Villous Maturation Research Articles

Placentas From Women of Advanced Maternal Age.

The percentage of pregnant women with advanced maternal age (AMA) has increased during the past several decades due to various socioeconomic factors and advances in assisted reproduction. These pregnancies are associated with adverse maternal and fetal outcomes. However, the underlying placental pathology has not been well described. To investigate the placental histopathology associated with AMA pregnancies. Placental pathology from 168 AMA women 35 years or older at delivery was reviewed. The cases were subdivided into 2 age subgroups, ages 35 to 39 and 40 or older, as well as a "pure AMA" subgroup where the only indication for placental examination was AMA. A group of 60 consecutive non-AMA placentas was also identified and used as comparison. The spectrum of histologic features in each case was catalogued. Of the overall AMA cases, meconium deposition was seen in 55% (93 of 168), chorangiosis in 40% (68 of 168), and acute chorioamnionitis in 36% (60 of 168). Fetal vascular malperfusion was also seen with high frequency (30%; 50 of 168). Two histologic alterations found to be significantly different between the 35 to 39 and greater than 40 age subgroups were fetal vascular malperfusion (11% [7 of 65] versus 42% [43 of 103]; P = .001) and delayed villous maturation (1.5% [1 of 65] versus 13% [13 of 103]; P = .02). The pure AMA subgroup showed no statistically significant differences compared with the overall AMA group. Chronic deciduitis was the only statistically significant difference between the overall AMA group and the non-AMA comparison group (14% [23 of 168] versus 30% [18 of 60]; P = .02). Our findings, particularly the high frequency of fetal vascular malperfusion, suggest that AMA should be an independent indication for placental pathologic examination.

Placental changes in diabetic pregnancies and the contribution of hypertension

Objective To evaluate placental abnormalities in pregnancies affected by diabetes compared to unaffected pregnancies from a single academic center. Methods This is a retrospective cohort study of women with singleton gestations delivered at the University of Arkansas for Medical Sciences from 2007 to 2016. Pathologic examination of placentas from pregestational and gestational diabetic pregnancies were compared to placentas from patients without diabetes using 12 histologic elements. Maternal and neonatal outcomes were extracted from the medical record and compared between groups. Findings were adjusted for hypertensive disorders of pregnancy. Placental lesions were also correlated with diabetic control. Results Pathology reports of 590 placentas along with corresponding medical records were reviewed. The diabetic group (N = 484) consisted of 188 patients with pregestational diabetes and 296 patients with gestational diabetes. The nondiabetic group consisted of 106 patients. The diabetic group was older, had a higher average BMI, and more hypertensive disorders (p < .0001). Out of the 12 histologic elements investigated, accelerated villous maturation (aOR = 8.45, 95%CI (1.13–62.95)) and increased placental weight (aOR = 3.131, 95% CI (1.558–6.293)) were noted to be significantly increased in placentas from diabetic pregnancies after controlling for hypertension. Intervillous thrombi were not significantly increased in pregnancies affected by diabetes. Neonates of the diabetic group were more likely to be large for gestational age (p < .0001) and had a higher rate of preterm delivery (p < .0001). Conclusions Accelerated villous maturation was found to be more frequent in pregnancies complicated by pregestational diabetes, even after controlling for hypertension. In pregnancies complicated by gestational diabetes, the placental findings were not significant after controlling for hypertension. In contrast with prior studies, there was no increase in thrombotic lesions of the placenta in patients with diabetes.

Histological villous maturation in placentas of complicated pregnancies.

Chorioamnionitis and preeclampsia account for the majority of preterm births worldwide. Thus far, adequate methods for early detection or prevention of these diseases are lacking. In preeclampsia, accelerated villous maturation is believed to compensate placental insufficiency. However, little is known about the effects of placental inflammation in chorioamnionitis on villous maturation. Therefore, we established a set of morphological parameters to evaluate histological villous maturity in pregnancies complicated by chorioamnionitis and preeclampsia. Preterm placentas complicated by chorioamnionitis or preeclampsia were compared to idiopathic preterm placentas and term controls. Histological villous maturation was analyzed by means of 17 histological markers. Fourteen of these markers provided information on absolute and relative numbers of the terminal villi (TV), the extent of their vascularization (using CD31-stained sections) and their exchange capacities. In addition, the numbers of syncytial bridges, syncytial apoptotic knots and shed syncytiotrophoblasts were counted. Accelerated villous maturation in preeclampsia was demonstrated by means of histological villous remodeling and confirmed by 11 relevant markers. Chorioamnionitis, however, only showed increased area of fetal capillaries. In preeclampsia, placentas may transition from growth to maturation earlier than placentas in normal pregnancies, whereas in chorioamnionitis placental changes are more acute and therefore less elaborated at a structural level. Regression analysis suggests the number of all villi and the number of terminal villi as a percentage of all villi as parameters to evaluate histological villous maturity in preeclamptic placentas and to assist diagnosis. However, we would recommend to analyze all 11 relevant parameters to judge placental maturity in detail.

Pre-conception blood pressure and evidence of placental malperfusion

BackgroundEvidence of placental maternal vascular malperfusion is associated with significant perinatal outcomes such as preeclampsia, intrauterine growth restriction and preterm birth. Elevations in pre-pregnancy blood pressure increase the risk for poor perinatal outcomes; however, the evidence linking pre-pregnancy blood pressure and placental malperfusion is sparse.Materials and methodsWe conducted a retrospective case-control study of women with singleton gestations with placental evaluations who delivered at Magee-Womens Hospital in 2012. Charts from 100 deliveries with placental malperfusion lesions (vasculopathy, advanced villous maturation, infarct, or fibrin deposition) and 102 deliveries without placental malperfusion were randomly selected for screening. Blood pressure, demographic, and clinical data were abstracted from pre-pregnancy electronic medical records and compared between women with and without subsequent placental malperfusion lesions.ResultsOverall, 48% of women had pre-pregnancy records, and these were similarly available for women with and without placental malperfusion. Women with placental malperfusion demonstrated a reduction in their pre- to early pregnancy decrease in diastolic blood pressure (DBP). Adjusted for race, pre-pregnancy BMI, age, pre-conception interval, and gestational age at the first prenatal visit, the difference in pre- to early pregnancy DBP was significantly less in women with placental malperfusion compared to those without this pathologic finding (− 1.35 mmHg drop vs − 5.6mmg, p < 0.05).ConclusionA blunted early gestation drop in DBP may be a risk factor for placental malperfusion, perhaps related to early pregnancy vascular maladaptation. The ability of the electronic medical record to provide pre-pregnancy data serves as an underutilized approach to study pre-pregnancy health.

326: Placental changes in diabetic pregnancies and the contribution of hypertension

To evaluate placental abnormalities in pregnancies affected by diabetes compared to unaffected pregnancies from a single academic center This is a retrospective cohort study of women with singleton gestations delivered from 2007 to 2016. Pathologic examination of placentas from pregestational and gestational diabetic pregnancies were compared to placentas from patients without diabetes using twelve histologic elements. Maternal and neonatal outcomes were extracted from the medical record and compared between groups. Findings were adjusted for hypertensive disorders of pregnancy. Pathology reports of 590 placentas along with corresponding medical records were reviewed. The diabetic group (N=484) consisted of 188 patients with pregestational diabetes and 296 patients with gestational diabetes. The nondiabetic group consisted of 106 patients. The diabetic group was older, had a higher average BMI, and more hypertensive disorders (p< 0.0001). Out of the 12 histologic elements investigated, accelerated villous maturation (aOR 8.45, 95%CI (1.13-62.95)) and increased placental weight (aOR 3.131, 95% CI (1.558-6.293)) were noted to be significantly increased in placentas from diabetic pregnancies after controlling for hypertension. Intervillous thrombi were not significantly increased in pregnancies affected by diabetes. Neonates of the diabetic group were more likely to be large for gestational age (p< 0.0001) and had a higher rate of preterm delivery (p< 0.0001). Accelerated villous maturation was found to be more frequent in pregnancies complicated by diabetes. Accelerated villous maturation is a placental finding that indicates maternal vascular malperfusion. In contrast with prior studies, there was no increase in thrombotic lesions of the placenta in patients with diabetes.View Large Image Figure ViewerDownload Hi-res image Download (PPT)

The value of histopathology of the placenta in a tertiary referral hospital in South Africa

Background. Unexplained intrauterine death (IUD) remains the most common cause of perinatal death in babies of 24 weeks’ gestation. Results. The total sample ( N =822) comprised 60.9% live-birth placentas and 39.1% IUD placentas. In the IUD group, the cause of death was clinically unexplained in 55.9% of cases. Histopathology identified in this group included chorioamnionitis (CA) (34.5%), maternal vascular malperfusion (32.1%), abruptio placentae (31.5%), delayed villous maturation (17.8%) and toxoplasmosis, other agents, rubella, cytomegalovirus and herpes simplex (TORCH) infections (6.1%), most commonly syphilis. No pathology was found in only 2% of IUD cases. Among live births, preterm labour accounted for 41.9% of placental submissions, of which the cause was unknown in 46.2% of cases. Clinically indicated and histologically defined CA was poorly correlated. Conclusion. This study demonstrates the value of placental histopathology in cases of adverse perinatal outcome.

Unique transcriptomic landscapes identified in idiopathic spontaneous and infection related preterm births compared to normal term births.

Preterm birth (PTB) is leading contributor to infant death in the United States and globally, yet the underlying mechanistic causes are not well understood. Histopathological studies of preterm birth suggest advanced villous maturity may have a role in idiopathic spontaneous preterm birth (isPTB). To better understand pathological and molecular basis of isPTB, we compared placental villous transcriptomes from carefully phenotyped cohorts of PTB due to infection or isPTB between 28–36 weeks gestation and healthy term placentas. Transcriptomic analyses revealed a unique expression signature for isPTB distinct from the age-matched controls that were delivered prematurely due to infection. This signature included the upregulation of three IGF binding proteins (IGFBP1, IGFBP2, and IGFBP6), supporting a role for aberrant IGF signaling in isPTB. However, within the isPTB expression signature, we detected secondary signature of inflammatory markers including TNC, C3, CFH, and C1R, which have been associated with placental maturity. In contrast, the expression signature of the gestational age-matched infected samples included upregulation of proliferative genes along with cell cycling and mitosis pathways. Together, these data suggest an isPTB molecular signature of placental hypermaturity, likely contributing to the premature activation of inflammatory pathways associated with birth and providing a molecular basis for idiopathic spontaneous birth.

Recurrent intrauterine growth restriction: characteristic placental histopathological features and association with prenatal vascular Doppler.

Intrauterine growth restriction (IUGR) is a leading cause of perinatal morbidity and mortality, carrying a 20% recurrence rate. The placental disease is a cardinal factor among IUGR underlying processes. This study describes placental histopathological features (HPf) characteristic of recurrent IUGR (rIUGR) and assesses association with antenatal Doppler studies. We conducted a retrospective case-control study, between the years 2005-2016, evaluating 34 placentae of 17 women with rIUGR, and 59 placentae of a gestational age-matched control. Doppler studies within a week prior to delivery were analyzed for the rIUGR group. Placental HPf characteristic of rIUGR is maternal and fetal vascular malperfusion lesions; maternal accelerated villous maturation and villous infarcts, repetitive feature rate 88.8% (95% CI 37.2-97), and fetal chorionic plate/stem villous thrombi, repetitive feature rate 66.6% (95% CI 30-90.3). Among women with abnormal Doppler, 83.3% had a placenta HPf of maternal vascular malperfusion lesions and 66.7% presented with a hypertensive disorder. Women with rIUGR are a unique group of patients characterized by repetitive placental HPf of both maternal and fetal vascular malperfusion lesions. Specifically, maternal vascular malperfusion lesions are associated with abnormal Doppler findings. In conclusion, characteristic placental HPf may serve as predictors of future IUGR recurrence, thus offering early recognition of pregnancies that require "high-risk" antenatal care.

Gastroschisis Is Associated With Placental Delayed Villous Maturation.

Gastroschisis is a congenital abnormality characterized by visceral herniation through an abdominal wall defect. While the cause of gastroschisis is unknown, it has been linked to risk factors including young maternal age, smoking, and alcohol use during pregnancy. To date, the only established placental correlate is amniocyte vacuolization. Based on our clinical experience, we hypothesized that delayed villous maturation (DVM) is also associated with gastroschisis. We conducted a retrospective slide review of 23 placentas of neonates with gastroschisis. Additionally, we selected 2 control groups of placentas: 1 with a previous diagnosis of DVM and 1 with normal villous morphology. All placentas were randomized and reviewed by 2 perinatal pathologists, who were blinded to the group; DVM and amniocyte vacuolization were assessed. Gastroschisis was associated with increased placental DVM in 65.2% of cases (vs 13.6% of controls; P = .0007) and increased amniocyte vacuolization in 52.2% of cases (vs 9.1% of controls; P = .003) compared to the control group. Based on the normal and DVM groups, kappa agreement between current slide review and initial pathology diagnosis was 0.419, indicating moderate agreement. Our study shows that gastroschisis is associated with placental DVM. This association may be due to (1) a common upstream factor contributing to both gastroschisis and DVM or (2) DVM may be a consequence of the altered placental and amniotic environment in the context of gastroschisis.

Abstract P3044: Second Trimester Severe Fetal Growth Restriction Preceding Preterm Severe Hypertensive Disorder in Pregnancy

Background: Pregnancies complicated by hypertensive disorders are at risk of fetal growth restriction, abruption, and stillbirth. These complications are likely mediated through endothelial vascular disease of the placenta. Case: A 34 year old female G3P0111 with a history of HELLP syndrome was referred for severe fetal growth restriction at 23 weeks and 3 days. She was normotensive with normal fetal anatomic survey, low risk cell free DNA screen, negative antiphospholipid antibody panel and no evidence of TORCH infections. She returned to the clinic two weeks later with new onset hypertension, suboptimal interval fetal growth and oligohydramnios. She was admitted, and delivered at 25 weeks and 5 days for preeclampsia with severe features. Her female infant weighted 340 grams, and was intubated and admitted to the NICU. The NICU stay was complicated by respiratory distress syndrome, cholestasis, pancreatic insufficiency, dyschezia, growth failure, hydronephrosis, and vesicoureteral reflux. Today she is 12 months old and thriving. Placental pathology showed accelerated villous maturation suggestive of placenta underperfusion, consistent with clinical history of preeclampsia. Discussion: Preeclampsia is a complication of pregnancy typically characterized by elevated blood pressure and damage of other organs, most commonly the liver or kidney. While the exact mechanisms that cause preeclampsia are not known, the resultant endothelial vascular disease affecting the placenta can lead to fetal growth restriction or abruption. Second trimester fetal growth restriction can result from fetal aneuploidy, viral infections, or maternal conditions that lead to uteroplacental insufficiency such as chronic hypertension or pre-gestational diabetes. Few cases describe fetal growth restriction preceding the onset of preeclampsia, although this is not uncommon in clinical practice. Conclusion: Pregnancies complicated by severe, preterm fetal growth restriction preceding the development of hypertensive disorder appear to have a common etiologic pathway, and the absence of hypertension does not exclude the possibility of underlying preeclampsia. Increased vigilance for signs and symptoms of preeclampsia in these pregnancies is warranted.

Cord blood alpha klotho is decreased in small for gestational age preterm infants with placental lesions of accelerated aging

BackgroundIntrauterine growth restriction is often accompanied by placental vascular disease, of which histologic maternal vascular malperfusion is prominent. Maternal vascular malperfusion is characterized by accelerated villous maturation consistent with placental aging. Alpha klotho is an anti-aging protein produced by the placenta. We hypothesize that cord blood alpha klotho varies with maternal vascular malperfusion and small for gestational age infants through dysregulated angiogenesis. MethodsNested case-control study of 54 preterm infants (N = 22 small for gestational age infants, 32 appropriate for gestational age infants, mean gestational age = 33.7 ± 2.7 weeks) and validation sample (N = 39) from a longitudinal birth cohort at Prentice Women's Hospital, Chicago, IL. Cord blood alpha klotho was measured via enzyme-linked immunoassay; concentrations were linked to multiplex data of cord blood angiogenic growth factors. ResultsMedian cord blood alpha klotho was decreased in small for gestational age infants (1200 [859, 2083] pg/mL) versus controls (3193 [1703, 3963] pg/mL; p < 0.01) and with severe maternal vascular malperfusion (1170 [760, 2645] pg/mL; P < 0.01), consistent with validation sample. Alpha klotho was decreased with maternal vascular malperfusion sublesions signifying accelerated villous maturation, including increased syncytial knots (1230 [805, 3606] pg/mL; p < 0.05) and distal villous hypoplasia (1170 [770, 3390] pg/mL; p < 0.05). Among 15 angiogenic markers, alpha klotho correlated directly with angiopoietin-2 (beta-coefficient = 2.6, p = 0.01). ConclusionsCord blood alpha klotho is decreased with small for gestational infants and maternal vascular malperfusion sublesions of accelerated placental villous maturation, and correlated with angiopoietin-2. Alpha klotho may play a role in vascular-mediated accelerated placental aging leading to intrauterine growth restriction.

MRI to evaluate placental function

We evaluated the association between plasma soluble endoglin (sENG) and maternal vascular malperfusion (MVM) lesions of the placenta in women with preeclampsia. We measured sENG (sCD105) by ELISA in N = 70 women diagnosed with preeclampsia (median [IQR] GA at sampling = 36.4 [6.0] weeks) and available placental pathology. Placental pathology reports were reviewed for evidence of MVM based on the presence of ≥1 of the following: villous infarct, decidual vasculopathy, accelerated villous maturation, intervillous fibrin deposition, and/or low placental weight (<10th percentile for GA). We categorized plasma sENG concentrations into tertiles and used a modified Poisson regression approach to estimate the prevalence of MVM associated with sENG. We separately estimated the association between sENG and accelerated villous maturation, villous infarct, and low placental weight, the three most frequent lesions in the sample. We adjusted all models for age, parity, pre-pregnancy obesity, smoking, and infant sex. The prevalence of MVM in our sample of women with preeclampsia was 74%. Women in the highest sENG tertile had a higher prevalence of MVM (aPR[adjusted prevalence ratio] 1.70, 95% CI 1.15–2.52), low placental weight (aPR 3.26, 95% CI 1.25–8.50), and villous infarcts (aPR 2.93, 95% CI 1.27–6.73) compared with women in the lowest sENG tertile, after adjusting for covariates. Medium (aPR 2.57, 95% CI 1.17–5.66) and high (aPR 3.14, 95% CI 1.47–6.70) tertile concentrations of sENG were associated with higher accelerated villous maturation. Our results suggest that sENG may mark a more severe placental phenotype of preeclampsia, although findings should be replicated in larger cohorts.

Plasma concentrations of soluble endoglin in the maternal circulation are associated with maternal vascular malperfusion lesions in the placenta of women with preeclampsia

We evaluated the association between plasma soluble endoglin (sENG) and maternal vascular malperfusion (MVM) lesions of the placenta in women with preeclampsia. We measured sENG (sCD105) by ELISA in N = 70 women diagnosed with preeclampsia (median [IQR] GA at sampling = 36.4 [6.0] weeks) and available placental pathology. Placental pathology reports were reviewed for evidence of MVM based on the presence of ≥1 of the following: villous infarct, decidual vasculopathy, accelerated villous maturation, intervillous fibrin deposition, and/or low placental weight (<10th percentile for GA). We categorized plasma sENG concentrations into tertiles and used a modified Poisson regression approach to estimate the prevalence of MVM associated with sENG. We separately estimated the association between sENG and accelerated villous maturation, villous infarct, and low placental weight, the three most frequent lesions in the sample. We adjusted all models for age, parity, pre-pregnancy obesity, smoking, and infant sex. The prevalence of MVM in our sample of women with preeclampsia was 74%. Women in the highest sENG tertile had a higher prevalence of MVM (aPR[adjusted prevalence ratio] 1.70, 95% CI 1.15–2.52), low placental weight (aPR 3.26, 95% CI 1.25–8.50), and villous infarcts (aPR 2.93, 95% CI 1.27–6.73) compared with women in the lowest sENG tertile, after adjusting for covariates. Medium (aPR 2.57, 95% CI 1.17–5.66) and high (aPR 3.14, 95% CI 1.47–6.70) tertile concentrations of sENG were associated with higher accelerated villous maturation. Our results suggest that sENG may mark a more severe placental phenotype of preeclampsia, although findings should be replicated in larger cohorts.

Angiogenesis-related factors in the placenta of pregnant women with congenital heart diseases

To study the features of angiogenesis of the placental villous chorion in women whose gestation took place in congenital heart disease (CHD). Thirty-five placentas obtained from women with full-term pregnancy, including 20 cases of non-operated CHD and 15 as a result of physiological pregnancy and childbirth (a control group), were studied. A placental morphological examination was made according to the standard scheme using routine stains and immunohistochemical techniques involving reactions with mouse monoclonal antibodies against VEGF, CD34, and SMA. The placentas of women with CHD showed a set of pathological changes, including impaired chorionic villous maturation and marked dystrophic and necrobiotic changes, the latter being more common in the placental marginal zones. Placental VEGF expression in women with CHD was significantly higher than that in the controls, especially at the edge of the placental disc. On the contrary, CD34 expression in all placental sections was lower in CHD. The distribution of SMA in the myofibroblasts of chorionic villous vessels in CHD was characterized by diffuse growth of actin expression. The specific volume of the cell surface with a positive reaction to actin significantly increased in the center, especially in the peripheral zone. Thus, the analysis of the studies could establish that hemodynamic disturbance during gestation complicated by CHD was accompanied by remodeling of the villous chorion. Pathological changes in the placental barrier complicate metabolism and gas exchange in the fetoplacental complex. Microvascular remodeling is an important mechanism of placental adaptation to circulatory hypoxic conditions in the presence of CHD and a prerequisite for successful pregnancy termination and childbirth in disease.

ОСОБЕННОСТИ МОРФОЛОГИЧЕСКОГО СТРОЕНИЯ ПЛАЦЕНТЫ У РОДИЛЬНИЦ С ГЕСТАЦИОННЫМ САХАРНЫМ ДИАБЕТОМ В СОЧЕТАНИИ С АНЕМИЕЙ

Objective: To study the features of the morphological structure of placenta in puerperas with gestational diabetes mellitus (GDM) and anemia. Methods: The study targeted 42 afterbirths, including 13 placentae from puerperas in GDM combined with anemia, 10 from puerperas with only GDM and 8 from puerperas with only the anemia. Comparison group accounted for 11 placentae from healthy puerperas. For histological research prepared paraffin slices of thickness from 3 to 5 microns, hematoxylin and eosin used for the review coloring. The morphological features were evaluated on the Olympus CX-21 microscope. Results: Women in GDM combined with anemia have had a decrease in placenta size, an increase in placental fetal ratio and a shortening of the umbilical cord with its eccentric attachment to the placenta. At the same time microscopically dominated dissociated forms of villous maturation, syncytiotrophoblast dystrophy with alternating syncytium atrophy sites, villous fibrosis, and stromal edema with inflammatory changes, which indicated circulatory-metabolic disorders associated with placental insufficiency. Compensatory adaptive reactions in the GDM group, combined with anemia, were mainly due to a relative increase in the number of terminal and specialized villi, along with the pronounced phenomena of angiomatosis. Conclusion: Gestational diabetes and anemia in pregnant women lead to the development of placental insufficiency, pathomorphologically manifested involutive and dystrophic changes, circulatory disorders, inflammatory processes and compensatory adaptive reactions, which are expressed more in the combination of these diseases. Keywords: Gestational diabetes, anemia, morphological structure of the placenta, involutive and dystrophic changes, compensatory-adaptive reactions.

Placental Peripartum Pathologies in Women with Preeclampsia and Eclampsia.

Objective To determine the pattern of pathological changes in placentas of preeclamptic/eclamptic parturients and its correlation with the clinical severity as well as the perinatal outcome. Methods A cross-sectional analytical study of placental pathologies in preeclamptic/eclamptic patients was performed in a blinded pattern and compared with matched normal controls. Data were analyzed using Epi-Info 2008 version 3.5.1. Results Placental pathologies were evaluated in 61 preeclamptic/eclamptic patients and in 122 controls. Of the 61 placentas, 53 (4.7%) were of preeclampsia while 8 (0.71%) were of eclampsia. Of the preeclamptic group, 14 (23%) had mild preeclampsia while 39 (63.9%) had severe preeclampsia. Infarction, haematoma, and some histological changes increased with the severity of preeclampsia (p < 0.001). When comparing placentas in eclampsia, severe preeclampsia, mild preeclampsia, and normal controls, there was respective increase in the presence of any infarction (75%, 66.7%, 35.7% vs. 12.3%) or any haematoma (100%, 100%, 71.4% vs. 35.2%), decidual arteriopathy (87.5%, 76.9%, 64.3% vs. 35.2%), cytotrophoblastic proliferation (75%, 71.8%, 42.9% vs. 25.4%), and accelerated villous maturation (75%, 69.2%, 57.1% vs. 31.1%). There was no statistically significant difference in placental calcifications, stromal oedema, stromal fibrosis, and syncytial knots. Degree of placental infarction was correlated with the fetal birth weight. The fetal birth weight with placental involvement of >10% was significant (p=0.01). Conclusion In mild or severe preeclampsia/eclampsia, placentas had significant histological signs of ischaemia and degree of placental involvement by infarction is inversely proportional to fetal birth weight. While feto-placental ratio was higher with increased severity of the disease, the mean weight was less. This trial is registered with researchregistry3503.

Race and risk of maternal vascular malperfusion lesions in the placenta

IntroductionThe biological mechanisms that underlie racial disparities in placenta-mediated pregnancy complications remain unknown. Placental evidence of maternal vascular malperfusion (MVM), a common pathologic feature of these outcomes, represents hypoxic-ischemic damage to the placenta. We sought to separately estimate the risk of MVM and individual lesions associated with maternal race. MethodsThis was a retrospective cohort study of black and white women with singleton live births and placental pathology data at Magee-Womens Hospital during 2008–2012 (n = 15,581). MVM consisted of ≥1 individual lesions: low placental weight, decidual vasculopathy, accelerated villous maturation, infarcts, and fibrinoid deposition. We separately compared the incidence of MVM and individual lesions in black and white women using logistic regression with generalized estimating equations. ResultsAfter adjusting for covariates, black women had increased risks of MVM (aOR 1.14, 95% CI 1.05–1.23), low placental weight (aOR 1.41, 95% CI 1.28–1.55), and decidual vasculopathy (aOR 1.58, 95% CI 1.36–1.83), also observed in uncomplicated, preterm, and term births. Conversely, black women had decreased risk of infarcts (aOR 0.84, 95% CI 0.75–0.95) compared with white women, also observed in uncomplicated and full-term births. Race was not associated with accelerated villous maturation or fibrinoid deposition. Inverse probability weighting to account for potential selection bias generated similar results. DiscussionOur findings suggest that excess risks of MVM, specifically low placental weight and decidual vasculopathy in black women may be due to a pathological susceptibility to an underlying high-risk vascular phenotype. The clinical significance of race differences in the occurrence of infarcts warrants further investigation.

Association of Maternal Prepregnancy Body Mass Index With Placental Histopathological Characteristics in Uncomplicated Term Pregnancies.

IntroductionPrepregnancy 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.MethodsIn this analysis, we studied data of the Netherlands Amniotic Fluid study, a prospective study of women delivering in Utrecht, the Netherlands, between 2006 and 2007. We included women with uncomplicated pregnancies, vaginal delivery, and data on prepregnancy weight and height (n = 382). Placental histopathology was compared between women of normal BMI (≤24.9 kg/m2), overweight (25–29.9 kg/m2), and obese (≥30 kg/m2).ResultsIncreasing prepregnancy BMI was associated with heavier placentas and higher mean infant’s birth weight. In addition, obesity was positively associated with high-grade chronic villitis (odds ratio [OR]: 18.1, 95% confidence interval [CI]: 1.6–205.2), 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 (OR: 0.5, 95% CI: 0.3–1.0). There was a substantial effect of parity on maternal, placental, and neonatal weights.ConclusionsEven in uncomplicated pregnancies, maternal obesity is associated with characteristic changes in placental pathology. Further research is needed to evaluate these changes in view of later-life health of infants born to obese mothers.

Re-view and view on maturation disorders in the placenta.

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

Placental pathology predicts infantile physical development during first 18 months in Japanese population: Hamamatsu birth cohort for mothers and children (HBC Study).

The present study aimed to investigate the relationship between placental pathological findings and physiological development during the neonate and infantile periods. Study participants were 258 infants from singleton pregnancies enrolled in the Hamamatsu Birth Cohort for Mothers and Children (HBC Study) whose placentas were stored in our pathological division. They were followed up from birth to 18 months of age. Physiological development (body weight and the ponderal index [PI]) was assessed at 0, 1, 4, 6, 10, 14, and 18 months. Placental blocks were prepared by random sampling and eleven pathological findings were assessed, as follows: ‘Accelerated villous maturation’, ‘Decidual vasculopathy’, ‘Thrombosis or Intramural fibrin deposition’, ‘Avascular villi’, ‘Delayed villous maturation’, ‘Maternal inflammatory response’, ‘Fetal inflammatory response’, ‘Villitis of unknown etiology (VUE)’, ‘Deciduitis’, ‘Maternal vascular malperfusion’, and ‘Fetal vascular malperfusion’. Mixed model analysis with the use of the xtmixed command by the generic statistical software, Stata version 13.1., identified ‘Accelerated villous maturation’ and ‘Maternal vascular malperfusion’ as significant predictors of a lower body weight and ‘Deciduitis’ as a significant predictor of a small PI, throughout the first 18 months of life. In conclusion, the present study is the first to demonstrate that some pathological findings of the placenta are associated with changes in infantile physical development during the initial 18 months of life in the Japanese population.