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Introduction:
Prepregnancy obesity is a growing global health problem and has several risks for mother and child. The aim of this study was to systematically examine the effect of increased maternal body mass index (BMI) on placental pathology in otherwise uneventful term pregnancies.
Methods:
In this analysis, we studied data of the Netherlands...
Context in source publication
Context 1
... included 382 women with 273 women with a normal BMI, 77 patients were overweight, and 32 were obese. Table 1 presents the baseline characteristics of the groups. Compared with patients who had a normal BMI, overweight and obese women were significantly less often nulliparous (43.6% vs 24.7% and 21.9%, respectively, P .001) ...
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Citations
... Collectively, placental (mal)adaption in response to suboptimal maternal metabolic status, infection, and/or preterm birth may have negative effects on placental function, and thus, offspring growth and development [9]. While previous studies have associated maternal BMI with placental pathology at term, these studies do not include the full range of suboptimal maternal BMI groups, or consider preterm pregnancies with or without infection [22,23]. Others have observed placental pathological and inflammatory lesions, yet fail to exclude maternal conditions associated with inflammation and placental pathology (such as chorioamnionitis and chronic maternal inflammatory conditions) [7]. ...
... Descriptions of all characteristics are included in Table 1. As previous studies in term cohorts have included accelerated villous maturation as diagnostic criteria [23,33], we assessed placental hypermaturity at both preterm and term. No placentae had both immature and hypermature characteristics. ...
... Here, we assessed placental morphometry and maturity among preterm (with and without chorioamnionitis) and term pregnancies to better understand the influence of the full range of suboptimal maternal BMI at these gestational periods on placental development. To our knowledge, only one other study has evaluated placental histopathology in pregnancies with obesity without complications or comorbidities, and this study reported only moderate associations between increasing maternal BMI and accelerated villous maturation and chronic villitis among term pregnancies [23]. In contrast, a study by Bar et al. investigating high prepregnancy BMI with maternal conditions including pre-eclampsia and GDM, but not hypertension or other pro-inflammatory conditions [22], showed increased maternal inflammatory lesions among pregnancies complicated by obesity compared to normal-weight pregnancies; these findings were consistent when comparing mothers with and without complications [22]. ...
Background: The placenta undergoes morphological and functional adaptations to adverse exposures during pregnancy. The effects ofsuboptimal maternal body mass index (BMI), preterm birth, and infection on placental histopathological phenotypes are not yet well understood, despite the association between these conditions and poor offspring outcomes. We hypothesized that suboptimal maternal prepregnancy BMI and preterm birth (with and without infection) would associate with altered placental maturity and morphometry, and that altered placental maturity would associate with poor birth outcomes. Methods: Clinical data and human placentae were collected from 96 pregnancies where mothers were underweight, normal weight, overweight, or obese, without other major complications. Placental histopathological characteristics were scored by an anatomical pathologist. Associations between maternal BMI, placental pathology (immaturity and hypermaturity), placental morphometry, and infant outcomes were investigated for term and preterm births with and without infection. Results: Fetal capillary volumetric proportion was decreased, whereas the villous stromal volumetric proportion was increased in placentae from preterm pregnancies with chorioamnionitis compared to preterm placentae without chorioamnionitis. At term and preterm, pregnancies with maternal overweight and obesity had a high percentage increase in proportion of immature placentae compared to normal weight. Placental maturity did not associate with infant birth outcomes. We observed placental hypermaturity and altered placental morphometry among preterm pregnancies with chorioamnionitis, suggestive of altered placental development, which may inform about pregnancies susceptible to preterm birth and infection. Conclusions: Our data increase our understanding of how common metabolic exposures and preterm birth, in the absence of other comorbidities or complications, potentially contribute to poor pregnancy outcomes and developmental programming.
... Pathologic changes have been reported in the placenta in association with maternal obesity, though results have been inconsistent. For example, several studies have reported increased placental weight in women with obesity, while others have not [15][16][17][18]. Variable histopathological changes have also been reported in placentas of women with obesity, including both delayed and accelerated villous maturation, maternal vascular lesions, and chronic villitis [15][16][17][18][19]. ...
... For example, several studies have reported increased placental weight in women with obesity, while others have not [15][16][17][18]. Variable histopathological changes have also been reported in placentas of women with obesity, including both delayed and accelerated villous maturation, maternal vascular lesions, and chronic villitis [15][16][17][18][19]. Some of these studies cite small sample sizes, while others have a study design that is limited to term gestation, which could explain the mixed results. ...
... Previous studies have shown women with obesity to present with chronically higher levels of inflammatory cytokines during pregnancy [7,10]. This long-standing inflammatory state could extend to the maternal-fetal interface, and subsequently show signs in the placenta, in the form of chronic villitis (CV), as shown both in our previous and current studies [18,22]. This same increase has been shown in smaller studies, including a study by Brouwers et al., that looked exclusively at uncomplicated pregnancies [18,22]. ...
Background
The rising prevalence of maternal obesity presents a significant health concern because of the possible implications for obstetric complications and neonatal outcomes. Understanding the impact of obesity on placental structure and function as well as fetal growth and infant outcomes is important to improve the care of these potentially high-risk pregnancies. This study aimed to determine the effect of elevated maternal BMI on histopathologic patterns of placental injury and its consequences on fetal growth.
Methods
Data were collected from an ongoing cohort of maternal-infant dyads in the UCSD Obstetric Registry spanning 2011–2020. Maternal characteristics, including BMI, hypertensive disease and diabetes, placental gross and histopathology, and infant characteristics, including sex and birthweight, were recorded and analyzed. ANOVA and chi-square tests were used in initial analyses, followed by log-binomial and linear regression models adjusted for relevant confounders to determine associations between maternal BMI, specific patterns of placental injury, and infant birthweight percentiles.
Results
Among 1366 maternal-infant dyads, placentas from mothers with overweight and obesity were heavier and demonstrated higher adjusted relative risks of chronic villitis (CV), decidual vasculopathy, intervillous thrombosis, and normoblastemia. Placental efficiency, determined by fetal-placental weight ratio, was decreased with increasing BMI. Maternal obesity was associated with higher rates of preterm birth and higher birthweight percentiles. Multiple placental lesions, including maternal (MVM) and fetal vascular malperfusion (FVM), exhibited significant effects on birthweight percentiles; however, only MVM showed a differential effect based on maternal obesity.
Conclusions
Presence of obesity in pregnancy is associated with increased rates of placental patterns of injury, decreased placental efficiency, and increased birthweight percentiles. While placental lesions, such as CV, have the potential to negatively impact fetal growth, the resulting birthweight percentiles demonstrate a more complex relationship between maternal obesity and fetal growth, that likely involves placental and fetal adaptation to the altered in utero environment.
... Our findings indicate that higher pre-pregnancy BMI and younger maternal age were the main contributors to elevated levels of inflammatory and metabolic markers in pregnancy. In addition, the positive association between hs-CRP and placental weight might be explained by increased pre-pregnancy BMI, which has been shown previously (50). However, concentrations of inflammatory and metabolic markers were similar to those in healthy pregnancies (51)(52)(53). ...
Background
Conditions in utero influence intrauterine and postnatal infant growth and a few studies indicate that maternal inflammation and insulin resistance might affect birth and breastfeeding outcomes. Furthermore, hormones in human milk (HM) may influence infant appetite-regulation and thereby milk intake, but the associations are less understood.
Objective
(1) To investigate associations between maternal inflammatory, lipid and metabolic markers and birth and breastfeeding outcomes, and (2) to assess predictors of maternal inflammatory, lipid and metabolic markers in pregnancy.
Methods
Seventy-one mother-infant dyads participating in the Mothers, Infants and Lactation Quality (MILQ) study were included in the present study. Fasting blood samples were collected around 28th gestational week, and HM samples at three time points from 1.0 to 8.5 months, where milk intake was assessed using 24-h test weighing. Maternal plasma inflammatory, lipid and metabolic markers included high-sensitive C-reactive protein (hs-CRP), tumor-necrosis factor-α (TNFα), interferon-γ (IFNγ), Interleukin (IL)-6, IL-8, high-, low-, and very-low-density lipoprotein (HDL, LDL, VLDL), total-cholesterol, triglycerides, leptin, adiponectin, insulin, C-peptide, the homeostasis model assessment of insulin resistance (HOMA-IR) and glucose concentration at t = 120 min following an oral glucose tolerance test. Of these, TNFα, IFNγ, IL-6, IL-8, leptin, adiponectin and insulin were also measured in HM samples.
Results
HDL in pregnancy was inversely associated with gestational age (GA) at birth and GA-adjusted birthweight z-score, whereas triglycerides and glucose (t = 120) were positively associated with GA-adjusted birthweight z-score. Higher hs-CRP, VLDL and triglycerides were associated with a higher placental weight. Furthermore, higher HDL, insulin, leptin and HOMA-IR were associated with longer duration of exclusive breastfeeding (EBF). Higher pre-pregnancy BMI was the main predictor of higher levels of hs-CRP, log-TNFα, leptin, insulin, C-peptide, and HOMA-IR.
Conclusion
Maternal lipid and metabolic markers influenced birthweight z-score and placental weight as well as duration of EBF. Furthermore, pre-pregnancy BMI and maternal age predicted levels of several inflammatory and metabolic markers during pregnancy. Our findings indicate that maternal lipid and metabolic profiles in pregnancy may influence fetal growth and breastfeeding, possibly explained by overweight and/or higher placental weight.
Clinical trial registration
https://clinicaltrials.gov/, identifier NCT03254329.
... These reference values may also be used to help resolve medico-legal issues related to neonatal death due to trauma (infanticide/fresh neonatal homicide), medical misadventure, negligence, and in deaths where natural and traumatic causes co-exist. 25 Women with high pre-pregnancy BMI have been reported to deliver heavyweight placentae, 26 in keeping with the present study (P < 0.001), but BMI in the present study was calculated at the earliest antenatal visit in the first trimester followed the missed menstrual period. Women with a higher pre-pregnancy BMI are at risk of several obstetric complications (e.g., gestational diabetes mellitus, preeclampsia, and large-for-gestational-age babies) associated with higher morbidity for both mother and child. ...
Objective:
Placental pathology is a well-known cause of perinatal and neonatal mortality and morbidity, and may correlate with placental growth, which can be assessed indirectly by anthropometric placental measurements. The aim of this cross-sectional study was to investigate mean placental weight and its relationship with birthweight and maternal body mass index (BMI).
Methods:
Fresh (not formalin fixed) consecutively delivered placentae of term newborns (37-42 weeks), collected between February 2022 and August 2022, and the mothers and newborns, were included. Mean placental weight, birthweight and maternal BMI were calculated. Pearson's correlation coefficient, linear regression, and one-way analysis of variance were used to analyse continuous and categorical data.
Results:
Out of 390 samples, 211 placentae (with 211 newborns and mothers) were included in this study after exclusion criteria were applied. Mean placental weight was 494.45 ± 110.39 g, and mean term birth weight/placental weight ratio was 6.21 ± 1.21 (range, 3.35-11.62 g). Placental weight was positively correlated with birthweight and maternal BMI, but not with newborn sex. Linear regression effect estimation of placental weight on birthweight revealed a medium correlation (R2 = 0.212; formula, 1.4553 × X + 2246.7, where X is placental weight [g]).
Conclusion:
Placental weight was revealed to positively correlate with birthweight and maternal BMI.
... accelerated villous maturation (OR: 1.1, 95% CI: 1.0-1.2), and lower incidence of placental weight below the 10th percentile for gestational age" [16]. ...
The present case study reports about Placental mesenchymal dysplasia co-existing with high grade villitis of unknown aetiology (VUE). Placental Mesenchymal Dysplasia (PMD) is a rare placental lesion characterized by unusual abnormality of the stem villi of the placenta that could be mistaken for hydatidiform mole due to the presence of both cysts and normal-appearing parenchyma. A 30-year-old G2 P1 (full-term normal delivery) seen in fetal medicine clinic at 20 weeks within view of high risk on combined screening (low PAPP-A and high HCG). An ultrasound scan showed an appropriately grown baby with an abnormal placenta consisting of multiple lacunae more than 50% of the placental mass with increased thickness. A second opinion at tertiary care hospital confirmed the presence of prominent lakes on the placenta. Growth scans also showed IUGR with increasingly abnormal Doppler scans as the pregnancy progressed. At 35 weeks, EFW was < 3rd centile with static growth and patient had Induction of labour at 35 +4 weeks with vaginal delivery of a live male neonate weighing 2325g admitted to the neonatal intensive care unit (NICU) admission Case Report 17 due to prematurity. The baby was discharged from NICU at day 5, achieving developmental milestones at the age of 23 weeks post-delivery. On microscopic histological examination, the chorionic plate showed no significant abnormality. The villous architecture was highly abnormal, and some villi were markedly enlarged with myxoid stroma and central degeneration. There were very occasional foci of apparent trophoblastic proliferation with villous architecture abnormalities seen in the form of clusters of large, immature intermediate villi. These features were in keeping with mesenchymal dysplasia. A highly unusual finding in this context was a florid infiltrate of CD3 positive T cells consistent with high-grade villitis of unknown aetiology concluding very rare coexistence of both conditions.
... Obesity during pregnancy can affect placental physiology and structure. Indeed, some studies suggest that mothers with high body mass indices (BMI) display heavier placentas [67], similar to HFD-fed mice [68]. The alterations in a placenta due to obesity can have a negative impact on offspring, as recent studies indicate that a HFD can affect placental function, leading to fetal growth restriction [69,70]. ...
While a dramatic increase in obesity and related comorbidities is being witnessed, the underlying mechanisms of their spread remain unresolved. Epigenetic and other non-genetic mechanisms tend to be prominent candidates involved in the establishment and transmission of obesity and associated metabolic disorders to offspring. Here, we review recent findings addressing those candidates, in the context of maternal and paternal influences, and discuss the effectiveness of preventive measures.
... In T1DM, hypervascularization is associated with fetal hyperinsulinaemia 158,161 . In pregnancies in women with obesity, the placenta does not show signs of hypervascularization 174,175 , which could reflect a milder degree of hyperinsulinaemia and hypoxia than in pregnancies with T1DM, if indeed present. ...
Despite improvements in clinical management, pregnancies complicated by pre-existing diabetes mellitus, gestational diabetes mellitus or obesity carry substantial risks for parent and offspring. Some of the endocrine and metabolic changes in parent and fetus in diabetes mellitus and obesity lead to fetal oxygen deficit, mostly due to insulin-induced accelerated fetal metabolism. The human fetus deals with reduced oxygenation through a wide range of adaptive responses that act at various levels in the placenta as well as the fetus. These responses ensure adequate oxygen delivery to the fetus, increase the oxygen transport capacity of fetal blood and redistribute oxygen-rich blood to vital organs such as the brain and heart. The liver has a central role in adapting to reduced oxygenation by increasing its oxygen extraction and stimulating erythropoietin synthesis to increase haematocrit. The type of adaptive response depends on the onset and duration of hypoxia and the severity of the metabolic disturbance. In pregnancies characterized by diabetes mellitus or obesity, these adaptive systems come under additional strain owing to the increased maternal supply of glucose and resultant fetal hyperinsulinaemia, both of which stimulate oxidative metabolism. In the rare situation that the adaptive responses are overwhelmed, stillbirth can ensue.
... They examined the prevalence of placental findings, grouped as per Amsterdam criteria, in 115 women with preterm birth (with 210 patients with term birth as control) and found that patients with preterm birth and MVM had higher total cholesterol and systolic blood pressure at time of follow-up (4-12 years) compared with controls. Although Bustamante Helfrich and colleagues 43 found no association between MVM and obesity, Brouwers and colleagues 14 found a correlation between obesity and AVM, as well as obesity and high-grade chronic villitis (see previous section). In this study, placental weight was overall high and positively correlated with prepregnancy BMI, as well as with mean infant's birth weight. ...
... In this study, placental weight was overall high and positively correlated with prepregnancy BMI, as well as with mean infant's birth weight. 14 In addition to maternal morbidity, MVM as currently defined is also associated with adverse fetal and neonatal outcomes. A large study by Kulkarni and colleagues 44 included 1633 patients from India and Pakistan (814 with fetal death, 618 with preterm live birth and subsequent neonatal death, and 201 with term live birth). ...
The Amsterdam Placental Workshop Group Consensus Statement on Sampling and Definitions of Placental Lesions has become widely accepted and is increasingly used as the universal language to describe the most common pathologic lesions found in the placenta. This review summarizes the most salient aspects of this seminal publication and the subsequent emerging literature based on Amsterdam definitions and criteria, with emphasis on publications relating to diagnosis, grading, and staging of placental pathologic conditions. We also provide an overview of the recent expert recommendations on the pathologic grading of placenta accreta spectrum, with insights on their clinical context. Finally, we discuss the emerging entity of SARS-CoV2 placentitis.
... Histopathological analyses of placentas from obese women show evidence of inflammatory processes and under-perfusion, even in the absence of pre-eclampsia. 106 As early as the first trimester, obesity alters the expression of cell cycle regulatory genes in the placenta, which may impact on further placental growth and development and the capacity to maintain function at later stages of pregnancy. 107 Among the hormones secreted by the placenta are leptin and adiponectin. ...
The prevalence of overweight and obesity is rising in all parts of the world and among young women it presents a very clear danger during pregnancy. Women who are overweight or who gain excessive weight during pregnancy are at greater risk of complications in pregnancy and labour, and are more likely to lose their child to stillbirth, or themselves die during pregnancy. This narrative review considers the evidence that in addition to increasing risk of poor pregnancy outcomes, obesity has the capacity to programme fetuses to be at greater risk of cardiometabolic disorders later in life. An extensive body of evidence from prospective and retrospective cohorts, and record linkage studies demonstrates associations of maternal obesity and/or gestational diabetes with cardiovascular disease, type‐1 and type‐2 diabetes. Studies in animals suggest that these associations are underpinned by adaptations that occur in fetal life, which remodel the structures of major organs including the brain, kidney and pancreas. This article is protected by copyright. All rights reserved.
... Patients with high BMI are more likely to have early miscarriage and placental hypertrophy (30)(31)(32)(33)(34). In this study, BMI was negatively correlated with epiblast cell number but positively correlated with total nuclei, suggesting increased growth in the trophoblast population that becomes the placenta. ...
Objective
To determine what patient and embryo characteristics are correlated with the developmental potential of the peri-implantation embryo.
Design
Retrospective study.
Setting
Research laboratory.
Patients
Six hundred fifty-one cryopreserved human blastocysts donated for research with informed patient consent.
Interventions
Not applicable.
Main Outcome Measures
Blastocyst attachment to fibronectin-coated plates, trophectoderm outgrowth area, epiblast cell number, total cell number, human chorionic gonadotropin secretion.
Results
Patients’ body mass index, age, follicle-stimulating hormone: luteinizing hormone ratio on menstrual cycle day 3, antral follicle count on menstrual cycle day 3, antimüllerian hormone level on menstrual cycle day 3, and blastocyst morphological grade were correlated with peri-implantation development outcomes. After controlling for good-quality morphological grades, blastocysts from patients of advanced maternal age developed fewer epiblast cells than blastocysts from younger patients.
Conclusions
Extended embryo culture during the peri-implantation period mirrors several disparities in fertility treatment outcome that we see clinically, including those from patients with advanced maternal age, high body mass index, and low ovarian reserve and from embryos with lower-quality morphological grades. This model system may be useful by providing an alternative or more sensitive endpoint assessment in studying patient, clinical, or laboratory factors that may influence preimplantation embryo developmental potential.
