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Drucilla J Roberts - One of the best experts on this subject based on the ideXlab platform.
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Chapter 69 – Placental Pathology
Reproductive and Developmental Toxicology, 2020Co-Authors: Drucilla J RobertsAbstract:Examination of the placenta offers insight into the development and welfare of the fetus. By looking at the placenta divided into three compartments—fetal, maternal, and Placental—correlating the Pathology with the clinical story is facilitated. This review highlights the utility of this approach and focuses on the importance of Placental Pathology in assessing neonatal risks.
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Chapter 81 – Placental Pathology
Reproductive and Developmental Toxicology, 2020Co-Authors: Drucilla J RobertsAbstract:Publisher Summary This overview of Placental Pathology is ordered by compartment – maternal, fetal and Placental. The placenta is a still poorly studied organ that may offer significant insights into human reproduction; its immunobiology may answer questions regarding transplant biology and “autoimmune diseases”, and provide risk assessment into the health of the mother neonatal, and the adult outcome from the neonate is broadly defined. Placental Pathology involves insults in either the maternal or fetal vascular compartments or to the placenta itself. The clinical effects of these pathologies are, for a large part, dependent on Placental reserve. Whereas large well-developed placentas can function despite pathologies, a small placenta has little reserve; therefore, any Pathology will likely have clinical effects. Malimplantation must be a defect in the trophoblast biology and results in maladaption of the implantation site vessels. This is evidenced by persistence of the muscularized vascular walls in the decidua and can be diagnosed by Placental bed biopsies or decidua, which remains on the placenta after deliver. If the uterine vessels are remodeled appropriately and maternal blood pressure is normotensive, then perfusion to the placenta may still be inhibited by pathologies within the placenta. These include predominantly abnormal fibrin/fibrinoid deposition in the intervillous space. Developmentally – the placenta being a fetal organ – Placental maldevelopment can be considered a fetal Pathology, and this is discussed in the section on primary Placental pathologies.
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Placental Pathology in live births conceived with in vitro fertilization after fresh and frozen embryo transfer
American Journal of Obstetrics and Gynecology, 2020Co-Authors: C R Sacha, Amy L Harris, Kaitlyn E James, Kristen M Basnet, Taylor S Freret, Anjali J Kaimal, Irene Souter, Drucilla J RobertsAbstract:Background The availability and use of frozen embryos after ovarian hyperstimulation for assisted reproduction has increased with improvement in vitrification techniques and the rise of preimplantation genetic testing. However, there are conflicting data regarding whether obstetric outcomes differ between fresh and frozen embryo transfer cycles. Objective To compare Placental Pathology from live births arising from fresh and frozen embryo transfer cycles. Materials and Methods A cohort of 1140 live births with Placental Pathology arising from autologous in vitro fertilization cycles with fresh or frozen programmed transfer performed at MGH Fertility Center between 2004 and 2017 was retrospectively reviewed. An experienced Placental pathologist categorized the reported Placental Pathology as anatomic, infectious, inflammatory, or vascular/thrombotic. Our primary outcomes were differences in these Placental pathologies between the 2 groups. Patient demographic, cycle, and birth outcomes were compared with the use of χ2 tests, Student t test, or nonparametric tests, as appropriate. Multivariate logistic regression models were used to compare Placental Pathology between the fresh and frozen transfer groups. Results Of the 1140 cycles included in our analysis, 929 arose from fresh embryo transfers (81.3%) and 211 arose from programmed frozen embryo transfers (18.5%). For both transfer types, the average age of the women at time of treatment was 35 years; mean body mass indices were within the normal range (23.6 kg/m2 for fresh transfers and 23.2 kg/m2 for frozen transfers, P = .26), and mean day 3 follicle-stimulating hormone values were 7.1 and 7.0 IU/L (P = .44), respectively. Deliveries occurred on average at 37.5 and 38.0 weeks’ gestational age (P = .04) in the fresh versus frozen transfer group, with similar rates of obstetric complications. However, frozen transfers were more likely to be associated with marginal cord insertion (adjusted odds ratio, 1.87; confidence interval, 1.21, 2.91; P = .01), accessory lobe formation (adjusted odds ratio, 2.96; confidence interval, 1.12, 7.79; P = 0.03), subchorionic thrombi (adjusted odds ratio, 3.72; confidence interval, 1.80, 7.71; P Conclusion Pregnancies arising from frozen embryo transfers demonstrated more anatomic and vascular Placental Pathology than those from fresh transfers in our cohort of patients, despite similar maternal outcomes. More research is needed to explore how these differences in Pathology may influence obstetric and perinatal outcomes.
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Placental Pathology in live births conceived with in vitro fertilization after fresh and frozen embryo transfer.
American Journal of Obstetrics and Gynecology, 2019Co-Authors: C R Sacha, Amy L Harris, Kaitlyn E James, Kristen M Basnet, Taylor S Freret, Anjali J Kaimal, Irene Souter, Drucilla J RobertsAbstract:Abstract Background The availability and use of frozen embryos after ovarian hyperstimulation for assisted reproduction has increased with improvement in vitrification techniques and the rise of pre-implantation genetic testing. However, there is conflicting data regarding whether obstetric outcomes differ between fresh and frozen embryo transfer cycles. Objective To compare Placental Pathology from live births arising from fresh and frozen embryo transfer cycles. Study Design A cohort of 1140 live births with Placental Pathology arising from autologous in vitro fertilization cycles with fresh or frozen programmed transfer performed at MGH Fertility Center between 2004 and 2017 was retrospectively reviewed. An experienced Placental pathologist categorized the reported Placental Pathology as anatomic, infectious, inflammatory, or vascular/thrombotic. Our primary outcomes were differences in these Placental pathologies between the two groups. Patient demographic, cycle, and birth outcomes were compared with chi square tests, Student’s t-test, or nonparametric tests, as appropriate. Multivariate logistic regression models were used to compare Placental Pathology between the fresh and frozen transfer groups. Results Of the 1140 cycles included in our analysis, 929 arose from fresh embryo transfers (81.3%) and 211 arose from programmed frozen embryo transfers (18.5%). For both transfer types, the average age of the women at time of treatment was 35 years; mean BMIs were within the normal range (23.6 kg/m2 for fresh transfers and 23.2 kg/m2 for frozen transfers, p = 0.26); and mean day 3 FSH was 7.1 and 7.0 IU/L (p = 0.44), respectively. Deliveries occurred on average at 37.5 and 38.0 weeks gestational age (p = 0.037) in the fresh vs. frozen transfer group, with similar rates of obstetric complications. However, frozen transfers were more likely to be associated with marginal cord insertion [aOR 1.87 (CI 1.21, 2.91); p = 0.01], accessory lobe formation [aOR 2.96 (CI 1.12, 7.79); p = 0.03], subchorionic thrombi [aOR 3.72 (CI 1.8, 7.71); p Conclusions Pregnancies arising from frozen embryo transfers demonstrated more anatomic and vascular Placental Pathology than those from fresh transfers in our cohort of patients, despite similar maternal outcomes. More research is needed to explore how these differences in Pathology may influence obstetric and perinatal outcomes.
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a systematic review of Placental Pathology in maternal diabetes mellitus
Placenta, 2015Co-Authors: Jennifer Huynh, Drucilla J Roberts, D Dawson, Rhonda BentleylewisAbstract:Abstract Introduction During a pregnancy complicated by diabetes, the human placenta undergoes a number of functional and structural pathologic changes, such as increased Placental weight and increased incidence of Placental lesions including villous maturational defects and fibrinoid necrosis. The pathologic findings reported have differed among studies, potentially reflecting differences in type of diabetes, study methodology, or glycemic control of study participants. Alternatively, these discrepancies may represent different biologic adaptations to distinct metabolic diseases. Methods We conducted a comprehensive review of English language citations in Pubmed and Embase using the keywords “diabetes”, “placenta”, AND “Pathology”. Abstracts were reviewed for relevance then full-text articles were reviewed in order to extract a comprehensive summary of current pathological findings associated with pregestational and gestational diabetes mellitus, as well as an understanding of the impact of glycemic control on Placental Pathology. Results Placental abnormalities most consistently associated with maternal diabetes are an increased incidence of villous immaturity, increased measures of angiogenesis, and increased Placental weight. Conclusions The literature suggests that, despite similarities in Placental abnormalities, differences in Placental Pathology may reflect differences in pathophysiology among different types of diabetes. Consequently, standardization of terminology used to define Placental lesions is warranted. Moreover, further research is needed to investigate the impact of pathophysiology, glycemic control and clinical factors, such as infant sex, weight and race, on Placental structure and function.
John Kingdom - One of the best experts on this subject based on the ideXlab platform.
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defining early vs late fetal growth restriction by Placental Pathology
Acta Obstetricia et Gynecologica Scandinavica, 2019Co-Authors: Amir Aviram, Christopher Sherman, John Kingdom, Arthur Zaltz, Jon Barrett, Nir MelamedAbstract:INTRODUCTION: Although early and late fetal growth restriction have been suggested to be distinct entities, the optimal gestational age cut-off that differentiates the two conditions is currently unclear and has been arbitrarily set in previous studies between 32 and 37 weeks. We aimed to use Placental Pathology findings to determine that optimal gestational age cut-off between early and late fetal growth restriction. MATERIAL AND METHODS: A retrospective cohort study of all women with singleton gestation who gave birth to a neonate diagnosed as small-for-gestational age (small-for-gestational age, defined as birthweight <10th percentile for gestational age) at a tertiary referral center between January 2001 and December 2015, and for whom Placental Pathology was available. Placental abnormalities were classified into lesions associated with maternal vascular malperfusion (MVM), fetal vascular malperfusion, Placental hemorrhage and chronic villitis. Placental findings were analyzed as a function of gestational age at birth. The analysis was repeated in the subgroups of women without hypertensive complications of pregnancy (to reflect changes associated with isolated small-for-gestational age) and of neonates with severe small-for-gestational age (defined as birthweight <5th percentile), which are more likely to represent true fetal growth restriction. RESULTS: A total of 895 women met the inclusion criteria. The only histological finding that changed with gestational age was MVM Pathology, which decreased in frequency with increasing gestational age. We identified a considerable drop in the rate of MVM lesions at 33 weeks of gestation. The rate of MVM Pathology in placentas of infants born before 330/7 weeks was significantly higher than that observed in placentas of infants born at 330/7 weeks or longer: 71.6% vs 27.4%, P < 0.001 for ≥2 MVM lesions, and 35.5% vs 3.5%, P < 0.001 for ≥3 MVM lesions. These findings persisted in the subgroups of women without hypertensive complications of pregnancy (n = 662) and of neonates with severe small-for-gestational age (n = 464). CONCLUSIONS: Using Placental Pathology as a direct measure of the mechanisms underlying fetal growth restriction, the optimal gestational age at birth cut-off which differentiates early from late fetal growth restriction appears to be 330/7 weeks.
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Defining early vs late fetal growth restriction by Placental Pathology
Acta Obstetricia et Gynecologica Scandinavica, 2018Co-Authors: Amir Aviram, Christopher Sherman, John Kingdom, Arthur Zaltz, Jon Barrett, Nir MelamedAbstract:Although early and late fetal growth restriction have been suggested to be distinct entities, the optimal gestational age cut-off that differentiates the two conditions is currently unclear and has been arbitrarily set in previous studies between 32 and 37 weeks. We aimed to use Placental Pathology findings to determine that optimal gestational age cut-off between early and late fetal growth restriction. A retrospective cohort study of all women with singleton gestation who gave birth to a neonate diagnosed as small-for-gestational age (small-for-gestational age, defined as birthweight <10th percentile for gestational age) at a tertiary referral center between January 2001 and December 2015, and for whom Placental Pathology was available. Placental abnormalities were classified into lesions associated with maternal vascular malperfusion (MVM), fetal vascular malperfusion, Placental hemorrhage and chronic villitis. Placental findings were analyzed as a function of gestational age at birth. The analysis was repeated in the subgroups of women without hypertensive complications of pregnancy (to reflect changes associated with isolated small-for-gestational age) and of neonates with severe small-for-gestational age (defined as birthweight <5th percentile), which are more likely to represent true fetal growth restriction. A total of 895 women met the inclusion criteria. The only histological finding that changed with gestational age was MVM Pathology, which decreased in frequency with increasing gestational age. We identified a considerable drop in the rate of MVM lesions at 33 weeks of gestation. The rate of MVM Pathology in placentas of infants born before 330/7 weeks was significantly higher than that observed in placentas of infants born at 330/7 weeks or longer: 71.6% vs 27.4%, P < 0.001 for ≥2 MVM lesions, and 35.5% vs 3.5%, P < 0.001 for ≥3 MVM lesions. These findings persisted in the subgroups of women without hypertensive complications of pregnancy (n = 662) and of neonates with severe small-for-gestational age (n = 464). Using Placental Pathology as a direct measure of the mechanisms underlying fetal growth restriction, the optimal gestational age at birth cut-off which differentiates early from late fetal growth restriction appears to be 330/7 weeks. © 2018 Nordic Federation of Societies of Obstetrics and Gynecology.
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Placental Pathology in relation to uterine artery doppler findings in pregnancies with severe intrauterine growth restriction and abnormal umbilical artery doppler changes
American Journal of Perinatology, 2016Co-Authors: Khrystyna Levytska, Nir Melamed, Mary Higgins, Sarah Keating, Melissa Walker, Neil J Sebire, John KingdomAbstract:Objectives Current guidelines for diagnosis and management of early-onset intrauterine growth restriction (IUGR) rely on umbilical artery Doppler (UAD), without including uterine artery Doppler (UtAD). We hypothesized that IUGR cases with abnormal UAD but normal UtAD has a different spectrum of Placental Pathology compared with those with abnormal UtAD. Study Design Retrospective review of pregnancies with sonographic evidence of IUGR and abnormal UAD prior to delivery. Cases with ≥ 1 UtAD record(s) after 18+0 weeks' gestation and Placental Pathology were included. Cases were stratified according to initial UtAD pulsatility index (PI) values (n = 196): normal (n = 19; PI Results Women in the normal group delivered later than those in the abnormal group (30.1 ± 3.5 vs. 28.0 ± 3.5 weeks; mean ± standard deviation; p = 0.03). Their placentas exhibited higher rates of chronic intervillositis (15.8 vs. 0.9%; p = 0.01), chorangiosis (15.8 vs. 0.9%; p Conclusion Approximately 10% of pregnancies with early-onset IUGR and abnormal UAD exhibited normal UtAD waveforms. They delivered later, and their placentas exhibited unusual Placental pathologies.
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mri reveals increased superior vena caval blood flow in human fetuses with congenital heart disease abnormal Placental Pathology and neonatal brain white matter changes
Journal of Cardiovascular Magnetic Resonance, 2015Co-Authors: Sujana Madathil, John Kingdom, Brahmdeep S Saini, Edgar Jaeggi, Lars Grossewortmann, Edward J Hickey, Steven P Miller, Christopher K Macgowan, Mike SeedAbstract:Background Delayed brain development in newborns with congenital heart disease (CHD) results in increased vulnerability to white matter injury before and after cardiac surgery [1]. Doppler showing reductions in pulsatility index (PI) in the middle cerebral arteries (MCA) of fetuses with CHD is interpreted as evidence of “brain sparing physiology”. It supports the hypothesis that in utero brain dysmaturation in CHD is due to reduced cerebral oxygen delivery [2]. We were interested in the relationship between cerebral blood flow, Placental Pathology and white matter changes in CHD fetuses using ultrasound and MRI.
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emerging role of sumoylation in Placental Pathology
Placenta, 2013Co-Authors: Dora Baczyk, Sascha Drewlo, John KingdomAbstract:Abstract Introduction Small ubiquitin-like modifiers (SUMO) conjugate to target proteins in a dynamic, reversible manner to function as post-translational modifiers. SUMOylation of target proteins can impinge on their localization, in addition to their activity or stability. Differential expression of deSUMOylating enzymes (SENP 1 and 2) contributes to altered mammalian Placental development and function in mice. Severe preeclampsia (sPE) is associated with abnormal Placental development and chronic ischemic injury. Extra- and intracellular stimuli/stressors that include hypoxic-activated pathways are known modulators of SUMOylation. In this current study we hypothesized that placentas from sPE patients will display up regulation in the SUMO regulatory pathway. Methods Utilizing qRT-PCR, immuno-blotting and Western techniques, we determined the expression levels of SUMO pathway genes in healthy and diseased placentas. We also exposed Placental explants to hypoxia to study the effect on the SUMOylation pathway. Results We observed steady-state expression of SUMO1–3, SUMO-conjugated enzyme-UBC9 and deSUMOylating enzymes – SENPs, throughout normal gestation. An elevated level of free SUMO1–3 and SUMO-protein conjugates was observed in sPE placentas. Furthermore, Placental UBC9 levels were strikingly increased in the same sPE patients. Hypoxia-induced SUMOylation in first trimester Placental explants. Discussion Our data demonstrate an elevated steady-state of SUMOylation in sPE placentas compared with gestational aged-matched controls. The observed hyper-SUMOylation in sPE placentas correlates with elevated expression of UBC9 rather than with reduced expression of SENPs Hypoxia may contribute to alterations in Placental SUMOylation pathway. Conclusion Increased Placental SUMOylation may contribute to the pathogenesis of serious Placental Pathology that causes extreme preterm birth.
Nir Melamed - One of the best experts on this subject based on the ideXlab platform.
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defining early vs late fetal growth restriction by Placental Pathology
Acta Obstetricia et Gynecologica Scandinavica, 2019Co-Authors: Amir Aviram, Christopher Sherman, John Kingdom, Arthur Zaltz, Jon Barrett, Nir MelamedAbstract:INTRODUCTION: Although early and late fetal growth restriction have been suggested to be distinct entities, the optimal gestational age cut-off that differentiates the two conditions is currently unclear and has been arbitrarily set in previous studies between 32 and 37 weeks. We aimed to use Placental Pathology findings to determine that optimal gestational age cut-off between early and late fetal growth restriction. MATERIAL AND METHODS: A retrospective cohort study of all women with singleton gestation who gave birth to a neonate diagnosed as small-for-gestational age (small-for-gestational age, defined as birthweight <10th percentile for gestational age) at a tertiary referral center between January 2001 and December 2015, and for whom Placental Pathology was available. Placental abnormalities were classified into lesions associated with maternal vascular malperfusion (MVM), fetal vascular malperfusion, Placental hemorrhage and chronic villitis. Placental findings were analyzed as a function of gestational age at birth. The analysis was repeated in the subgroups of women without hypertensive complications of pregnancy (to reflect changes associated with isolated small-for-gestational age) and of neonates with severe small-for-gestational age (defined as birthweight <5th percentile), which are more likely to represent true fetal growth restriction. RESULTS: A total of 895 women met the inclusion criteria. The only histological finding that changed with gestational age was MVM Pathology, which decreased in frequency with increasing gestational age. We identified a considerable drop in the rate of MVM lesions at 33 weeks of gestation. The rate of MVM Pathology in placentas of infants born before 330/7 weeks was significantly higher than that observed in placentas of infants born at 330/7 weeks or longer: 71.6% vs 27.4%, P < 0.001 for ≥2 MVM lesions, and 35.5% vs 3.5%, P < 0.001 for ≥3 MVM lesions. These findings persisted in the subgroups of women without hypertensive complications of pregnancy (n = 662) and of neonates with severe small-for-gestational age (n = 464). CONCLUSIONS: Using Placental Pathology as a direct measure of the mechanisms underlying fetal growth restriction, the optimal gestational age at birth cut-off which differentiates early from late fetal growth restriction appears to be 330/7 weeks.
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Defining early vs late fetal growth restriction by Placental Pathology
Acta Obstetricia et Gynecologica Scandinavica, 2018Co-Authors: Amir Aviram, Christopher Sherman, John Kingdom, Arthur Zaltz, Jon Barrett, Nir MelamedAbstract:Although early and late fetal growth restriction have been suggested to be distinct entities, the optimal gestational age cut-off that differentiates the two conditions is currently unclear and has been arbitrarily set in previous studies between 32 and 37 weeks. We aimed to use Placental Pathology findings to determine that optimal gestational age cut-off between early and late fetal growth restriction. A retrospective cohort study of all women with singleton gestation who gave birth to a neonate diagnosed as small-for-gestational age (small-for-gestational age, defined as birthweight <10th percentile for gestational age) at a tertiary referral center between January 2001 and December 2015, and for whom Placental Pathology was available. Placental abnormalities were classified into lesions associated with maternal vascular malperfusion (MVM), fetal vascular malperfusion, Placental hemorrhage and chronic villitis. Placental findings were analyzed as a function of gestational age at birth. The analysis was repeated in the subgroups of women without hypertensive complications of pregnancy (to reflect changes associated with isolated small-for-gestational age) and of neonates with severe small-for-gestational age (defined as birthweight <5th percentile), which are more likely to represent true fetal growth restriction. A total of 895 women met the inclusion criteria. The only histological finding that changed with gestational age was MVM Pathology, which decreased in frequency with increasing gestational age. We identified a considerable drop in the rate of MVM lesions at 33 weeks of gestation. The rate of MVM Pathology in placentas of infants born before 330/7 weeks was significantly higher than that observed in placentas of infants born at 330/7 weeks or longer: 71.6% vs 27.4%, P < 0.001 for ≥2 MVM lesions, and 35.5% vs 3.5%, P < 0.001 for ≥3 MVM lesions. These findings persisted in the subgroups of women without hypertensive complications of pregnancy (n = 662) and of neonates with severe small-for-gestational age (n = 464). Using Placental Pathology as a direct measure of the mechanisms underlying fetal growth restriction, the optimal gestational age at birth cut-off which differentiates early from late fetal growth restriction appears to be 330/7 weeks. © 2018 Nordic Federation of Societies of Obstetrics and Gynecology.
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Placental Pathology in Relation to Uterine Artery Doppler Findings in Pregnancies with Severe Intrauterine Growth Restriction and Abnormal Umbilical Artery Doppler Changes.
American journal of perinatology, 2016Co-Authors: Khrystyna Levytska, Nir Melamed, Mary Higgins, Sarah Keating, Melissa Walker, Neil J Sebire, John C P KingdomAbstract:Objectives Current guidelines for diagnosis and management of early-onset intrauterine growth restriction (IUGR) rely on umbilical artery Doppler (UAD), without including uterine artery Doppler (UtAD). We hypothesized that IUGR cases with abnormal UAD but normal UtAD has a different spectrum of Placental Pathology compared with those with abnormal UtAD. Study Design Retrospective review of pregnancies with sonographic evidence of IUGR and abnormal UAD prior to delivery. Cases with ≥ 1 UtAD record(s) after 18+0 weeks' gestation and Placental Pathology were included. Cases were stratified according to initial UtAD pulsatility index (PI) values (n = 196): normal (n = 19; PI
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Placental Pathology in relation to uterine artery doppler findings in pregnancies with severe intrauterine growth restriction and abnormal umbilical artery doppler changes
American Journal of Perinatology, 2016Co-Authors: Khrystyna Levytska, Nir Melamed, Mary Higgins, Sarah Keating, Melissa Walker, Neil J Sebire, John KingdomAbstract:Objectives Current guidelines for diagnosis and management of early-onset intrauterine growth restriction (IUGR) rely on umbilical artery Doppler (UAD), without including uterine artery Doppler (UtAD). We hypothesized that IUGR cases with abnormal UAD but normal UtAD has a different spectrum of Placental Pathology compared with those with abnormal UtAD. Study Design Retrospective review of pregnancies with sonographic evidence of IUGR and abnormal UAD prior to delivery. Cases with ≥ 1 UtAD record(s) after 18+0 weeks' gestation and Placental Pathology were included. Cases were stratified according to initial UtAD pulsatility index (PI) values (n = 196): normal (n = 19; PI Results Women in the normal group delivered later than those in the abnormal group (30.1 ± 3.5 vs. 28.0 ± 3.5 weeks; mean ± standard deviation; p = 0.03). Their placentas exhibited higher rates of chronic intervillositis (15.8 vs. 0.9%; p = 0.01), chorangiosis (15.8 vs. 0.9%; p Conclusion Approximately 10% of pregnancies with early-onset IUGR and abnormal UAD exhibited normal UtAD waveforms. They delivered later, and their placentas exhibited unusual Placental pathologies.
Michal Kovo - One of the best experts on this subject based on the ideXlab platform.
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pregnancy outcome and Placental Pathology in emergent cesarean deliveries for non reassuring fetal heart rate in laboring versus non laboring women
Journal of Maternal-fetal & Neonatal Medicine, 2016Co-Authors: Eran Weiner, Letizia Schreiber, Nataly Fainstein, Adam Pomeranz, Michal KovoAbstract:AbstractObjective: The objective of this study is to correlate between pregnancy outcome and Placental Pathology in emergent cesarean deliveries (ECD) for non-reassuring-fetal-heart-rate (NRFHR) performed in women in their active phase of labor versus those performed in non-laboring women.Methods: A retrospective cohort study. Data were reviewed for all pregnancies necessitating ECD for NRFHR between January 2009 and December 2013. Maternal outcome, neonatal outcome, and Placental Pathology parameters were compared between ECDs performed during active phase of labor and those performed before the active phase of labor (non-labor group).Results: During the study period, a total of 661 ECDs were performed due to NRFHR. Compared with the active labor group (n = 335), the non-labor group (n = 326) had more pre-eclampsia (p = 0.033), small for gestational age (SGA) (p = 0.016), and preterm labor (p < 0.001). Worse composite neonatal outcome was observed in the non-labor group compared with the active labor gro...
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the effect of placenta previa on fetal growth and pregnancy outcome in correlation with Placental Pathology
Journal of Perinatology, 2016Co-Authors: Eran Weiner, Hadas Miremberg, Ehud Grinstein, Yossi Mizrachi, Letizia Schreiber, Michal KovoAbstract:The effect of placenta previa on fetal growth and pregnancy outcome, in correlation with Placental Pathology
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pregnancy outcome and Placental Pathology differences in term gestational diabetes with and without hypertensive disorders
Journal of Maternal-fetal & Neonatal Medicine, 2016Co-Authors: Michal Kovo, Letizia Schreiber, Yoav Granot, Michael Divon, Avi BenharoushAbstract:AbstractObjective: To compare pregnancy outcome and Placental Pathology in pregnancies complicated by gestational diabetes mellitus (GDM A1 and A2), with and without hypertensive disorders.Methods: Pregnancy outcome and Placental Pathology from term deliveries of women complicated with GDM with (GDM + H) and without (GDM − H) hypertensive disorders were compared. Results of the GDM + H group were compared also with the non-diabetic patients but with hypertensive disorders (non-GDM + H). Composite neonatal outcome was defined as one or more of early complications: respiratory distress or need of ventilation support, sepsis, phototherapy, transfusion, seizure, hypoxic-ischemic encephalopathy. Placental lesions were categorized to lesions related to maternal and fetal vascular supply abnormalities, and maternal and fetal inflammatory responses.Results: Of the 192 women with GDM, the GDM + H group (n = 41) were more obese, p < 0.001, with higher rate of Placental maternal and fetal vascular supply lesions, p ...
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Pregnancy outcome and Placental Pathology in emergent cesarean deliveries for non-reassuring fetal heart rate in laboring versus non-laboring women
Journal of Maternal-fetal & Neonatal Medicine, 2015Co-Authors: Eran Weiner, Letizia Schreiber, Nataly Fainstein, Adam Pomeranz, Michal KovoAbstract:AbstractObjective: The objective of this study is to correlate between pregnancy outcome and Placental Pathology in emergent cesarean deliveries (ECD) for non-reassuring-fetal-heart-rate (NRFHR) performed in women in their active phase of labor versus those performed in non-laboring women.Methods: A retrospective cohort study. Data were reviewed for all pregnancies necessitating ECD for NRFHR between January 2009 and December 2013. Maternal outcome, neonatal outcome, and Placental Pathology parameters were compared between ECDs performed during active phase of labor and those performed before the active phase of labor (non-labor group).Results: During the study period, a total of 661 ECDs were performed due to NRFHR. Compared with the active labor group (n = 335), the non-labor group (n = 326) had more pre-eclampsia (p = 0.033), small for gestational age (SGA) (p = 0.016), and preterm labor (p
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Pregnancy outcome and Placental Pathology differences in term gestational diabetes with and without hypertensive disorders
Journal of Maternal-fetal & Neonatal Medicine, 2015Co-Authors: Michal Kovo, Letizia Schreiber, Yoav Granot, Michael Divon, Avi Ben-haroushAbstract:AbstractObjective: To compare pregnancy outcome and Placental Pathology in pregnancies complicated by gestational diabetes mellitus (GDM A1 and A2), with and without hypertensive disorders.Methods: Pregnancy outcome and Placental Pathology from term deliveries of women complicated with GDM with (GDM + H) and without (GDM − H) hypertensive disorders were compared. Results of the GDM + H group were compared also with the non-diabetic patients but with hypertensive disorders (non-GDM + H). Composite neonatal outcome was defined as one or more of early complications: respiratory distress or need of ventilation support, sepsis, phototherapy, transfusion, seizure, hypoxic-ischemic encephalopathy. Placental lesions were categorized to lesions related to maternal and fetal vascular supply abnormalities, and maternal and fetal inflammatory responses.Results: Of the 192 women with GDM, the GDM + H group (n = 41) were more obese, p
Amir Aviram - One of the best experts on this subject based on the ideXlab platform.
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defining early vs late fetal growth restriction by Placental Pathology
Acta Obstetricia et Gynecologica Scandinavica, 2019Co-Authors: Amir Aviram, Christopher Sherman, John Kingdom, Arthur Zaltz, Jon Barrett, Nir MelamedAbstract:INTRODUCTION: Although early and late fetal growth restriction have been suggested to be distinct entities, the optimal gestational age cut-off that differentiates the two conditions is currently unclear and has been arbitrarily set in previous studies between 32 and 37 weeks. We aimed to use Placental Pathology findings to determine that optimal gestational age cut-off between early and late fetal growth restriction. MATERIAL AND METHODS: A retrospective cohort study of all women with singleton gestation who gave birth to a neonate diagnosed as small-for-gestational age (small-for-gestational age, defined as birthweight <10th percentile for gestational age) at a tertiary referral center between January 2001 and December 2015, and for whom Placental Pathology was available. Placental abnormalities were classified into lesions associated with maternal vascular malperfusion (MVM), fetal vascular malperfusion, Placental hemorrhage and chronic villitis. Placental findings were analyzed as a function of gestational age at birth. The analysis was repeated in the subgroups of women without hypertensive complications of pregnancy (to reflect changes associated with isolated small-for-gestational age) and of neonates with severe small-for-gestational age (defined as birthweight <5th percentile), which are more likely to represent true fetal growth restriction. RESULTS: A total of 895 women met the inclusion criteria. The only histological finding that changed with gestational age was MVM Pathology, which decreased in frequency with increasing gestational age. We identified a considerable drop in the rate of MVM lesions at 33 weeks of gestation. The rate of MVM Pathology in placentas of infants born before 330/7 weeks was significantly higher than that observed in placentas of infants born at 330/7 weeks or longer: 71.6% vs 27.4%, P < 0.001 for ≥2 MVM lesions, and 35.5% vs 3.5%, P < 0.001 for ≥3 MVM lesions. These findings persisted in the subgroups of women without hypertensive complications of pregnancy (n = 662) and of neonates with severe small-for-gestational age (n = 464). CONCLUSIONS: Using Placental Pathology as a direct measure of the mechanisms underlying fetal growth restriction, the optimal gestational age at birth cut-off which differentiates early from late fetal growth restriction appears to be 330/7 weeks.
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Defining early vs late fetal growth restriction by Placental Pathology
Acta Obstetricia et Gynecologica Scandinavica, 2018Co-Authors: Amir Aviram, Christopher Sherman, John Kingdom, Arthur Zaltz, Jon Barrett, Nir MelamedAbstract:Although early and late fetal growth restriction have been suggested to be distinct entities, the optimal gestational age cut-off that differentiates the two conditions is currently unclear and has been arbitrarily set in previous studies between 32 and 37 weeks. We aimed to use Placental Pathology findings to determine that optimal gestational age cut-off between early and late fetal growth restriction. A retrospective cohort study of all women with singleton gestation who gave birth to a neonate diagnosed as small-for-gestational age (small-for-gestational age, defined as birthweight <10th percentile for gestational age) at a tertiary referral center between January 2001 and December 2015, and for whom Placental Pathology was available. Placental abnormalities were classified into lesions associated with maternal vascular malperfusion (MVM), fetal vascular malperfusion, Placental hemorrhage and chronic villitis. Placental findings were analyzed as a function of gestational age at birth. The analysis was repeated in the subgroups of women without hypertensive complications of pregnancy (to reflect changes associated with isolated small-for-gestational age) and of neonates with severe small-for-gestational age (defined as birthweight <5th percentile), which are more likely to represent true fetal growth restriction. A total of 895 women met the inclusion criteria. The only histological finding that changed with gestational age was MVM Pathology, which decreased in frequency with increasing gestational age. We identified a considerable drop in the rate of MVM lesions at 33 weeks of gestation. The rate of MVM Pathology in placentas of infants born before 330/7 weeks was significantly higher than that observed in placentas of infants born at 330/7 weeks or longer: 71.6% vs 27.4%, P < 0.001 for ≥2 MVM lesions, and 35.5% vs 3.5%, P < 0.001 for ≥3 MVM lesions. These findings persisted in the subgroups of women without hypertensive complications of pregnancy (n = 662) and of neonates with severe small-for-gestational age (n = 464). Using Placental Pathology as a direct measure of the mechanisms underlying fetal growth restriction, the optimal gestational age at birth cut-off which differentiates early from late fetal growth restriction appears to be 330/7 weeks. © 2018 Nordic Federation of Societies of Obstetrics and Gynecology.