Placental Infarction Research Articles

P10.06: Congenital fetal anomalies are associated with placental pathologic change

The aim of this research was to systematically examine the placenta in congenital anomalies. The placental pathological section was examined in 217 cases with congenital fetal anomalies including 87 cases with congenital heart diseases, 41 cases facial abnormalities, genitourinary abnormalities, 62 cases with neurologic abnormalities. Placental infarction or villus degeneration was observed in 4 cases and chorangiosis was found in 12 cases with congenital heart diseases corresponding to the overall placental disease rate being 16.1%; chorangiosis was observed in 5 cases with facial abnormalities corresponding to the placental disease rate being 12.1%; chorangiosis was found in 2 cases with genitourinary abnormalities corresponding to the placental disease rate being 7.4%. In addition, chorangiosis was observed in 10 cases with neurologic abnormalities corresponding to the placental disease rate being 14.5%. Relative to other system abnormalities the placental disease rate was more higher in cases with congenital fetal heart anomalies.

P05.04: Placental histology and sFlt‐1/PlGF in pregnancies complicated by hypertensive disorders

Redline classification correlates the histology of placental lesions with the pathogenesis of the correspondent obstetric disorder. Our work evaluates the correlation between hypertensive disorders of pregnancy (HDP), placental histology and circulating angiogenic factors (sFlt-1, PlGF). In this observational study, 30 pregnant patients affected by HDP (gestational hypertension, pre-eclampsia) were recruited: 20 HDP with intrauterine growth restriction (HDP-IUGR) and 10 HDP with an appropriate for gestational age fetus (HDP-AGAf); 16 controls with uneventful pregnancies were also included. Diagnosis of HDP was based on Canadian Guidelines (SOGC 2014). Diagnosis of IUGR was made for fetuses with abdominal circumference (AC) < 10th percentile or with AC measure deflecting at least 40 percentiles. The patients underwent a blood sampling for the dosage of sFlt-1 and PlGF. Placentas were analysed for histological examination, executed in blind by a dedicated pathologist, using Redline classification. HDP-IUGR shows vascular lesions on the placental maternal side in 95% of cases, significantly more than HDP-AGA (p=0.03) and also than controls (p<0.001). These lesions result from early placental oxidative stress, due to incomplete spiral arteries remodelling; they include developmental anomalies (decidual arteriopathy 50%, villous hypoplasia 40%) and obstructive vascular lesions (syncytial knots 65%, placental infarcts 40%). HDP-AGA predominantly shows vascular lesions on the placental fetal side in 70% of cases. These lesions are represented for 70% by developmental anomalies, especially hyper-ramification and villous immaturity, indicating late placental oxidative stress. sFlt-1/PlGF ratio correlates with vascular lesions on the placental maternal side, typical of HDP-IUGR group. Placental histology and angiogenic markers correlate with the severity of placental damage and with the different fetoplacental phenotypes of HDP, supporting investigations about their pathogenesis.

Investigating in utero fetal death: outcome of internal medicine consultation.

The objectives were to determine the frequency of in utero fetal death (IUFD) related to placental disorders and to assess the frequency of antiphospholipid antibodies syndrome (APS) among women referred to the internal medicine department. A retrospective clinical study conducted in Rennes University Hospital, France. From January 2007 to December 2014, 53 women who presented an IUFD at 14 weeks or more of gestational age were included. The main cause for each IUFD was determined by expert agreement. Primary outcome was to analyze the final etiologies diagnosed and the prevalence of IUFD related to placental disorders. Secondary outcomes included the frequency of APS among patients with IUFD of placental origin and the pathological and clinical features associated with APS. IUFD resulted from placental disorders in 36/53 (68%) patients, and remained unexplained in 11 cases (20.8%). Among the 36 patients with placental disorders, APS was diagnosed in five (13.9%) cases, and four (11.1%) patients were considered as having 'non-criteria' APS. History of thrombosis (P = 0.001) and placental infarcts (P = 0.047) were significantly associated with APS. Placental disorders were the major cause for IUFD in patients who were referred to internal medicine specialists. Importantly, APS was seldom found in patients with placental disorders. Venous thromboembolism history and placental infarcts were both significantly associated with APS. Further studies are needed in order to deepen our understanding of the physiopathology of placental disorders and its underlying causes among non-APS women, and to determine the best treatment regimen for future pregnancies.

Placental Pathology Findings Associated With Adverse Outcomes Among Women With Sickle Cell Hemoglobinopathies [8N

INTRODUCTION: The objective of this study is to investigate the relationship between placental pathology findings among women with sickle cell hemoglobinopathies (SCH) and adverse perinatal outcomes (APO). METHODS: This is a retrospective cohort study of non-anomalous, singleton infants born to mothers with laboratory confirmed SCH and placental pathology results. Medical charts were reviewed for maternal and neonatal outcomes as we sought to identify histologic findings associated with APOs. APOs included fetal death, small for gestational age neonates, umbilical cord pH &lt; 7.2, 5 minute Apgar &lt; 7, and neonatal death. RESULTS: One hundred thirty-five patients met inclusion criteria. Eighty-six percent had sickle cell trait, 12% had sickle cell disease, and 2% had hemoglobin SC disease. Twenty-seven pregnancies (20%) were complicated by APOs. There was no difference in presence of the following placental findings among the APO group as compared to the group without APOs: delayed villous maturation (p=0.59), perivillous fibrin deposition (p=0.58), placental infarction (p=0.62), chorioamnionitis (p=0.63), funisitis (p=0.24), villous congestion (p=0.39), and increased syncytial knots (p=0.10). When placental pathology findings among patients with sickle cell anemia were compared to patients with other types of SCH, there was a difference among groups with respect to increased syncytial knots (p &lt; 0.01). CONCLUSION: There was no difference in placental pathology findings among patients with SCH with and without APOs. Severity of maternal disease was associated with a higher rate of increased syncytial knots; which are associated with reduced uteroplacental perfusion and may be induced by exposure of the placenta to hypoxia or oxidative stress as seen in SCH.

Enhancement of trophoblast differentiation and survival by low molecular weight heparin requires heparin-binding EGF-like growth factor.

Does low molecular weight heparin (LMWH) require heparin-binding epidermal growth factor (EGF)-like growth factor (HBEGF) signaling to induce extravillous trophoblast differentiation and decrease apoptosis during oxidative stress? LMWH increased HBEGF expression and secretion, and HBEGF signaling was required to stimulate trophoblast extravillous differentiation, increase invasion in vitro and reduce trophoblast apoptosis during oxidative stress. Abnormal trophoblast differentiation and survival contribute to placental insufficiency syndromes, including preeclampsia and intrauterine growth restriction. Preeclampsia often manifests as a pro-thrombotic state, with unsuccessful transformation of the spiral arteries that reduces oxygen supply and can produce placental infarction. LMWH improves placental function by increasing blood flow. Recent data suggest that the actions of LMWH transcend its anti-coagulative properties, but the molecular mechanism is unknown. There is evidence that LMWH alters the expression of human HBEGF in trophoblast cells, which regulates human trophoblast pathophysiology. HBEGF, itself, is capable of increasing trophoblast survival and invasiveness. First-trimester placental explants and the HTR-8/SVneo cell line, established using extravillous trophoblast outgrowths from first-trimester villous explants, were treated in vitro with LMWH to examine the effects on HBEGF signaling and trophoblast function under normal physiological and pathological conditions. A highly specific antagonist of HBEGF and other inhibitors of HBEGF downstream signaling were used to determine the relationship between LMWH treatment and HBEGF. Placental tissues (n = 5) were obtained with IRB approval and patient consent from first-trimester terminations. Placental explants and HTR-8/SVneo cells were cultured on plastic or Matrigel™ and treated with a therapeutic dose of LMWH (Enoxaparin; 10 IU/ml), with or without CRM197, pan Erb-B2 Receptor Tyrosine Kinase (ERBB) inhibitor, anti-ERBB1 or ERBB4 blocking antibodies, or pretreatment of cells with heparitinase I. Extravillous differentiation was assessed by immunocytochemistry to determine the relative levels of integrins α6β4 and α1β1. Trophoblast invasiveness was assessed in villous explants by measuring outgrowth from villous tips cultured on Matrigel, and by invasion assays with HTR-8/SVneo cells cultured on Matrigel-coated transwell insert. Placental explants and HTR-8/SVneo cells were exposed to oxidative stress in a hypoxia-reoxygenation (H-R) model, measuring cell death by TUNEL assay, caspase 3 cleavage, and BCL-2α expression. LMWH induced extravillous differentiation, according to trophoblast invasion assays and integrin (α6β4-α1β1) switching. Treatment with LMWH rescued cytotrophoblasts and HTR-8/SVneo cells from apoptosis during exposure to reoxygenation injury, based on TUNEL, caspase 3 cleavage and BCL-2α expression. Experiments using CRM197, ERBB1 and ERBB4 blocking antibodies, pan-ERBB inhibitor and removal of cell surface heparin demonstrated that the effects of LMWH on trophoblast invasion and survival were dependent upon HBEGF signaling. N/A. The primary limitation of this study was the use of only in vitro experiments. Patient demographics from elective terminations were not available. These data provide new insights into the non-coagulation-related aspects of perinatal LMWH treatment in the management of placental insufficiency disorders. This research was supported by grants from the National Institutes of Health (HD071408 and HL128628), the March of Dimes, and the W. K. Kellogg Foundation. There were no conflicts or competing interests.

Placental Pathology in Small-for-Gestational-Age Fetuses with Different Doppler Studies

Objectives: To describe and compare placental pathologies and neonatal outcomes in pregnancies with small-for-gestational-age (SGA) fetuses with their umbilical artery (UA) and middle cerebral artery (MCA) Doppler studies. Materials and Methods: A retrospective study was conducted in pregnant women delivered between gestational ages of 24 to 42 week at King Chulalongkorn Memorial Hospital. Only singletons without infection, chromosomal abnormalities or major structural abnormalities were included. Those with no Doppler study within 7 days prior to delivery were excluded. Sixty-nine subjects enrolled were classified into Group 1 (n=16): normal UA and MCA pulsatility index (PI), Group 2 (n=28): normal UA but abnormal MCA PI and Group 3 (n=25): abnormal UA PI/absent or reversed end diastolic flow (AREDF). Data were compared between each group. Results: Fetuses in Group 3 were found to be delivered at earlier gestational age with lower birth weight, higher Cesarean delivery rate, higher proportion of fetuses with Apgar score less than 7, higher NICU admission, and higher neonatal resuscitation rate than those in Group 1 and Group 2. There was no significant difference in placental weight, gross umbilical cord abnormality, and overall placental underperfusion pathology. Placental infarct in Group 3 was found to be more prevalent than those in Group 1 and Group 2. Conclusion: Placental infarct was the only abnormal placental pathology that was significantly found in SGA fetuses with abnormal UA PI/AREDF. These SGA fetuses carried a higher morbidity and mortality than those with normal UA Doppler study regardless of normality of MCA Doppler.

Decidual Vasculopathy: Placental Location and Association With Ischemic Lesions.

Decidual vasculopathy (DV) is a general term for a number of lesions involving uteroplacental vessels. It is often seen in preeclamptic placentas and indicates a disorder of uteroplacental malperfusion and is associated with placental ischemia and infarction. Although some have advocated submitting special sections in order to better document DV, it is unclear which placental sections have the highest yield in demonstrating these abnormal vessels. Seventy-six consecutive cases of decidual vasculopathy were identified and evaluated for location of DV, as well as presence of other lesions of ischemic change, infarcts, and retroplacental hematomas. Sections reviewed were the membrane roll (MR), full thickness (FT) sections of the placental disc, and sections specifically of the basal plate (BP). DV was found in the MR in 67.1% of cases, in FT sections in 32.9%, and in the BP in 25.0% of cases ( P value = .004). DV was exclusive to the MR in 53.9%, the FT in 14.5%, and the BP in 9.2%. DV was present in 2 locations in 19.7% and in all 3 locations in 2.6%. The presence of DV in any location (MR, FT, and BP) was associated with placental ischemic change but not specifically with infarcts or retroplacental hematomas. The specific location of DV showed no difference in the presence of placental lesions. Our findings indicate DV is often present in 1 location and is associated with lesions of malperfusion. It is recommended that when clinically indicated, additional sections are submitted to demonstrate decidual vasculopathy.

Uterine artery embolization for management of placenta accreta, a single-center experience and literature review

“Morbidly adherent placenta” is a term that describes the continuum of placenta accreta, increta, and percreta. Placenta accreta is the least invasive form, whereas placenta percreta represents a complete penetration of the trophoblast through the uterus that reaches the serosal surface and potentially invades the bladder, rectal wall, and pelvic vessels. Leaving the placenta in situ in the setting of abnormally invasive placenta is now widely practiced. We herein present three cases of abnormal placental implantation diagnosed by antenatal ultrasound and magnetic resonance imaging, in which uterine artery embolization was performed to induce placental infarction and eventually rapid regression but most importantly to minimize peripartum and postpartum bleeding. As we do this, we sought to review the risks of placenta accreta, increta, and percreta and evaluate the role of endovascular therapy to improve maternal outcomes when abnormal placental implantation occurs.

Uterine Artery Embolization for Management of Placenta Accreta, a Single-center Experience and Literature Review

Abstract“Morbidly adherent placenta” is a term that describes the continuum of placenta accreta, increta, and percreta. Placenta accreta is the least invasive form, whereas placenta percreta represents a complete penetration of the trophoblast through the uterus that reaches the serosal surface and potentially invades the bladder, rectal wall, and pelvic vessels. Leaving the placenta in situ in the setting of abnormally invasive placenta is now widely practiced. We herein present three cases of abnormal placental implantation diagnosed by antenatal ultrasound and magnetic resonance imaging, in which uterine artery embolization was performed to induce placental infarction and eventually rapid regression but most importantly to minimize peripartum and postpartum bleeding. As we do this, we sought to review the risks of placenta accreta, increta, and percreta and evaluate the role of endovascular therapy to improve maternal outcomes when abnormal placental implantation occurs.

Pathological findings associated with stillborn babies

Introduction: Fetal death rate and Perinatal Mortality rate are important indicators of a country’s Health care system. Stillbirth forms a prime contributing factor in deciding these rates. But the causes of Stillbirth and autopsy findings associated with Stillbirth remains a gray zone. The aim of this study is to analyse the pathological autopsy findings associated with spontaneously expelled stillbirth babies and placenta. Materials and Methods: This is a retrospective study conducted in Department of Pathology, Govt. Kilpauk Medical College, Chennai for a period of 1 and half years. 29 Stillborn cases were received in our department during this period. Fetal autopsy was done in these cases by using a standard protocol. The external, internal examination findings and histopathological findings of both fetus and Placenta were analysed and compared with the Antenatal clinical findings. Results: Stillbirth is more common in the third trimester constituting 72.4% cases and peaks at 27-30 weeks of gestation. Placental pathology is more frequently associated with stillbirth with 44.8% followed by Fetal causes with 34.5% and maternal causes identified in 6.9% cases. In the second trimester stillbirths fetal causes are common and in third trimester placental pathologies were common. Among the fetal causes, congenital anamolies are seen in all cases with CNS and Kidney anamolies being the commonest. Among the Placental causes, placental infarct is seen in most of the cases. In 13.8% cases, no pathology identified even after complete autopsy. Conclusion: A Complete schematic autopsy of fetus and placenta along with a good knowledge and correlation of pathological and clinical findings help in arriving at a diagnosis of cause of fetal demise. A correct diagnosis of the cause of stillbirth can alleviate parents worries and helps the clinician in deciding the counselling, care and management of future pregnancies.

SMI for imaging of placental infarction

Since superb Micro-vascular Imaging (SMI) is a new blood flow imaging technique that employs a unique algorithm to minimize motion artifacts, it can visualize low-velocity blood flow in small vessels. We demonstrate SMI imaging of the placental infarction in a case with fetal growth restriction, comparing a normal placenta on the same gestation. While SMI image in normal placenta clearly shows structures from the branching vessels to the peripheral villous trees in the cotyledons, they could not be seen in the case of fetal growth restriction. We think that the clinical value and future potential of SMI in placental evaluation have been clearly demonstrated.

Frequency and risk factors for the birth of small-for-gestational-age newborns in a public maternity hospital.

ABSTRACTObjective:To determine the frequency and risk factors of small-for-gestational-age newborns in a high-risk maternity.Methods:This is an observational, cross-sectional, and case-control study, conducted in a public tertiary care maternity hospital. Data from 998 newborns and their mothers were collected through interviews and review of medical records and prenatal care cards. Some placentas underwent histopathological analysis. The variables of small-for-gestational-age and non-small-for-gestational-age newborns and of their mothers were statistically compared by means of Student's t test, Fisher's exact test, and odds ratio. The significance level used was 0.050.Results:There was a 17.9% frequency of small-for-gestational-age newborns. The statistically significant factors associated with the birth of these babies were female sex (p=0.012); positive history of another small-for-gestational-age child (p=0.006); inadequate prenatal care (p=0.019); smoking (p=0.003); hypertensive disorders of pregnancy (p=0.007); placental bleeding (p=0.009) and infarction (p=0.001).Conclusion:In the population studied, the frequency of small-for-gestational-age newborns was high and associated with sex, inappropriate prenatal care, presence of maternal diseases and addictions, and placental abnormalities.

The human placenta: Function and morphological assessments using ultrasound and magnetic resonance elastography

s / Placenta 45 (2016) 63e133 74 P1.6 THE HUMAN PLACENTA: FUNCTION AND MORPHOLOGICAL ASSESSMENTS USING ULTRASOUND AND MAGNETIC RESONANCE ELASTOGRAPHY Richard K. Miller , Stephan McAleavey , Juvenal Ormachea , Eva Pressman, Loralei Thornburg , David Dombroski , Jianhui Zhong, Marvin Doyley , Ronald W. Wood, Jonathan Carrol-Nellenback , Ollivier Hyrien , Philip Katzman , Christopher Stodgell , Kam Szlachetka, Henry Wang, Kevin Parker . University of Rochester School of Medicine and Dentistry, Rochester, New York, USA; University of Rochester Haijm School of Engineering, Rochester, New York, USA Objective: In utero evaluations of placental anatomy and function offer the promise of associating placental pathophysiology with neonatal outcomes, and thus potential for enhanced management of perinatal complications and improved long-term health of the mother and child. Ultrasound Elastography (USE) and Magnetic Resonance Elastography (MRE) provide means to evaluate tissue stiffness in utero. In conjunction with measures of vascular anatomy and perfusion, we can test mechanistic hypotheses about the relationship with anatomical function and deviations associated with disease states. For example, The Parker Hypothesis (Parker, Phys. Med. Biol. 59: 4443,14) proposes that viscoelastic measures of soft tissue stiffness are related to the fractal branching properties of the vascular anatomy. Methods: Term human placentae were obtained immediately upon delivery and evaluated directly either in a 3T GE MRI with Elastography or using a Siemens Antares US scanner and VF10-5 Probe with custom single track location shear wave elasticity imaging pulse sequences and accelerated processing. Other placentae were perfused through the umbilical cord and imaging, Doppler measures and elastography were conducted. At the end of the experiments, a barium gel was infused to enhance subsequent CT imaging of the fetal vasculature. Results: The utility of elastography in functional evaluation of the placenta are readily demonstrated in the following examples: 1) Placental tissue anomalies (e.g., infarcted areas) are stiff, and provided dramatic examples of the sensitivity USE and MRE methodologies for the detection of placental pathology; 2) Ex vivo placental perfusions have been used to relate placental stiffness to fetal vasculature when measured by USE, as seen when fetal vascular dynamics were pharmacologically manipulated. Clinical and high-resolution microCT systems can and have been used on placentae to provide additional post-delivery anatomical characterization and quantification of the vascular beds. These CT observations provide confirmation of in vivo Doppler US and the potential use of MR angiography for vascular characterization. We demonstrated that these datasets are amenable to automated identification and characterization of branching morphology, including centerline tree and Sholl analyses. Conclusion: These USE and MRE technologies enable promising new approaches for the prediction of risks during and after pregnancy. (Support: Goode Foundation) MRI localization of a placental infarct with associated elastographic ortho slice A: gross examination of placental lesion. B, MR segmented volume. C. Superimposed MRE. Yellow arrow directs attention to lesion.

Placental pathology and outcome after perinatal asphyxia and therapeutic hypothermia.

To assess the relationship between placental pathology, pattern of brain injury and neurodevelopmental outcome in term infants with perinatal asphyxia receiving therapeutic hypothermia. Studies were performed in 76 infants. Death or survival with impairments at 18 to 24 months was used as a composite adverse outcome. Multivariable analysis was performed. Among the 75 infants analyzed, the predominant pattern of brain injury was: no injury (n=27), a white matter/watershed pattern (n=14), basal-ganglia-thalamic injury (n=13) or near-total brain injury (n=21). An adverse outcome was seen in 35 of the 76 infants. Elevated nucleated red blood cells were associated with white matter involvement. Small placental infarcts were more common among infants without brain injury. All other placental abnormalities were not related to both outcome measures. In our population of term infants receiving therapeutic hypothermia, no type of placental pathology was related to extensive brain injury or adverse neurodevelopmental outcome.

Decidual Vasculopathy: Placental Location and Association with Ischemic Lesions

Decidual vasculopathy (DV) is a general term for a number of lesions involving uteroplacental vessels. It is often seen in preeclamptic placentas and indicates a disorder of uteroplacental malperfusion and is associated with placental ischemia and infarction. Although some have advocated submitting special sections in order to better document DV, it is unclear which placental sections have the highest yield in demonstrating these abnormal vessels. 76 consecutive cases of decidual vasculopathy were identified and evaluated for location of DV, as well as presence of other lesions of ischemic change, infarcts and retroplacental hematomas. Sections reviewed were the membrane roll, full thickness sections of the placental disc, and sections specifically of the basal plate. DV was found in the membrane roll (MR) in 67.1% of cases, in full thickness sections (FT) in 32.9% and in the basal plate (BP) in 25.0% of cases (p value = 0.004). DV was exclusive to the MR in 53.9%, the FT in 14.5% and the BP in 9.2%. DV was present in 2 locations in 19.7% and in all 3 locations in 2.6%. The presence of DV in any location (MR, FT, BP) was associated with placental ischemic change but not specifically with infarcts or retroplacental hematomas. The specific location of DV showed no difference in the presence of placental lesions. Our findings indicate DV is often present in one location, and is associated with lesions of malperfusion. It is recommended that when clinically indicated, additional sections are submitted to demonstrate decidual vasculopathy.

Abstract 3449: Placental characteristics and risk of cryptorchidism among populations at high and low risk of testicular germ cell tumors

Abstract Background: Testicular germ cell tumors, which are significantly more common among white men than black men in the U.S., are thought to be part of a Testicular Dysgenesis Syndrome (TDS) that also includes impaired fertility, hypospadias and cryptorchidism. The etiology of the TDS conditions is not well understood, but the in-utero milieu is likely to be a significant factor. As the placenta is a critically important determinant of the in-utero milieu, placental characteristics may play a role in determining risk of the TDS conditions. Prior evidence suggests that placental weight, in particular, may be associated with cryptorchidism. Methods: We examined placental characteristics (weight, thickness, placental weight/birth weight ratio, infarct size, disorders of membrane development, presence of macrophages in the amniotic fluid) and cryptorchidism in a nested case-control study within the Collaborative Perinatal Project (CPP). The CPP was a maternal-child cohort study conducted in 12 medical centers in the U.S. between 1959 and 1965. Diagnoses of cryptorchidism made during the first year of life were included in the case group. The analysis contrasted 413 (232 white, 181 black) boys with cryptorchidism to 23,799 (12,092 white, 11,707 black) boys without cryptorchidism. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated using unconditional logistic regression, stratified by race. Results: Among white boys, cryptorchidism was significantly associated with circummarginate placenta (OR: 1.7, 95% CI: 1.1-2.7) or a combination of circummarginate/circumvallate (OR: 1.3, 95% CI: 1.0-1.8) placenta. Among black boys, cryptorchidism was significantly associated with having at least one placental infarct greater than 3 cm (OR: 2.3, 95% CI: 1.1-4.8) and with placental weight in the lower (OR: 1.7, 95% CI: 1.1-2.6) or higher (OR: 1.5, 95% CI: 1.0-2.3) tertile compared with the middle tertile. No significant associations were found between cryptorchidism and the other placental characteristics in either white or black boys. Conclusion: These results suggest that there may be associations between cryptorchidism and certain placental characteristics which differ between white and black births. The race-specific findings suggest an area where future research may prove fruitful. Citation Format: Armen A. Ghazarian, Britton Trabert, Barry Graubard, Matthew Longnecker, Mark Klebanoff, Katherine McGlynn. Placental characteristics and risk of cryptorchidism among populations at high and low risk of testicular germ cell tumors. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 3449.

Importancia de la autopsia y del estudio de la placenta en la evaluación de la muerte fetal en el Hospital Universitario de Santander

Objetivo: evaluar las causas de muerte fetal, mediante antecedentes clínicos maternos, análisis de los hallazgos de la autopsia fetal y estudio de la placenta. Materiales y Métodos: se realizó un análisis retrospectivo de 332 muertes fetales durante el periodo comprendido de 2005-2009 ocurridas en el Hospital Universitario de Santander (HUS) Bucaramanga, Colombia. Se incluyeron análisis histopatológicos de la placenta y el feto. Se planteó la siguiente clasificación de las causas de muerte fetal 1) Hipoxia fetal intrínseca 2) Anomalías congénitas 3) Infecciones ascendentes 4) Traumatismos del parto 5) Hidrops fetal. Se determinaron como no clasificables a fetos macerados. Se establecieron subgrupos de análisis de la población como edad materna, edad fetal y se analizan los datos mediante porcentajes y promedios. Resultados: el promedio de edad materna fue de 25,9 años, el promedio de edad gestacional fue de 28,9 semanas. Se conoció el tipo de muerte en el 87,96% de los casos. Las causas más frecuentes de muerte fueron la hipoxia fetal intrínseca 46,67%: insuficiencia placentaria 17,5%, desprendimiento placentario 6,6%, infarto placentario 6,3%, HTA materna 4,5%. Anomalías congénitas 18,07%, infección bacteriana ascendente 16,26%, causa desconocida 12,04%. En gestaciones entre 20-29 semanas la principal causa de muerte fue patología placentaria (43.97%); en cuanto a 37-42 semanas la principal causa fue las anomalías congénitas (5,1%). Conclusiones: el presente estudio muestra que las principales causas de óbito fetal están vinculadas con patologías que pueden ser detectadas y manejadas de manera adecuada y expone la importancia de la autopsia fetal sumado al estudio anatomopatologico de la placenta a la hora de determinar dichas causas.

Expression changes of proteins associated with the development of preeclampsia in maternal plasma: A case-control study.

Defective deep placentation, involving abnormal transformation of the spiral arteries in the junctional zone of the myometrium, is known to cause significant obstetric complications, such as preeclampsia (PE), fetal growth restriction, and placental infarction leading to fetal death. Serological biomarkers to predict and diagnose PE would help antenatal care and reduce obstetric complications. To discover candidate PE biomarkers, we first performed global proteomic profiling of three pairs of plasma samples obtained from pregnant women in the early second trimester, who subsequently developed PE, and controls to identify candidate proteins that were abundant in the patients. We further evaluated the changes in the expression of PE-representing proteins in stored plasma samples of a cohort that subsequently developed PE and their matched controls by MRM-MS analysis. We identified that both complement C1s subcomponent (C1S) and protein AMBP were elevated in the plasma samples of the PE cohort before the manifestation of clinical disease. We propose that these proteins may be involved in the remodeling process of the spiral arteries even before PE manifestation. These proteins can serve as potential plasma biomarkers to predict the pregnant women having an increased risk of developing PE.

Maternal and placental risk factors for light-for-gestational-age births.

We conducted a cross-sectional study to investigate risk factors for births of light-for-gestational-age (LGA) infants. A survey was conducted at the Department of Obstetrics and Gynecology at Sapporo Medical University Hospital in Sapporo, Japan from 2013 to 2014. LGA and appropriate for gestational age (AGA) are defined as having a birthweight below the 10th percentile and between the 10th percentile and 90th percentile for gestational age at birth in the population standard of gestational age, sex, and parity, respectively. An odds ratio (OR) and its 95% confidence interval (95%CI) for LGA were calculated by analysis using the logistic regression model. In total, 307 inpatients (94.2%) participated in the study out of 326 consecutive post-partum inpatients. Among them, 37 infants and 237 infants were classified into the LGA and AGA groups, respectively. As a result of multivariable analysis, prevalence of gestational hypertension (OR = 8.96, 95%CI 1.81-44.35) and the presence of placental infarction (OR = 9.65, 95%CI 1.76-53.01) were significantly associated with an increased risk of LGA. Placentas weighing 510-603 g and ≥604 g were significantly associated with reduced risk of LGA (OR = 0.04, 95%CI 0.01-0.29 and OR = 0.03, 95%CI 0.01-0.32, respectively), and higher placental weights were significantly observed in the trend for reduced LGA risk (P for trend < 0.001). We found that the prevalence of gestational hypertension, lower placental weight, and the presence of placental infarctions were all independently associated with the risk of LGA. Placental abnormalities may be etiologically important for LGA risk, though further research is necessary.

Placental changes in pregnancy induced hypertension

Objective: To study the histomorphological changes in placentae of pre-eclamptic mothers and to compare them with placentae of normotensive mothers. Method: This study was carried out in 34 placentas of mothers who had pregnancy induced hypertension (PIH) and 34 placentas of normotensive non diabetic mothers in the Department of Pathology, University of Sri Jayewardenepura. Placentae were fixed in normal saline for 48 hours. After fixation the placentae were divided into four quadrants and 5mm pieces of tissue were taken from the center, upper and lower quadrants. After tissue processing and staining, the histomorphological changes were studied in both normotensive and hypertensive groups after obtaining clinical details from the bed head tickets. Results: Infarctions, small villi and numbers of syncytial knots and vasculosyncytial membrane were significantly higher in the study group compared with the control group. The severity of hypertension correlated with the extent of the placental infarcts. Conclusion: A significant number of both macroinfarcts and microinfarcts with an increased number of syncytial knots was observed in the hypertensive group as compared to normotensive group which may be due to placental hypoxia. Journal of Diagnostic Pathology 2015;10(1):14-22