CCTs) have not helped to monitor hemostasis in this population. Compared with normal pregnancy, TEG/ROTEM in PE reveals an excessive hypercoagulability analogous with the severity of the disease, characterized by higher-stability fibrin clots. The TEG/ROTEM parameters can reflect PE severity and may be used for monitoring and as predictive markers for the disease. [ABSTRACT FROM AUTHOR]

Introduction: Infection by Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2) has been shown to affect multiple organs in the human body. Research shows that Coronavirus Disease (COVID-19)-positive pregnant women experience poorer perinatal outcomes related to placental infection, including higher risks of miscarriage, preeclampsia, preterm birth, and stillbirth. Aim: To evaluate the histopathological changes in the placentas of COVID-19-positive mothers and the associated foetal outcomes. Materials and Methods: This cohort study was conducted at Kalinga Institute of Medical Sciences (KIMS) Bhubaneswar, Odisha, India, over a period of one year and eight months, from November 2020 to July 2022. It included 23 COVID-19-positive pregnant females admitted for safe confinement during the first and second COVID-19 waves. Thirty COVID-19-negative pregnant women admitted for safe delivery during the same period served as controls. Placentas were collected, processed, and stained according to standard protocols. Descriptive data were interpreted as frequencies and percentages, and associations were tested using the Chi-square test. A p-value <0.05 was considered statistically significant. Results: The study included 23 cases (mean gestational age: 37 weeks and 5 days) and 30 controls (mean gestational age: 38 weeks and 6 days). The prevalence of Maternal Vascular Malperfusion (MVM) and Foetal Vascular Malperfusion (FVM) was found to be higher among cases than controls. Conclusion: Compared to controls, COVID-19-positive placentas showed a higher prevalence of both MVM and FVM. This might be attributable to the hypercoagulable state associated with COVID-19. Further research is needed to explore the potential effects of intrauterine inflammation on neonates exposed to COVID-19. [ABSTRACT FROM AUTHOR]

Objectives: Severe Acute Respiratory Syndrome Coronavirus 2 (SARS‐CoV‐2) virus infection in pregnancy is associated with higher incidence of placental dysfunction, referred to by a few studies as a 'preeclampsia‐like syndrome'. However, the mechanisms underpinning SARS‐CoV‐2‐induced placental malfunction are still unclear. Here, we investigated whether the transcriptional architecture of the placenta is altered in response to SARS‐CoV‐2 infection. Methods: We utilised whole‐transcriptome, digital spatial profiling, to examine gene expression patterns in placental tissues from participants who contracted SARS‐CoV‐2 in the third trimester of their pregnancy (n = 7) and those collected prior to the start of the coronavirus disease 2019 (COVID‐19) pandemic (n = 9). Results: Through comprehensive spatial transcriptomic analyses of the trophoblast and villous core stromal cell subpopulations in the placenta, we identified SARS‐CoV‐2 to promote signatures associated with hypoxia and placental dysfunction. Notably, genes associated with vasodilation (NOS3), oxidative stress (GDF15, CRH) and preeclampsia (FLT1, EGFR, KISS1, PAPPA2) were enriched with SARS‐CoV‐2. Pathways related to increased nutrient uptake, vascular tension, hypertension and inflammation were also enriched in SARS‐CoV‐2 samples compared to uninfected controls. Conclusions: Our findings demonstrate the utility of spatially resolved transcriptomic analysis in defining the underlying pathogenic mechanisms of SARS‐CoV‐2 in pregnancy, particularly its role in placental dysfunction. Furthermore, this study highlights the significance of digital spatial profiling in mapping the intricate crosstalk between trophoblasts and villous core stromal cells, thus shedding light on pathways associated with placental dysfunction in pregnancies with SARS‐CoV‐2 infection. [ABSTRACT FROM AUTHOR]