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Background Pregnancy in women with systemic lupus erythematosus (SLE) and nephritis (LN) is at risk of foetal and maternal complications. Objective To evaluate the effect of LN on pregnancy with respect to foetal and maternal outcome. Methods We retrospectively studied all pregnant SLE patients with and without diagnosis of LN, who attended the Materno Neonatal Hospital in Cordoba city, Argentina, from January 2015 to April 2017. Demographic, clinical, and laboratory data were collected. The presence of antiphospholipid syndrome (APS) and antiphospholipid antibodies (AAF), and maternal and foetal outcome were evaluated. Results 121 pregnancies in 79 patients were included. Pregnancies were divided into those with LN (69) and those without LN (52). The presence of APS and AAF was more frequent in the LN group as well as higher basal SLEDAI. The LN group received more immunosuppressive therapy and increased steroid dose treatment. Of the patients, 47.5% had Class IV LN. Lupus flares occurred more frequently in the LN group 25.8% vs 10.9% in the group without LN (P = .041), mainly renal flares in the LN group. No patients developed end-stage renal failure. Preeclampsia was more frequent in the LN group, 18.8% vs 6.3% in the group without LN (P = .047). There was only one maternal death. A caesarean section was required in 68.5% of the LN group vs 31.5 in the group without LN, and urgent caesarean section was also performed in the LN group. There were no differences in foetal outcomes in either group: live birth, gestational age, weight birth, perinatal death, foetal distress. Conclusions Patients with LN experienced more maternal complications such as lupus flares and preeclampsia. However, LN does not lead to a worse pregnancy and foetal outcome. Patients should be strictly monitored before and after conception.

Systemic lupus erythematosus (SLE) patients have more pregnancy complications than healthy patients. Data regarding pregnancy outcomes in women with undifferentiated connective tissue disease (UCTD) are more limited, and existing studies are concentrated in Italy and predominantly in patients with a new diagnosis. Our objective was to compare pregnancy outcomes for UCTD and SLE patients with established disease.Between 2008 and 2017, patients with UCTD and SLE at an academic medical center were recruited to a prospective pregnancy registry. UCTD was defined as a positive autoantibody plus connective tissue disease symptoms not meeting criteria for another rheumatic diagnosis. SLE was defined by American College of Rheumatology or Systemic Lupus International Collaborating Clinics classification criteria or by physician diagnosis. Data were collected throughout pregnancy and postpartum. Comparator groups included UCTD, low-activity SLE, and high-activity SLE.A total of 150 SLE and 51 UCTD pregnancies were analyzed. Disease activity was low in most patients, although more patients with SLE had severe activity during pregnancy (12% versus 2%; P = 0.05). The frequencies of prematurity and preeclampsia were significantly lower in UCTD than in high-activity SLE patients (preterm 17% versus 45% [P = 0.004] and preeclampsia 6% versus 34% [P = 0.0008]), although similar to low-activity SLE patients. More infants who were small for gestational age were born to SLE than UCTD patients (33% versus 7% [P = 0.0005]), regardless of disease activity level.Pregnancies in women with UCTD managed by a rheumatologist have a high rate of pregnancy success and fewer risks than those in women with active SLE.

Objective To identify the prevalence of pre-pregnancy overweight/obesity in pregnant women and its relationship with socio-demographic factors and to describe the maternal and perinatal outcomes in a Barcelona hospital (Spain). Method A descriptive cross-association study, with retrospective data collection, was performed Barcelona Hospital. The data of 5447 pregnant women who delivered at >=23 weeks of gestation were included. Body Mass Index (BMI) data were categorised into World Health Organization classifications. p values Results The prevalence of pre-pregnancy obesity was 8.4% and 18.9% for overweight. Gestational diabetes was more frequent in pre-pregnancy overweight/obesity (OR 1.92: 95% CI 1.54–2.40 and OR 3.34: 95% CI 2.57–4.33), as were preeclampsia (OR 2.08: 95% CI 1.55–2.79 and OR 3.35: 95% CI 2.38–4.71), induction of labour (OR 1.19: 95% CI 1.02–1.38 and OR 1.94: 95% CI 1.57–2.10), caesarean section (OR 1.41: 95% CI 1.21–1.65 and OR 2.68: 95% CI 2.18–3.29), prematurity (OR 1.28: 95% CI 1–1.65 and OR 1.79: 95% CI 1.32–2.44) and macrosomia (OR 1.87: 95% CI 1.43–2.46 and OR 2.03: 95% CI 1.40–2.93). Conclusions One in four pregnant women had pre-pregnancy overweight or obesity. This study shows the relationship between pre-pregnancy overweight or obesity with adverse maternal and perinatal outcomes.

Contains fulltext : 249888.pdf (Publisher’s version ) (Open Access) BACKGROUND: In-depth insight into haemodynamic changes during normotensive pregnancy may help identify women at risk for gestational hypertensive complications. OBJECTIVES: To determine the magnitude of changes in cardiac output and its determinants stroke volume and heart rate, and total peripheral vascular resistance during singleton normotensive and hypertensive pregnancies. SEARCH STRATEGY: PubMed (NCBI) and Embase (Ovid) databases were searched from their inception up to November 2019. SELECTION CRITERIA: Studies reporting original measurements of haemodynamic parameters during pregnancy together with a non-pregnant reference measurement. Studies including women using antihypertensive medication were excluded. DATA COLLECTION AND ANALYSIS: Pooled mean differences between pregnant and non-pregnant women, and absolute values of haemodynamic parameters were calculated for predefined gestational intervals using a random-effects model in normotensive and hypertensive pregnancy. Meta-regression analysis was used to analyse group differences in adjustments and absolute values during pregnancy. MAIN RESULTS: In normotensive pregnancies, cardiac output increased from the first weeks on, reaching its highest level early in the third trimester (mean difference, 1.41 l·min(1) ; 95% CI 1.18-1.63 l·min). In parallel, vascular resistance decreased progressively until its nadir in the early third trimester (mean difference, -331 dyn·sec(-1) ·cm(-5) ; 95% CI -384 to -277 dyn·sec(-1) ·cm(-5) ) and then increased slightly at term. In hypertensive pregnancies, the initial cardiac output increase was higher and vascular resistance did not change throughout gestation compared with reference values. CONCLUSIONS: Hemodynamic changes in women who eventually develop hypertensive complications are substantially different. Serial monitoring and plotting against developed normograms can identify women at risk and may allow timely intervention. TWEETABLE ABSTRACT: Monitoring haemodynamic changes in pregnancy helps identify women at risk for hypertensive complications.

Objective s : There is a need for markers to facilitate the diagnosis of preeclampsia, one of the most chief causes of maternal and infant mortality. Preeclampsia causes damage to the glomeruli and vascular endothelium in pregnant women. Podocalyxin is a sialoglycoprotein found in both glomeruli and vascular endothelium. In this study, we investigated the levels of podocalyxin in preeclampsia, and studied its potential to predict preeclampsia. Material and methods: Women admitted to the Health Sciences University Derince Training and Research Hospital, Department of Obstetrics and Gynecology between February–November 2018 due to high direct blood and diagnosed with preeclampsia according to the 2013 American College of Obstetricians and Gynecologists criteria were included in the study. The control group consisted of healthy volunteers having similar demographic features ‎(gestational week, gravida, parity, and age) with the preeclampsia group. The main outcome variable was serum podocalyxin levels. Results: ‎The mean (± SD) podocalyxin levels of the study and control groups were 124.15 ± ‎39.63 ng/mL and ‎71.47 ± ‎16.86 ng/mL, respectively (‎t = 7.845‎, ‎p < 0.001‎). Using a cut-off of 91.7123, podocalyxin could predict preeclampsia with 90% sensitivity and 98% specificity. Furthermore, podocalyxin levels were significantly higher than the normotensive participants in both early (‎14‎‎3.81‎ ± ‎5‎‎1.96 ng/mL‎ vs. ‎75.‎‎35 ± ‎1‎‎9.36 ng/mL‎) and late-onset (‎11‎‎0.22 ± ‎1‎‎9.11 ng/mL‎ vs ‎68.‎‎26 ± ‎1‎‎4.13 ng/mL‎) preeclampsia (p < 0.001). Conclusions: Serum podocalyxin levels increase in preeclampsia. We conclude that podocalyxin is a candidate for predicting preeclampsia.

Background: Hypertensive disorders of pregnancy (HDP) cause substantial preventable maternal morbidity and mortality. Postpartum hypertension that worsens after women are discharged is particularly...

OBJECTIVE This study evaluated urinary angiotensinogen in preeclampsia. METHODS Normal pregnant (n = 57) and preeclamptic patients (n = 31); Normal pregnant (n = 10) and preeclamptic rats (n = 10) were studied. Urinary angiotensinogen and plasma angiotensin II were assayed by enzyme-linked immunosorbent assay (ELISA). RESULTS Urinary angiotensinogen in preeclampsia patients (2.0 ± 1.1 ng/mg creatinine) was suppressed (*p

Background: Preeclampsia (PE) is a pregnancy complication with serious maternal and neonatal consequences worldwide. Our understanding of PE pathophysiology has significantly evolved over the last decades by recognizing that endothelial dysfunction and systemic inflammation, with an associated angiogenic imbalance, are key pieces of this incomplete puzzle. In the present era, where no single treatment to cure or treat this obstetric condition has been developed so far, PE prevention and early prediction are the most useful clinical approach to reduce the PE burden. Introduction: Although most PE episodes occur in healthy nulliparous women, the identification of specific clinical conditions that increase the risk of PE dramatically provides a critical opportunity to improve outcomes by acting on potentially reversible factors, and also contributes to better understand this pathophysiologic enigma. Methods: Pertinent studies were searched in PubMed/Medline and Google Scholar (updated August 2020) using common keywords applied in the field of preeclampsia, inflammation and endothelial dysfunction. Given the design of this work as a narrative review, no formal criteria for study selection or appraisal were utilized. Conclusion: In this review, we highlight major clinical contributors of PE and shed light on their potential link with endothelial dysfunction and inflammation.

Objective In this brief review, the authors focus on the effects of gestational exposures to urban air pollution on fetal development and neonatal outcomes. Source of data In this review the authors used PubMed, Web of Science and SciELO research platforms, analyzing papers from the last 30 years. Summary of the findings Epidemiological and experimental evidence agree that gestational exposure to air pollution in urban increases the risks for low birth weight, preterm birth, congenital malformation, intrauterine growth restriction, and neonatal mortality. Furthermore, exposures are associated with increased risks for preeclampsia, hypertension, gestational diabetes. Conclusions Therefore, it is time for greater involvement and engagement of the health sector in the discussion of public policies that may affect the quality of the environment, and that directly or indirectly impact the health of those who were not yet born.

Preeclampsia and eclampsia is a complication in the labor process whose incidence is always high. The purpose of this study was to study the relationship between Birth Weight and the incidence of preeclampsia in RSUD dr. M. Yunus, Bengkulu city in 2017. The type of research used in this study is Survey Analytic using the Cross Sectional method. The population in this study was overall in the hospital of Dr. M. Yunus City of Bengkulu in January to December in 2017 which is 362 babies. The sampling technique in this study was 78 proportional sampling. The data used is secondary data obtained from the patient register at Dr. M Yunus Hospital in Bengkulu. Data were analyzed using univariate and bivariate analysis with Chi-Square test (2) and Contingency Coefficient (C) test. The results obtained: Of the 78 newborns sampled there were 60 infants (76.9%) normal birth weight, 55 people (70.5%) did not experience preeclampsia, there was a significant relationship between preeclampsia and low infant weight in RSUD dr. M. Yunus Bengkulu in the tight category. It is expected that health workers can maintain and improve the quality of their abilities and skills to deal with babies with low birth weight born by preeclampsia patients or other patients.

OBJECTIVES: To determine whether the full spectrum of hypertensive disorders of pregnancy (HDP) -- comprising gestational hypertension; preeclampsia with or without severe features; eclampsia; and Hemolysis, Elevated Liver enzymes, and Low Platelets (HELLP) Syndrome -- is increased at high (≥2500 m, 8250 ft) compared with lower altitudes in Colorado independent of maternal background characteristics, and if so their relationship to neonatal well-being. METHODS: A retrospective cohort study was conducted using statewide birth-certificate data to compare the frequency of gestational hypertension, preeclampsia (with or without severe features), eclampsia, HELLP Syndrome, or all HDP combined in 617,958 Colorado women who lived at high vs. low altitude (2500 m)- vs. low (

Objectives: Fetal growth restriction is associated with chronic fetal hypoxia, poor perinatal outcome and increased perinatal mortality. There are no reliable methods to detect cell damage in the central nervous system (CNS) in these patients. The findings of increased an acidic calcium-binding protein (S100B) concentration in biological fluids of infants after brain injury have supported the use of S100B as a biochemical marker of CNS damage. The purpose of the study was to assess blood S100B concentrations in small for gestational age (SGA) and appropriate for gestational age (AGA) newborns and to evaluate the usefulness of S100B for early detection of hypoxia. Material and methods: The investigation was carried out between November 2011 and April 2014. Serum S100B protein level was assessed in cord blood collected from newborns after birth. Medical records of mothers of neonates studied were reviewed for pregnancy induced hypertension (PIH), preeclampsia, maternal smoking during pregnancy and abnormalities in umbilical artery (UA) Doppler ultrasound examination. Results: The study was carried out in 88 SGA neonates and 80 AGA neonates. The median value of S100B protein concentration in the SGA study group was significantly higher than in AGA controls (p < 0.001). Cord blood serum S100B concentration in SGA neonates with prenatal normal UA Doppler ultrasound findings (n = 32) did not differ from that SGA neonates with abnormal prenatal UA Doppler findings (n = 25) (p = 0.74), but was significantly higher than in AGA newborns (p < 0.001). Conclusions : Elevated S100B protein levels in cord blood collected from SGA newborns may be helpful in detecting infants at higher risk of postnatal neurologic disturbances at an early stage.

Women with hypertensive disorders of pregnancy (HDP) present with evidence of significant myocardial dysfunction on echocardiographic assessment at the time of diagnosis. Birth not only cures the syndrome of HDP, but is also associated with a reduction in cardiovascular (CV) volume and resistance load in the mother due to the delivery of the fetoplacental unit. The impact of this physiological change on maternal myocardial function in women with HDP has not been systematically evaluated. The aim of this study is to compare echocardiographic findings immediately before and after childbirth in women with HDP. In this prospective longitudinal study, 30 women with a diagnosis of HDP underwent two consecutive transthoracic echocardiography (TTE) examinations: the first prepartum and the second in the early postpartum period. Paired comparisons of these assessments were performed. Left ventricular (LV) concentric remodelling or hypertrophy were found in 21 (70%) patients and there were no significant differences in cardiac morphology indices: LV mass index (78.9±16.3 g/m vs 77.9 ±15.4 g/m , p=0.611) and relative wall thickness (0.45±0.1 vs 0.44±0.1, p=0.453). LV diastolic function did not demonstrate any peripartum variation: left atrial volume (52.40±15.3 vs 50.97±15.6, p=0.433); lateral E' (0.12±0.03 vs 0.12±0.03, p=0.307) and E/E' ratio (7.88±2.19 vs 7.91±1.74, p=0.934). Systolic function indices such as LV ejection fraction (57.5±4.4% vs 56.4±2.1%, p=0.295) and global longitudinal strain (-15.3±2.6% vs -15.1±3.1%, p=0.715) also remained unchanged. Maternal hemodynamic changes associated with birth did not significantly influence peripartum TTE indices in women with HDP. Suboptimal maternal echocardiographic findings in HDP are likely to be the consequence of chronic pregnancy CV load changes or pre-existing maternal CV impairment. Severity and persistence of myocardial dysfunction into the postpartum period may be related to the long-term maternal CV disease legacy of HDP. This article is protected by copyright. All rights reserved. [Abstract copyright: This article is protected by copyright. All rights reserved.]

The reported incidence of eclampsia is 1.6 to 10 per 10,000 deliveries in developed countries, whereas it is 50 to 151 per 10,000 deliveries in developing countries. In addition, low-resource countries have substantially higher rates of maternal and perinatal mortalities and morbidities. This disparity in incidence and pregnancy outcomes may be related to universal access to prenatal care, early detection of preeclampsia, timely delivery, and availability of healthcare resources in developed countries compared to developing countries. Because of its infrequency in developed countries, many obstetrical providers and maternity units have minimal to no experience in the acute management of eclampsia and its complications. Therefore, clear protocols for prevention of eclampsia in those with severe preeclampsia and acute treatment of eclamptic seizures at all levels of healthcare are required for better maternal and neonatal outcomes. Eclamptic seizure will occur in 2% of women with preeclampsia with severe features who are not receiving magnesium sulfate and in

Although the most recent guidance from the International Society for the Study of Hypertension in Pregnancy (ISSHP) has highlighted the role of angiogenic marker assessment in the diagnosis of pre-eclampsia (PE) in women with chronic hypertension, the ISSHP has withheld recommending its implementation due to the limited available evidence in this group of women. Therefore, we aimed to investigate the value of soluble fms-like tyrosine kinase-1 (sFlt-1) and placental growth factor (PlGF) assessment in women with chronic hypertension and suspected superimposed PE.This was a retrospective analysis of prospectively collected data recorded in an electronic database between January 2013 and October 2019. Women with chronic hypertension and singleton pregnancy who had suspected superimposed PE were included. Superimposed PE was suspected in women presenting with worsening hypertension, epigastric pain, new-onset edema, dyspnea or neurological symptoms. The exclusion criteria were delivery within 1 week after assessment for reasons other than PE, chronic kidney disease, history of cardiac disease, fetal aneuploidy, genetic syndrome or major structural anomaly and missing pregnancy outcome. Maternal serum angiogenic markers (sFlt-1, PlGF and sFlt-1/PlGF ratio) were measured. The primary outcome was the utility of angiogenic markers in the prediction of superimposed PE. Predictive accuracy was assessed for superimposed PE diagnosed at different timepoints, including within 1 week after assessment and any time before birth. The secondary outcome was comparison of adverse maternal and perinatal outcomes between women with superimposed PE diagnosed according to the traditional ISSHP criteria and those diagnosed according to extended criteria including angiogenic markers. The predictive accuracy of each angiogenic marker was assessed using receiver-operating-characteristics-curve analysis. Area under the curve (AUC) values were compared using De Long's test. A sensitivity analysis was planned for gestational age at assessment. The association of various variables with composite adverse maternal and perinatal outcomes was assessed using binomial regression.The study included 142 pregnant women with chronic hypertension and suspected superimposed PE, of whom 25 (17.6%) developed PE within 1 week after assessment, 52 (36.6%) developed PE at any timepoint before birth and 90 (63.4%) delivered without PE. Maternal serum angiogenic imbalance was associated significantly with superimposed PE diagnosed according to the ISSHP criteria within 1 week or at any time after assessment (P 0.001 for both). The predictive accuracy of maternal serum sFlt-1/PlGF ratio for superimposed PE diagnosed within 1 week after assessment was superior to that of maternal serum PlGF level (AUC, 0.91 vs 0.86; P = 0.032). The addition of angiogenic imbalance to the traditional ISSHP diagnostic criteria was associated with an increase in the detection rate (35.1% increase; 95% credible interval (CrI), 16.6-53.6%) and positive (9.6% increase; 95% CrI, 0.0-20.6%) and negative (3.1% increase; 95% CrI, 1.3-4.9%) predictive values for composite adverse maternal outcome, with high posterior probabilities of an increase in each predictive accuracy parameter ( 99.9%, 95.6% and 99.9%, respectively), without a meaningful decrease in specificity. The addition of angiogenic imbalance improved the detection rate for composite adverse perinatal outcome (20.6% increase; 95% CrI, 0.0-42.2%), with a high posterior probability (96.9%). There was a corresponding drop in specificity (5.7% decrease; 95% CrI, -2.3% to 13.6%), with a posterior probability of 91.8%.In women with chronic hypertension and suspected superimposed PE, addition of maternal serum angiogenic markers to the traditional diagnostic criteria for superimposed PE improved significantly the sensitivity for the prediction of both maternal and perinatal adverse outcomes. Implementation of angiogenic marker assessment in the evaluation of pregnant women with chronic hypertension should therefore be considered. © 2021 International Society of Ultrasound in Obstetrics and Gynecology.

The opinion on the mechanisms underlying the pathogenesis of preeclampsia still divides scientists and clinicians. This common complication of pregnancy has long been viewed as a disorder linked primarily to placental dysfunction, which is caused by abnormal trophoblast invasion, however, evidence from the previous two decades has triggered and supported a major shift in viewing preeclampsia as a condition that is caused by inherent maternal cardiovascular dysfunction, perhaps entirely independent of the placenta. In fact, abnormalities in the arterial and cardiac functions are evident from the early subclinical stages of preeclampsia and even before conception. Moving away from simply observing the peripheral blood pressure changes, studies on the central hemodynamics reveal two different mechanisms of cardiovascular dysfunction thought to be reflective of the early-onset and late-onset phenotypes of preeclampsia. More recent evidence identified that the underlying cardiovascular dysfunction in these phenotypes can be categorized according to the presence of coexisting fetal growth restriction instead of according to the gestational period at onset, the former being far more common at early gestational ages. The purpose of this review is to summarize the hemodynamic research observations for the two phenotypes of preeclampsia. We delineate the physiological hemodynamic changes that occur in normal pregnancy and those that are observed with the pathologic processes associated with preeclampsia. From this, we propose how the two phenotypes of preeclampsia could be managed to mitigate or redress the hemodynamic dysfunction, and we consider the implications for future research based on the current evidence. Maternal hemodynamic modifications throughout pregnancy can be recorded with simple-to-use, noninvasive devices in obstetrical settings, which require only basic training. This review includes a brief overview of the methodologies and techniques used to study hemodynamics and arterial function, specifically the noninvasive techniques that have been utilized in preeclampsia research.

The definition of preeclampsia is changing. However, with the addition of organ symptoms to the presence of hypertension in pregnancy instead of relying only on proteinuria, a more precise detection of women at risk of preeclampsia-associated adverse events has not been achieved. Instead, under the new definitions of the American College of Obstetricians and Gynecologists and of the International Society for the Study of Hypertension in Pregnancy, more women are classified as preeclamptic, with a tendency to milder disease. Furthermore, angiogenic and antiangiogenic factors have emerged as essential tools for predicting and diagnosing preeclampsia at high accuracies. Next to being rooted in the pathophysiology of the disease, they have been proven to be reliable tools for predicting and diagnosing the disease. In addition, 2 cutoffs have been evaluated for the clinical setting. As shown in the Prediction of Short-Term Outcome in Pregnant Women With Suspected Preeclampsia Study, at the soluble fms-like tyrosine kinase-1-to-placental growth factor ratio cutoff of 38, a preeclampsia can be ruled out for 1 week with a negative predictive value of 99.3% (95% confidence interval, 97.9-99.9) and ruled in with a positive predictive value of 36.7% (95% confidence interval, 28.4-45.7). The diagnostic cutoff of 85 has been shown to accurately identify women with preeclampsia, with a sensitivity of up to 88% and a specificity of 99.5%. In this review, we highlight the central role of angiogenic and antiangiogenic factors in the differential diagnosis of women presenting at high risk of the disease, such as patients with chronic hypertension or chronic kidney disease. We will focus on their ability to predict preeclampsia-associated adverse fetal and maternal outcomes. This is only possible when critically reviewing the evolution of the definition of "preeclampsia." We show how changes in this definition shape our clinical picture of the condition and how angiogenic and antiangiogenic biomarkers might be included to better identify women destined to develop preeclampsia-related adverse outcomes.

International audience; Objective: To explore the regulatory role of soluble CD146 (sCD146) and its interaction with galectin-1 (Gal1) in placenta-mediated complications of pregnancy.Design: Prospective pilot and experimental studies.Setting: University-affiliated hospital and academic research laboratory.Patient(s): One hundred fifteen women divided into three groups: 30 healthy, nonpregnant women, 50 women with normal pregnancies, and 35 with placenta-mediated pregnancy complications.Intervention(s): Wound-healing experiments were conducted to study trophoblast migration.Main outcome measure(s): Quantification of sCD146 and Gal1 by enzyme-linked immunosorbent assay. Analysis of trophoblast migration by wound closure.Result(s): Concomitant detection of sCD146 and Gal1 showed lower sCD146 and higher Gal1 concentrations in women with normal pregnancies compared with nonpregnant women. In addition, follow-up of these women revealed a decrease in sCD146 associated with an increase in Gal1 throughout pregnancy. In contrast, in women with preeclampsia, we found significantly higher sCD146 concentrations compared with women with normal pregnancies and no modification of Gal1. We emphasize the opposing effects of sCD146 and Gal, since, unlike Gal1, sCD146 inhibits trophoblast migration. Moreover, the migratory effect of Gal1 was abrogated with the use of an anti-CD146 blocking antibody or the use of small interfering RNA to silence VEGFR2 expression. This suggests that trophoblast migration is mediated though the interaction of Gal1 with CD146, further activating the VEGFR2 signaling pathway. Significantly, sCD146 blocked the migratory effects of Gal1 on trophoblasts and inhibited its secretion, suggesting that sCD146 acts as a ligand trap.Conclusion(s): Soluble CD146 could be proposed as a biomarker in preeclampsia and a potential therapeutic target. Clinical trial registration number: NCT 01736826.Trial registration: ClinicalTrials.gov NCT01736826.

Preeclampsia is a devastating medical complication of pregnancy that can lead to significant maternal and fetal morbidity and mortality. It is currently believed that there is abnormal placentation in as early as the first trimester in women destined to develop preeclampsia. Although the etiology of the abnormal placentation is being debated, numerous epidemiologic and experimental studies suggest that imbalances in circulating angiogenic factors released from the placenta are responsible for the maternal signs and symptoms of preeclampsia. In particular, circulating levels of soluble fms-like tyrosine kinase 1, an antiangiogenic factor, are markedly increased in women with preeclampsia, whereas free levels of its ligand, placental, growth factor are markedly diminished. Alterations in these angiogenic factors precede the onset of clinical signs of preeclampsia and correlate with disease severity. Recently, the availability of automated assays for the measurement of angiogenic biomarkers in the plasma, serum, and urine has helped investigators worldwide to demonstrate a key role for these factors in the clinical diagnosis and prediction of preeclampsia. Numerous studies have reported that circulating angiogenic biomarkers have a very high negative predictive value to rule out clinical disease among women with suspected preeclampsia. These blood-based biomarkers have provided a valuable tool to clinicians to accelerate the time to clinical diagnosis and minimize maternal adverse outcomes in women with preeclampsia. Angiogenic biomarkers have also been useful to elucidate the pathogenesis of related disorders of abnormal placentation such as intrauterine growth restriction, intrauterine fetal death, twin-to-twin transfusion syndrome, and fetal hydrops. In summary, the discovery and characterization of angiogenic proteins of placental origin have provided clinicians a noninvasive blood-based tool to monitor placental function and health and for early detection of disorders of placentation. Uncovering the mechanisms of altered angiogenic factors in preeclampsia and related disorders of placentation may provide insights into novel preventive and therapeutic options.

The study aimed to investigate whether serum sFlt-1 (soluble fms-like tyrosine kinase-1) at 11-13 weeks’ gestation in pregnancies that subsequently developed preeclampsia was different from those without preeclampsia and compare screening performance of the International Prediction of Pregnancy Complications (IPPIC) reported models, which include various combinations of maternal factors, systolic blood pressure, diastolic blood pressure, PlGF (placental growth factor) and sFlt-1 and the competing risk (CR) models, which include various combinations of maternal factors, mean arterial pressure (MAP) and PlGF for predicting any-onset, early-onset, and late-onset preeclampsia. This was a prospective multicenter study in 7877 singleton pregnancies. The differences of the predictive performance between the IPPIC and CR models were compared. There were 141 women (1.79%) who developed preeclampsia, including 13 cases (0.17%) of early-onset preeclampsia and 128 cases (1.62%) of late-onset preeclampsia. In pregnancies that developed preeclampsia compared to unaffected pregnancies, median serum sFlt-1 levels and its MoMs were not significantly different ( p >0.05). There was no significant association between gestational age at delivery and log 10 sFlt-1 and log 10 sFlt-1 MoM ( p >0.05). The areas under the curve of CR models were significantly higher than the IPPIC models for the prediction of any-onset and late-onset preeclampsia but not for early-onset preeclampsia. In conclusion, there are no significant differences in the maternal serum sFlt-1 levels at 11-13 weeks’ gestation between women who subsequently develop preeclampsia and those who do not. Moreover, the CR models for the prediction of any-onset and late-onset preeclampsia perform better than the IPPIC reported model.

Physiologic, mechanical and immunologic alterations in pregnancy could potentially affect susceptibility to and severity of COVID-19 during pregnancy. Due to lack of comparable incidence data and challenges with disentangling differences in susceptibility from different exposure risks, data are insufficient to determine whether pregnancy increases susceptibility to SARS-CoV-2 infection. Data support pregnancy as a risk factor for severe disease associated with COVID-19; some of the best evidence comes from the Centers for Disease Control and Prevention’s (CDC’s) COVID-19 surveillance system, which reported that pregnant persons were more likely to be admitted to an intensive care unit (ICU), require invasive ventilation, require extracorporeal membrane oxygenation, and die compared with nonpregnant women of reproductive age. Although intrauterine transmission of SARS-CoV-2 has been documented, it appears to be rare, possibly related to low levels of SARS-CoV-2 viremia and decreased co-expression of angiotensin-converting enzyme 2 (ACE2) and transmembrane serine protease 2 (TMPRSS2) needed for SARS-CoV-2 entry into cells in the placenta. Evidence is accumulating that SARS-CoV-2 infection during pregnancy is associated with a number of adverse pregnancy outcomes including preeclampsia, preterm birth, and stillbirth, especially among pregnant persons with severe COVID-19 disease. In addition to the direct impact of COVID-19 on pregnancy outcomes, there is evidence that the pandemic and its effects on healthcare systems have had adverse effects on pregnancy outcomes, such as increased stillbirths and maternal deaths. These trends may represent widening disparities and an alarming reversal of recent improvements in maternal and infant health. All three COVID-19 vaccines currently available under an Emergency Use Authorization by the United States Food and Drug Administration can be administered to pregnant or lactating persons, with no preference for vaccine type. Although safety data in pregnancy are rapidly accumulating and no safety signals in pregnancy have been detected, additional information about birth outcomes, particularly among persons vaccinated earlier in pregnancy, are needed.

الملخص: أهداف البحث: تسمم الحمل هو عامل خطر رئيس لوفيات ومراضة الأمهات والجنين. كانت هناك جهود هائلة لتحديد المؤشرات الحيوية في المصل، والتي يمكن أن تتنبأ بشكل موثوق بتسمم الحمل. تهدف الدراسة إلى تقييم المؤشرات الحيوية التي لها أفضل فائدة في تشخيص تسمم الحمل. طرق البحث: تم إجراء بحث منهجي في قاعدة بيانات ''بب ميد'' وتم استرداد المراجع المتسلسلة. تم تضمين المقالات البحثية الأصلية التي تضم ضوابط الحالة، والأتراب، وتجارب التحكم العشوائية، والدراسات المقطعية. تضمنت المتغيرات المسجلة تصميم الدراسة ونوعها وسنة ومكان الدراسة وقيمة المتوسط ± الانحراف المعياري للعلامات في المرضى والضوابط والوحدة وحجم عينة مجتمع الدراسة. تم تفسير النتائج بناء على قيم فرق المتوسط المعيارية. النتائج: تم استرجاع ما مجموعه ٣٨٩ دراسة من قاعدة بيانات ''بب ميد''. وأدى التحليل الإضافي ٨٩ دراسة لهذه المراجعة. تم تضمين ٤٧ دراسة إضافية من سلسلة المراجع. في وقت لاحق، تمت مراجعة ١٣٦ مقالة ذات نص كامل بالتفصيل وتم إدخال البيانات. أخيرا، تم اختيار ٢٥ دراسة لهذا التحليل التلوي، وقيمت ١٣ واصما حيويا في مصل الدم. كانت الواسمات المولدة للأوعية والتيروزين كيناز، وعامل النمو المشيمي، والإندوغلين مرتفعة بشكل ملحوظ في المرضى الذين يعانون من تسمم الحمل مقارنة بالضوابط العادية للحوامل. وكان عامل النمو المشيمي والعلامات الحيوية الدهنية عالية الكثافة والأديبونكتين منخفضة بشكل ملحوظ. في حين أن الدهون الثلاثية، وصميم البروتين ب، واللبتين كانت مرتفعة في مرضى مقدمات الارتعاج مقارنة بالضوابط العادية للحوامل. الاستنتاجات: في دراستنا، أظهرت قيم المؤشرات الحيوية في المصل؛ الواسمات المولدة للأوعية وعامل النمو المشيمي والدهون عالية الكثافة والأديبونكتين واللبتين والدهون الثلاثية وصميم البروتين ب، اختلافات كبيرة بين المرضى والضوابط. تتطلب هذه النتائج تقييما متقدما للواسمات الحيوية من أجل الفحص التشخيصي لمقدمات الارتعاج. Abstract: Objective: Preeclampsia is a major risk factor for maternal and foetal mortality and morbidity. There have been tremendous efforts to identify serum biomarkers which can reliably predict the occurrence of preeclampsia. The study aims to assess the biomarkers that have the greatest utility in the diagnosis of preeclampsia. Methods: A systematic search was performed on the PubMed literature database, and chain references were retrieved. Original research articles composed of case controls, cohorts, randomised control trials, and cross-sectional studies were included. The recorded variables included each study's design, type, year, and location; the value (mean ± standard deviation) of the markers in the patients and the pregnant controls; and the p-value, unit of measurement, and the sample size of each study. The results were interpreted based on the standardised mean difference (SMD) values. Results: A total of 398 studies were retrieved from the PubMed database. After further analysis, 89 studies were selected for this review. An additional 47 studies were included based on chain referencing. Later, 136 full-text articles were reviewed in detail and their data were entered. Finally, 25 studies, in which 13 serum biomarkers were assessed, were selected for this meta-analysis. The levels of the angiogenic markers fms-like tyrosine kinase (sFlt), sFlt/placental growth factor (PlGF), and endoglin were significantly higher in patients with preeclampsia than in the pregnant controls. The levels of PlGF and the lipid biomarkers high density lipoprotein (HDL) and adiponectin were significantly lower, while the levels of triglycerides, apolipoprotein B (APO-B), and leptin were elevated in the preeclamptic patients compared to the pregnant controls (p

Objective To estimate the annual cost associated with obstetric events in women of reproductive age with immune-mediated inflammatory diseases, from the perspective of the National Healthcare System. Methods A cost-analysis was developed to estimate the impact associated with obstetric events in women of reproductive age with psoriasis (PSO), psoriatic arthritis (PsA), rheumatoid arthritis (RA) and axial spondyloarthritis (axSpA). The analysis considered complications during fertility and conception, in pregnancy and in the postpartum. All parameters were validated and agreed by a multidisciplinary expert panel. Unitary costs (€, 2019) were obtained from national, local databases. Results During fertility and conception, an annual cost per patient of €229 was estimated for a preconception consultation in a patient with PSO, of €3,642 for a preconception consultation in patients with PsA, RA and axSpA and €4,339 for assisted reproduction. Women with complications in pregnancy had an annual cost per patient of €1,214 for a miscarriage in the first trimester, €4,419 for a late miscarriage in the second trimester, €11,260 for preeclampsia €3,188 for restricted intrauterine growth and €12,131 for threat of premature delivery. In the postpartum, an annual cost per patient of €120,364, €44,709, and €5,507 were estimated associated with admissions to neonatology of premature infants of Conclusions This analysis provides insight on the economic burden of complications associated with women of reproductive age for immune-mediated diseases (PSO, PsA, RA, axSpA). Individualization of treatment, additional and close monitoring may reduce the risk and burden of these complications.

Qualitative and quantitative measurement of urine protein excretion is one of the most common tests performed during pregnancy. For more than 100 years, proteinuria was necessary for the diagnosis of preeclampsia, but recent guidelines recommend that proteinuria is sufficient but not necessary for the diagnosis. Still, in clinical practice, most patients with gestational hypertension will be diagnosed as having preeclampsia based on the presence of proteinuria. Although the reference standard for measuring urinary protein excretion is a 24-hour urine collection, spot urine protein-to-creatinine ratio is a reasonable "rule-out" test for proteinuria. Urine dipstick screening for proteinuria does not provide any clinical benefit and should not be used to diagnose proteinuria. The classic cutoff cited to define proteinuria during pregnancy is a value of >300 mg/24 hours or a urine protein-to-creatinine ratio of at least 0.3. Using this cutoff, the rate of isolated proteinuria in pregnancy may reach 8%, whereas preeclampsia occurs among 3% to 8% of pregnancies. Although this threshold is widely accepted, its origin is not based on evidence on adverse pregnancy outcomes but rather on expert opinion and results of small studies. After reviewing the available data, the most important factor that influences maternal and neonatal outcome is the severity of blood pressures and presence of end organ damage, rather than the excess protein excretion. Because the management of gestational hypertension and preeclampsia without severe features is almost identical in frequency of surveillance and timing of delivery, the separation into 2 disorders is unnecessary. If the management of women with gestational hypertension with a positive assessment of proteinuria will not change, we believe that urine assessment for proteinuria is unnecessary in women who develop new-onset blood pressure at or after 20 weeks' gestation. Furthermore, we do not recommend repeated measurement of proteinuria for women with preeclampsia, the amount of proteinuria does not seem to be related to poor maternal and neonatal outcomes, and monitoring proteinuria may lead to unindicated preterm deliveries and related neonatal complications. Our current diagnosis of preeclampsia in women with chronic kidney disease may be based on a change in protein excretion, a baseline protein excretion evaluation is critical in certain conditions such as chronic hypertension, diabetes, and autoimmune or other renal disorders. The current definition of superimposed preeclampsia possesses a diagnostic dilemma, and it is unclear whether a change in the baseline proteinuria reflects another systemic disease such as preeclampsia or whether women with chronic disease such as chronic hypertension or diabetes will experience a different "normal" pattern of protein excretion during pregnancy. Finally, limited data are available regarding angiogenic and other biomarkers in women with chronic kidney disease as a potential aid in distinguishing the worsening of baseline chronic kidney disease and chronic hypertension from superimposed preeclampsia.

Maternal tolerance of the semiallogenic fetus necessitates conciliation of competing interests. Viviparity evolved with a placenta to mediate the needs of the fetus and maternal adaptation to the demands of pregnancy and to ensure optimal survival for both entities. The maternal-fetal interface is imagined as a 2-dimensional porous barrier between the mother and fetus, when in fact it is an intricate multidimensional array of tissues and resident and circulating factors at play, encompassing the developing fetus, the growing placenta, the changing decidua, and the dynamic maternal cardiovascular system. Pregnancy triggers dramatic changes to maternal hemodynamics to meet the growing demands of the developing fetus. Nearly a century of extensive research into the development and function of the placenta has revealed the role of placental dysfunction in the great obstetrical syndromes, among them preeclampsia. Recently, a debate has arisen questioning the primacy of the placenta in the etiology of preeclampsia, asserting that the maternal cardiovascular system is the instigator of the disorder. It was the clinical observation of the high rate of preeclampsia in hydatidiform mole that initiated the focus on the placenta in the etiology of the disease. Over many years of research, shallow trophoblast invasion with deficient remodeling of the maternal spiral arteries into vessels of higher capacitance and lower resistance has been recognized as hallmarks of the preeclamptic milieu. The lack of the normal decrease in uterine artery resistance is likewise predictive of preeclampsia. In abdominal pregnancies, however, an extrauterine pregnancy develops without remodeling of the spiral arteries, yet there is reduced resistance in the uterine arteries and distant vessels, such as the maternal ophthalmic arteries. Proponents of the maternal cardiovascular model of preeclampsia point to the observed maternal hemodynamic adaptations to pregnancy and maladaptation in gestational hypertension and preeclampsia and how the latter resembles the changes associated with cardiac disease states. Recognition of the importance of the angiogenic-antiangiogenic balance between placental-derived growth factor and its receptor soluble fms-like tyrosine kinase-1 and disturbance in this balance by an excess of a circulating isoform, soluble fms-like tyrosine kinase-1, which competes for and disrupts the proangiogenic receptor binding of the vascular endothelial growth factor and placental-derived growth factor, opened new avenues of research into the pathways to normal adaptation of the maternal cardiovascular and other systems to pregnancy and maladaptation in preeclampsia. The significance of the "placenta vs heart" debate goes beyond the academic: understanding the mutuality of placental and maternal cardiac etiologies of preeclampsia has far-reaching clinical implications for designing prevention strategies, such as aspirin therapy, prediction and surveillance through maternal hemodynamic studies or serum placental-derived growth factor and soluble fms-like tyrosine kinase-1 testing, and possible treatments to attenuate the effects of insipient preeclampsia on women and their fetuses, such as RNAi therapy to counteract excess soluble fms-like tyrosine kinase-1 produced by the placenta. In this review, we will present an integrated model of the maternal-placental-fetal array that delineates the commensality among the constituent parts, showing how a disruption in any component or nexus may lead to the multifaceted syndrome of preeclampsia.

Preeclampsia is a common hypertensive disorder of pregnancy associated with considerable neonatal and maternal morbidities and mortalities. However, the exact cause of preeclampsia remains unknown; it is generally accepted that abnormal placentation resulting in the release of soluble antiangiogenic factors, coupled with increased oxidative stress and inflammation, leads to systemic endothelial dysfunction and the clinical manifestations of the disease. Statins have been found to correct similar pathophysiological pathways that underlie the development of preeclampsia. Pravastatin, specifically, has been reported in various preclinical and clinical studies to reverse the pregnancy-specific angiogenic imbalance associated with preeclampsia, to restore global endothelial health, and to prevent oxidative and inflammatory injury. Human studies have found a favorable safety profile for pravastatin, and more recent evidence does not support the previous teratogenic concerns surrounding statins in pregnancy. With reassuring and positive findings from pilot studies and strong biological plausibility, statins should be investigated in large clinical randomized-controlled trials for the prevention of preeclampsia.

Preeclampsia evolves in 2 stages: a placental problem that generates signals to the mother to cause a range of responses that comprise the second stage (preeclampsia syndrome). The first stage of early-onset preeclampsia is poor placentation, which we here call malplacentation. The spiral arteries are incompletely remodeled, leading to later placental malperfusion, relatively early in the second half of pregnancy. The long duration of the first stage (several months) is unsurprisingly associated with fetal growth restriction. The first stage of late-onset preeclampsia, approximately 80% of total cases, is shorter (several weeks) and part of a process that is common to all pregnancies. Placental function declines as it outgrows uterine capacity, with increasing chorionic villous packing, compression of the intervillous space, and fetal hypoxia, and causes late-onset clinical presentations such as "unexplained" stillbirths, late-onset fetal growth restriction, or preeclampsia. The second stages of early- and late-onset preeclampsia share syncytiotrophoblast stress as the most relevant feature that causes the maternal syndrome. Syncytiotrophoblast stress signals in the maternal circulation are probably the most specific biomarkers for preeclampsia. In addition, soluble fms-like tyrosine kinase-1 (mainly produced by syncytiotrophoblast) is the best-known biomarker and is routinely used in clinical practice in many locations. How the stress signals change over time in normal pregnancies indicates that syncytiotrophoblast stress begins on average at 30 to 32 weeks' gestation and progresses to term. At term, syncytiotrophoblast shows increasing markers of stress, including apoptosis, pyroptosis, autophagy, syncytial knots, and necrosis. We label this phenotype the "twilight placenta" and argue that it accounts for the clinical problems of postmature pregnancies. Senescence as a stress response differs in multinuclear syncytiotrophoblast from that of mononuclear cells. Syncytiotrophoblast irreversibly acquires part of the senescence phenotype (cell cycle arrest) when it is formed by cell fusion. The 2 pathways converge on the common pathologic endpoint, syncytiotrophoblast stress, and contribute to preeclampsia subtypes. We highlight that the well-known heterogeneity of the preeclampsia syndrome arises from different pathways to this common endpoint, influenced by maternal genetics, epigenetics, lifestyle, and environmental factors with different fetal and maternal responses to the ensuing insults. This complexity mandates a reassessment of our approach to predicting and preventing preeclampsia, and we summarize research priorities to maximize what we can learn about these important issues.

Objective This study aimed to review pregnancy hypertension clinical practice guidelines to inform international clinical practice and research priorities. Study Eligibility Criteria Relevant national and international clinical practice guidelines, 2009-19, published in English, French, Dutch or German. Study Appraisal and Synthesis Methods Following published methods and prospective registration (CRD42019123787), a literature search was updated. CPGs were identified by 2 authors independently who scored quality and usefulness for practice (Appraisal of Guidelines for Research and Evaluation II instrument), abstracted data, and resolved any disagreement by consensus. Results Of note, 15 of 17 identified clinical practice guidelines (4 international) were deemed “clinically useful” and had recommendations abstracted. The highest Appraisal of Guidelines for Research and Evaluation II scores were from government organizations, and scores have improved over time. The following were consistently recommended: (1) automated blood pressure measurement with devices validated for pregnancy and preeclampsia, reflecting increasing recognition of the prevalence of white-coat hypertension and the potential usefulness of home blood pressure monitoring; (2) use of dipstick proteinuria testing for screening followed by quantitative testing by urinary protein-to-creatinine ratio or 24-hour urine collection; (3) key definitions and most aspects of classification, including a broad definition of preeclampsia (which includes proteinuria and maternal end-organ dysfunction, including headache and visual symptoms and laboratory abnormalities of platelets, creatinine, or liver enzymes) and a recognition that it can worsen after delivery; (4) preeclampsia prevention with aspirin; (5) treatment of severe hypertension, most commonly with intravenous labetalol, oral nifedipine, or intravenous hydralazine; (6) treatment for nonsevere hypertension when undertaken, with oral labetalol (in particular), methyldopa, or nifedipine, with recommendations against the use of renin-angiotensin-aldosterone inhibitors; (7) magnesium sulfate for eclampsia treatment and prevention among women with “severe” preeclampsia; (8) antenatal corticosteroids for preterm birth but not hemolysis, elevated liver enzymes, and low platelet count syndrome; (9) delivery at term for preeclampsia; (10) a focus on usual labor and delivery care but avoidance of ergometrine; and (11) an appreciation that long-term health complications are increased in incidence, mandating lifestyle change and risk factor modification. Lack of uniformity was seen in the following areas: (1) the components of a broad preeclampsia definition (specifically respiratory and gastrointestinal symptoms, fetal manifestations, and biomarkers), what constitutes severe preeclampsia, and whether the definition has utility because at present what constitutes severe preeclampsia by some guidelines that mandate proteinuria now defines any preeclampsia for most other clinical practice guidelines; (2) how preeclampsia risk should be identified early in pregnancy, and aspirin administered for preeclampsia prevention, because multivariable models (with biomarkers and ultrasonography added to clinical risk markers) used in this way to guide aspirin therapy can substantially reduce the incidence of preterm preeclampsia; (3) the value of calcium added to aspirin for preeclampsia prevention, particularly for women with low intake and at increased risk of preeclampsia; (4) emerging recommendations to normalize blood pressure with antihypertensive agents even in the absence of comorbidities; (5) fetal neuroprotection as an indication for magnesium sulfate in the absence of “severe” preeclampsia; and (6) timing of birth for chronic and gestational hypertension and preterm preeclampsia. Conclusion Consistent recommendations should be implemented and audited. Inconsistencies should be the focus of research.

The placenta is a highly metabolically active organ fulfilling the bioenergetic and biosynthetic needs to support its own rapid growth and that of the fetus. Placental metabolic dysfunction is a common occurrence in preeclampsia although its causal relationship to the pathophysiology is unclear. At the outset, this may simply be seen as an "engine out of fuel." However, placental metabolism plays a vital role beyond energy production and is linked to physiological and developmental processes. In this review, we discuss the metabolic basis for placental dysfunction and propose that the alterations in energy metabolism may explain many of the placental phenotypes of preeclampsia such as reduced placental and fetal growth, redox imbalance, oxidative stress, altered epigenetic and gene expression profiles, and the functional consequences of these aberrations. We propose that placental metabolic reprogramming reflects the dynamic physiological state allowing the tissue to adapt to developmental changes and respond to preeclampsia stress, whereas the inability to reprogram placental metabolism may result in severe preeclampsia phenotypes. Finally, we discuss common tested and novel therapeutic strategies for treating placental dysfunction in preeclampsia and their impact on placental energy metabolism as possible explanations into their potential benefits or harm.

Exudative retinal detachment (ERD) is a rare complication that occurring in 1% of patients with preeclampsia, its incidence is increased when it is associated with HELLP syndrome. Preeclampsia is defined by the development of arterial hypertension and proteinuira occurs after 20 weeks of gestation until postpartum. HELLP syndrome (low platelets, hemolysis and elevated liver enzymes) is a severe form of preeclampsia. ERD in preeclampsia is related to choroidal ischaemia, in the vast majority of the cases associated with hypertensive retinopathy. However, it has been proposed that the combination of hypertension with a microangiopathic hemolysis, hipercoagulability and hypoalbuminemia are the main factors contributing to the development of ERD. Its treatment includes a rapid resolution of labor to reverse ocular manifestations and prevent visual sequels. We describe the case of a pregnant woman with atypical preeclampsia who, in the postpartum of a cesarean, presented an ERD concomitantly with a HELLP syndrome.

Accurate assessment of blood pressure is fundamental to the provision of safe obstetrical care. It is simple, cost effective, and life-saving. Treatments for preeclampsia, including antihypertensive drugs, magnesium sulfate, and delivery, are available in many settings. However, the instigation of appropriate treatment relies on prompt and accurate recognition of hypertension. There are a number of different techniques for blood pressure assessment, including the auscultatory method, automated oscillometric devices, home blood pressure monitoring, ambulatory monitoring, and invasive monitoring. The auscultatory method with a mercury sphygmomanometer and the use of Korotkoff sounds was previously recommended as the gold standard technique. Mercury sphygmomanometers have been withdrawn owing to safety concerns and replaced with aneroid devices, but these are particularly prone to calibration errors and regular calibration is imperative to ensure accuracy. Automated oscillometric devices are straightforward to use, but the physiological changes in healthy pregnancy and pathologic changes in preeclampsia may affect the accuracy of a device and monitors must be validated. Validation protocols classify pregnant women as a "special population," and protocols must include 15 women in each category of normotensive pregnancy, hypertensive pregnancy, and preeclampsia. In addition to a scarcity of devices validated for pregnancy and preeclampsia, other pitfalls that cause inaccuracy include the lack of training and poor technique. Blood pressure assessment can be affected by maternal position, inappropriate cuff size, conversation, caffeine, smoking, and irregular heart rate. For home blood pressure monitoring, appropriate instruction should be given on how to use the device. The classification of hypertension and hypertensive disorders of pregnancy has recently been revised. These are classified as preeclampsia, transient gestational hypertension, gestational hypertension, white-coat hypertension, masked hypertension, chronic hypertension, and chronic hypertension with superimposed preeclampsia. Blood pressure varies across gestation and by ethnicity, but gestation-specific thresholds have not been adopted. Hypertension is defined as a sustained systolic blood pressure of ≥140 mm Hg or a sustained diastolic blood pressure of ≥90 mm Hg. In some guidelines, the threshold of diagnosis depends on the setting in which blood pressure measurement is taken, with a threshold of 140/90 mm Hg in a healthcare setting, 135/85 mm Hg at home, or a 24-hour average blood pressure on ambulatory monitoring of >126/76 mm Hg. Some differences exist among organizations with respect to the criteria for the diagnosis of preeclampsia and the correct threshold for intervention and target blood pressure once treatment has been instigated. Home blood pressure monitoring is currently a focus for research. Novel technologies, including early warning devices (such as the CRADLE Vital Signs Alert device) and telemedicine, may provide strategies that prompt earlier recognition of abnormal blood pressure and therefore improve management. The purpose of this review is to provide an update on methods to assess blood pressure in pregnancy and appropriate technique to optimize accuracy. The importance of accurate blood pressure assessment is emphasized with a discussion of preeclampsia prediction and treatment of severe hypertension. Classification of hypertensive disorders and thresholds for treatment will be discussed, including novel developments in the field.

Preeclampsia is defined as hypertension arising after 20 weeks of gestational age with proteinuria or other signs of end-organ damage and is an important cause of maternal and perinatal morbidity and mortality, particularly when of early onset. Although a significant amount of research has been dedicated in identifying preventive measures for preeclampsia, the incidence of the condition has been relatively unchanged in the last decades. This could be attributed to the fact that the underlying pathophysiology of preeclampsia is not entirely understood. There is increasing evidence suggesting that suboptimal trophoblastic invasion leads to an imbalance of angiogenic and antiangiogenic proteins, ultimately causing widespread inflammation and endothelial damage, increased platelet aggregation, and thrombotic events with placental infarcts. Aspirin at doses below 300 mg selectively and irreversibly inactivates the cyclooxygenase-1 enzyme, suppressing the production of prostaglandins and thromboxane and inhibiting inflammation and platelet aggregation. Such an effect has led to the hypothesis that aspirin could be useful for preventing preeclampsia. The first possible link between the use of aspirin and the prevention of preeclampsia was suggested by a case report published in 1978, followed by the first randomized controlled trial published in 1985. Since then, numerous randomized trials have been published, reporting the safety of the use of aspirin in pregnancy and the inconsistent effects of aspirin on the rates of preeclampsia. These inconsistencies, however, can be largely explained by a high degree of heterogeneity regarding the selection of trial participants, baseline risk of the included women, dosage of aspirin, gestational age of prophylaxis initiation, and preeclampsia definition. An individual patient data meta-analysis has indicated a modest 10% reduction in preeclampsia rates with the use of aspirin, but later meta-analyses of aggregate data have revealed a dose-response effect of aspirin on preeclampsia rates, which is maximized when the medication is initiated before 16 weeks of gestational age. Recently, the Aspirin for Evidence-Based Preeclampsia Prevention trial has revealed that aspirin at a daily dosage of 150 mg, initiated before 16 weeks of gestational age, and given at night to a high-risk population, identified by a combined first trimester screening test, reduces the incidence of preterm preeclampsia by 62%. A secondary analysis of the Aspirin for Evidence-Based Preeclampsia Prevention trial data also indicated a reduction in the length of stay in the neonatal intensive care unit by 68% compared with placebo, mainly because of a reduction in births before 32 weeks of gestational age with preeclampsia. The beneficial effect of aspirin has been found to be similar in subgroups according to different maternal characteristics, except for the presence of chronic hypertension, where no beneficial effect is evident. In addition, the effect size of aspirin has been found to be more pronounced in women with good compliance to treatment. In general, randomized trials are underpowered to investigate the treatment effect of aspirin on the rates of other placental-associated adverse outcomes such as fetal growth restriction and stillbirth. This article summarizes the evidence around aspirin for the prevention of preeclampsia and its complications.

Physiological transformation with remodeling of the uteroplacental spiral arteries is key to a successful placentation and normal placental function. It is an intricate process that involves, but is not restricted to, complex interactions between maternal decidual immune cells and invasive trophoblasts in the uterine wall. In normal pregnancy, the smooth muscle cells of the arterial tunica media of uteroplacental spiral arteries are replaced by invading trophoblasts and fibrinoid, and the arterial diameter increases 5- to 10-fold. Poor remodeling of the uteroplacental spiral arteries is linked to early-onset preeclampsia and several other major obstetrical syndromes, including fetal growth restriction, placental abruption, and spontaneous preterm premature rupture of membranes. Extravillous endoglandular and endovenous trophoblast invasions have recently been put forth as potential contributors to these syndromes as well. The well-acknowledged disturbed extravillous invasion of maternal spiral arteries in preeclampsia is summarized, as are briefly novel concepts of disturbed extravillous endoglandular and endovenous trophoblast invasions. Acute atherosis is a foam cell lesion of the uteroplacental spiral arteries associated with poor remodeling. It shares some morphologic features with early stages of atherosclerosis, but several molecular differences between these lesions have also recently been revealed. Acute atherosis is most prevalent at the maternal-fetal interface, at the tip of the spiral arteries. The localization of acute atherosis downstream of poorly remodeled arteries suggests that alterations in blood flow may trigger inflammation and foam cell development. Acute atherosis within the decidua basalis is not, however, confined to unremodeled areas of spiral arteries or to hypertensive disorders of pregnancy and may even be present in some clinically uneventful pregnancies. Given that foam cells of atherosclerotic lesions are known to arise from smooth muscle cells or macrophages activated by multiple types of inflammatory stimulation, we have proposed that multiple forms of decidual vascular inflammation may cause acute atherosis, with or without poor remodeling and/or preeclampsia. Furthermore, we propose that acute atherosis may develop at different gestational ages, depending on the type and degree of the inflammatory insult. This review summarizes the current knowledge of spiral artery remodeling defects and acute atherosis in preeclampsia. Some controversies will be presented, including endovascular and interstitial trophoblast invasion depths, the concept of 2-stage trophoblast invasion, and whether the replacement of maternal spiral artery endothelium by fetal endovascular trophoblasts is permanent. We will discuss the role of acute atherosis in the pathophysiology of preeclampsia and short- and long-term health correlates. Finally, we suggest future opportunities for research on this intriguing uteroplacental interface between the mother and fetus.

The study included 78 female patients aged 19–35 years (mean age 27.1 ± 0.5 years) with severe preeclampsia at gestational age 38.50 ± 0.15 weeks. All patients in the antepartum period underwent correction of hypovolemic disorders using Gecoton («Yuria-Pharm»): 4–6 ml/kg for 1–1.5 hours. The study was performed in 4 stages: I — before infusion, II — 60 min after the end of Gecoton infusion, III — 6 hours after and IV — by the end of the first day. The initial state of hemodynamics in patients with preeclampsia was characterized by hypertensive-hypodynamic dissociation with the manifestation of systolic and diastolic dysfunction. Inclusion in the infusion program of Gecoton provided a stable hemodynamic profile, the elimination of systolic and diastolic left ventricular dysfunction, contributed to the rapid transition of the extracellular fluid into the intravascular space, keeping the achieved increase of intravascular volume due to the high capacity of hydroxyethyl starch 130/0.4 to bind the water that ensures long-lasting effect of the drug.

Заболевания печени, связанные с беременностью, встречаются приблизительно у 3 % беременных и являются важной причиной как материнской, так и фетальной смертности. В последние годы были получены значимые данные относительно патогенеза, диагностики и лечения этих болезней. В публикуемом обзоре акцент сделан на изменении показателей функциональных печеночных тестов у беременных как при физиологически протекающей беременности, так и при заболеваниях печени, являющихся следствием беременности, а также на механизмах этих изменений. Приводятся сведения о сроках нормализации функциональных печеночных тестов после родоразрешения или при естественном течении заболевания.

In preeclamptic pregnancies, a variety of intrauterine alterations lead to abnormal placentation, release of inflammatory and/or antiangiogenic factors, and subsequent fetal growth restriction with significant potential to cause a primary insult to the developing fetal lung. Thus, modulation of the maternal intrauterine environment may be a key therapeutic avenue to prevent preeclampsia-associated developmental lung injury. A biologic therapy of interest is mesenchymal stromal cell–derived extracellular vesicles (MEx), which we have previously shown to ameliorate preeclamptic physiology through intrauterine immunomodulation. To evaluate the therapeutic potential of MEx to improve developmental lung injury in experimental preeclampsia, using the heme oxygenase-1–null mouse (Hmox1(−)(/−)) model, preeclamptic pregnant dams were administered intravenous antenatal MEx treatment during each week of pregnancy followed by analysis of fetal and postnatal lung tissues, amniotic fluid protein profiles, and lung explant and amniotic fluid cocultures in comparison with control and untreated preeclamptic pregnancies. We first identified that a preeclamptic intrauterine environment had a significant adverse impact on fetal lung development, including alterations in fetal lung developmental gene profiles in addition to postnatal alveolar and bronchial changes. Amniotic fluid proteomic analysis and fetal lung explant and amniotic fluid cocultures further demonstrated that maternally administered MEx altered the expression of multiple inflammatory mediators in the preeclamptic intrauterine compartment, resulting in the normalization of fetal lung branching morphogenesis and developmental gene expression. Our evaluation of fetal and postnatal parameters overall suggests that antenatal MEx treatment may provide a highly valuable preventative therapeutic modality for amelioration of lung development in preeclamptic disease.

Background Hypertensive disorders are important causes of maternal and perinatal morbidity and death. Considering the role of both physical and psychological factors in pregnancies complicated by hypertension, the aim of this study is to examine psychological factors and coping strategies in pregnancies complicated by hypertension. Methods Cross-sectional study. A sample of 552 pregnant women, 343 with pregnancies complicated by hypertension, were assessed in terms of depression, anxiety, stress and coping. Results The hypertensive group had higher scores of depression, stress and anxiety than the control one. Coping strategies were different between hypertensive and control groups (except for confrontive and self-reliant coping styles). When splitting up the hypertensive group into gestational hypertension, chronic hypertension and preeclampsia syndrome, differences between this new classification reached the statistical level. Our data suggests that women with preeclampsia have more symptoms of depression and worse coping strategies – they are less optimistic and more fatalistic. However, after a cluster analysis, two different subgroups of hypertensive women were found: one with worst coping strategies and more vulnerability to negative affective states and another with better coping and more resilient to mental health problems. Limitations Data were cross-sectional. We excluded women with some comorbidities, such as a diagnosis of kidney disease, diabetes or fetal malformation. Conclusions It is important to consider distinct profiles of pregnant women, in order to be able to better understand the peculiarities of mental health and coping during the gestation, especially in pregnancies complicated by hypertension.

First trimester circulating ADAM12 is reduced in fetal growth restriction (FGR) and preeclampsia. We measured plasma ADAM12 at 36 weeks' gestation preceding diagnosis of term preeclampsia or delivery of a small for gestational age (SGA; birthweight10th centile) infant in two independent cohorts (Cohort 1 90 SGA, 41 preeclampsia, 862 controls; Cohort 2121 SGA 23 preeclampsia; 190 controls). ADAM12 was reduced with SGA in both cohorts (p = 0.0015 and 0.011 respectively), and further reduced with birthweight5th centile (p = 0.0013 and 0.0058 respectively). This validates ADAM12 as an SGA biomarker near term. Circulating ADAM12 preceding preeclampsia was not consistently altered.

Diabetes mellitus, whether preexisting or gestational, poses significant risk to both the mother and the developing fetus. A myriad of potential fetal complications in the setting of diabetic pregnancies include, among others, congenital anomalies, delayed fetal lung maturity, macrosomia, and increased perinatal morbidity and mortality. Congenital anomalies most commonly involve the nervous, cardiovascular, genitourinary, and musculoskeletal systems. Delayed fetal lung maturity, probably secondary to hyperglycemia suppressing surfactant secretion, is a major determinant of perinatal morbidity and mortality. Besides the potential complications encountered during cesarean delivery in macrosomic fetuses, vaginal delivery is also associated with increased risks of shoulder dystocia, clavicular and humeral fractures, and brachial plexus palsy. Maternal complications are related to the increased risk of hypertensive diseases of pregnancy and associated preeclampsia and hemolysis, elevated liver function, and low platelets (HELLP) syndrome, as well as complications encountered at the time of delivery secondary to fetal macrosomia and cesarean delivery. Additional conditions encountered in the setting of maternal diabetes include polyhydramnios, placental thickening, and two-vessel umbilical cord, each of which is associated with adverse fetal and maternal outcomes including fetal growth restriction, preterm labor, placental abruption, and premature rupture of membranes. Imaging plays a vital role in the evaluation of the mother and the fetus and can provide invaluable information that can be used by maternal fetal medicine to manage this patient population effectively. The authors review the pathophysiologic alterations induced by diabetes in pregnancy, discuss the imaging spectrum of diabetic embryopathy, and provide a detailed review of potential associated maternal complications. Online supplemental material is available for this article.©RSNA, 2021.

Objective To analyse a cohort of pregnant patients with systemic lupus erythematosus and compare the outcomes of both the disease and pregnancy with the results of previous studies conducted in the same geographical area. Patients and methods Retrospective cohort study of 37 women with systemic lupus erythematosus (64 pregnancies) followed in a multidisciplinary unit. Comparative study with similar Spanish studies identified after literature search. Results Our cohort was characterized by an older age and by the presence of non-Caucasian patients. Although we found no clinical differences, from the serological point of view our cohort presented a higher frequency of antiphospholipid antibodies. Patients included in this study were treated more frequently with antimalarials and low-dose aspirin. Systemic lupus erythematosus flare frequency was very similar between the different studies, and we did not identify clear predictors for them. Although the rate of live births was similar among studies, the obstetric outcome of our series was better with a very low rate of preeclampsia, preterm birth and low birth weight newborn. The only predictor of adverse obstetric event was age. Conclusions Although changes in the therapeutic attitude and planning of pregnancy in recent years have not had a direct impact on the rate of systemic lupus erythematosus flares during pregnancy, they have meant an improvement in the obstetric results. The introduction of new variables independent of the disease such as age at conception, socio-cultural origin, or the availability of multidisciplinary units should be considered in the results of future studies.

To examine the performance of a model combining maternal risk factors, uterine artery pulsatility index (UtA-PI) and estimated fetal weight (EFW) at 19-24 weeks' gestation, for predicting all antepartum stillbirths and those due to impaired placentation, in a training dataset used for development of the model and in a validation dataset.The data for this study were derived from prospective screening for adverse obstetric outcome in women with singleton pregnancy attending for routine pregnancy care at 19 + 0 to 24 + 6 weeks' gestation. The study population was divided into a training dataset used to develop prediction models for placental dysfunction-related antepartum stillbirth and a validation dataset to which the models were then applied. Multivariable logistic regression analysis was used to develop a model based on a combination of maternal risk factors, EFW Z-score and UtA-PI multiples of the normal median. We examined the predictive performance of the model by, first, the ability of the model to discriminate between the stillbirth and live-birth groups, using the area under the receiver-operating-characteristics curve (AUC) and the detection rate (DR) at a fixed false-positive rate (FPR) of 10%, and, second, calibration by measurements of calibration slope and intercept.The study population of 131 514 pregnancies included 131 037 live births and 477 (0.36%) stillbirths. There are four main findings of this study. First, 92.5% (441/477) of stillbirths were antepartum and 7.5% (36/477) were intrapartum, and 59.2% (261/441) of antepartum stillbirths were observed in association with placental dysfunction and 40.8% (180/441) were unexplained or due to other causes. Second, placental dysfunction accounted for 80.1% (161/201) of antepartum stillbirths at 32 weeks' gestation, 54.2% (52/96) at 32 + 0 to 36 + 6 weeks and 33.3% (48/144) at ≥ 37 weeks. Third, the risk of placental dysfunction-related antepartum stillbirth increased with increasing maternal weight and decreasing maternal height, was 3-fold higher in black than in white women, was 5.5-fold higher in parous women with previous stillbirth than in those with previous live birth, and was increased in smokers, in women with chronic hypertension and in parous women with a previous pregnancy complicated by pre-eclampsia and/or birth of a small-for-gestational-age baby. Fourth, in screening for placental dysfunction-related antepartum stillbirth by a combination of maternal risk factors, EFW and UtA-PI in the validation dataset, the DR at a 10% FPR was 62.3% (95% CI, 57.2-67.4%) and the AUC was 0.838 (95% CI, 0.799-0.878); these results were consistent with those in the dataset used for developing the algorithm and demonstrate high discrimination between affected and unaffected pregnancies. Similarly, the calibration slope was 1.029 and the intercept was -0.009, demonstrating good agreement between the predicted risk and observed incidence of placental dysfunction-related antepartum stillbirth. The performance of screening was better for placental dysfunction-related antepartum stillbirth at 37 weeks' gestation compared to at term (DR at a 10% FPR, 69.8% vs 29.2%).Screening at mid-gestation by a combination of maternal risk factors, EFW and UtA-PI can predict a high proportion of placental dysfunction-related stillbirths and, in particular, those that occur preterm. Such screening provides poor prediction of unexplained stillbirth or stillbirth due to other causes. © 2021 International Society of Ultrasound in Obstetrics and Gynecology.

Background and objective Haramonting (Rhodomyrtus tomentosa) is an alternative herb to improve health because it has many biological activities and antioxidant. HSP-70 levels as biomarkers of preeclampsia affected the anti-apoptosis of damaged cells in the placenta. This study aimed to evaluate the role of HSP-70 expressions by investigating whether effect haramonting leaves in PE rats. Materials and methods The study design was control (C): pregnant rats without treatment, PE: Preeclamptic rats, PE+E: PE rats were given 1 mL EVOO kg-1 b.wt./day orally (pregnancy 13-19), PE+H: PE rats were given nano herbal haramonting 100 mg kg-1 b.wt. (pregnancy 13-19 days). PE+E+H: PE rats were given EVOO 0.5 mL kg-1 b.wt. and nano herbal haramonting 50 mg kg-1 b.wt. (pregnancy 13-19 day). Surgery was performed by taking blood from the heart for the SGOT/SGPT parameters, creatinine and HSP70. Results A significant difference was observed in all groups with the value p 0.05). Conclusion These findings indicate that Nano herbal haramonting and EVOO possess antioxidative effects and a promising drug for the future in the treatment of preeclampsia.

To assess pregnancy outcomes following first trimester combined screening for preterm preeclampsia in Australia.We compared pregnancy outcomes of women with singleton pregnancies who underwent first trimester combined preeclampsia screening with the Fetal Medicine Foundation algorithm between 2014 and 2017 in Melbourne and Sydney, Australia, with those from women who received standard care. The primary outcomes were preterm preeclampsia and screening performance. Effect estimates were presented as risk ratios with 95% confidence intervals.A total of 29 618 women underwent combined screening and 301 566 women received standard care. Women who had combined screening were less likely to have preeclampsia, preterm birth, small neonates, and low Apgar scores than the general population. Women with high-risk results (≥1 in 100) were more likely to develop preterm preeclampsia (2.1% vs. 0.7%, risk ratio [RR] 3.04, 95% CI 2.46-3.77), while low-risk women (risk1 in 100) had lower rates of preterm preeclampsia (0.2% vs. 0.7%, RR 0.26, 95% CI 0.19-0.35) and other pregnancy complications. Screening detected 65.2% (95% CI 56.4-73.2%) of all preterm preeclampsia cases, with improved performance after adjustment for treatment effect.First trimester screening for preeclampsia in clinical practice identified a population at high risk of adverse pregnancy outcomes and low-risk women who may be suitable for less intensive antenatal care.

Objective To investigate the relationship between NADPH oxidase p22phox subunit (CYBA; C242T) and superoxide dismutase 2 (SOD2; A16V) polymorphisms and the risk of preeclampsia (PE) in Chinese women. Methods This case-control study included 325 patients with PE and 1,294 controls. The genotypes were determined by polymerase chain reaction-restriction fragments length polymorphism method. Clinical, metabolic, and oxidative stress parameters were analyzed. Results Participants with T allele of the CYBA C242T polymorphism had a decreased risk of PE (OR = 0.62, 95% CI: 0.42-0.92, P = 0.016) and those with the A allele of the SOD2 A16V polymorphism had increased risk of PE (OR = 1.44, 95% CI: 1.09-1.89, P = 0.010). The coexistence of the SOD2 AA + AV genotypes and the CYBA CC genotype further increased the risk of PE (OR = 2.32, 95% CI: 1.31-4.10, P = 0.003) when the CT + TT/VV combined genotype was the reference category. Conclusion The T allele of the CYBA C242T polymorphism is related to a decreased risk of PE, while the A allele of the SOD2 A16V polymorphism and its combination with the CYBA CC genotype are associated with an increased risk of PE in Chinese women.

Introduction. Pre-eclampsia is a significant cause of maternal and fetal mortality and morbidity. Pre-eclampsia is characterized by hypertension (blood pressure ≥ 140/90 mmHg), oedema and amount of protein in urine 300 mg in the 24-hour, which appears after 20 weeks of gestation. Pre-eclampsia can cause complications, one of which is HELLP syndrome. This case report discusses the use of anaesthesia in a patient who underwent a cesarean section with indications for pre-eclampsia and partial HELLP syndrome.Case Presentation. A woman, 41 years old, G4P3A0 34 weeks pregnant with pre-eclampsia + syndrome HELLP will undergo emergency cesarean section with ASA IIE physical statusLabouror pain management was carried out using regional spinal anaesthesia technique, using bupivacaine 0.5% hyperbaric agent 12.5 mg. The operation lasted for 1 hour 30 minutes, with 300 ml bleeding, hemodynamically stable.Conclusion. Difficult intubation in emergency cases can be avoided by choosing of neuraxial anaesthesia technique is recommended. It will lead to better uteroplacental perfusion, good analgesia/anaesthesia quality, reducing surgical stress, reducing drugs that enter the uteroplacental circulation, and maternal psychological to be able to see the baby at birth.

Women with a history of preeclampsia and/or Hemolysis Elevated Liver enzymes Low Platelets (HELLP) syndrome report impaired cognitive functioning, such as concentration problems and decreased memory function. The presence of subjective cognitive impairment, depressive symptoms and cognitive deficits may affect working abilities.

Preeclampsia is a severe pregnancy complication characterized by hypertension and may cause maternal morbidity and mortality. A better understanding of the essential genes involved in preeclampsia pathophysiology is urgently needed. This study investigated the function and molecular mechanisms of pumilio RNA binding family member 1 (PUM1) in extravillous trophoblast cells (EVTs). The interaction between protein and mRNA was verified by RNA pull-down assays, RNA immunoprecipitation assays, and luciferase reporter assays. The mRNA and protein levels of the genes involved were determined by RT-qPCR and western blot assays, respectively. Our results demonstrated that PUM1 could bind to the 3′-untranslated region of low-density lipoprotein receptor-related protein 6 (LRP6) mRNA, resulting in reduced expression of LRP6 mRNA and protein. Repression of PUM1 resulted in enhanced colony formation, cell proliferation, migration, and invasion of EVTs. The PUM1-depletion-mediated promotion effects on EVTs could be abrogated by LRP6 knockdown. PUM1 regulates the growth and mobility of EVTs by modulating LRP6 expression. Developing strategies to balance PUM1 and LRP6 levels may be beneficial for the management of preeclampsia patients.

Atypical preeclampsia before 20 weeks of gestation without an underlying disease is very rare; however, the soluble Fms-like tyrosine kinase 1/placental growth factor (sFlt-1/PlGF) ratios remain unknown. Four pregnant women with no underlying disease, except for a history of childhood IgA vasculitis, developed preeclampsia at 13, 14, 17, and 18 weeks of gestation with sFlt-1/PlGF ratios of 1589, 1183, 500, and 1460 pg/mL, respectively. Their pregnancies were terminated, and they delivered within 2 weeks. All previously abnormal clinical findings normalized within 3 months. The sFlt-1/PlGF ratios were elevated in the four patients with atypical preeclampsia without underlying disease before 20 weeks of gestation. A high sFlt-1/PlGF ratio may be indicative of preeclampsia when no underlying disease is present in pregnancies of less than 20 weeks of gestation.

Background LDA triggers biosynthesis of endogenous anti-inflammatory molecules, aspirin-triggered 15-epi-lipoxin A4 (15-epi-LXA4), which may counteract inflammatory process of preeclampsia (PE), and play role in LDA’s mechanism of action in PE prevention in high-risk patients. Objective Investigate the effects of daily LDA on levels of 15-epi-LXA4 in pregnancies at high-risk for developing PE. Materials and methods Secondary analysis of multi-centered randomized controlled trial investigating effects of daily LDA (60 mg) in high-risk pregnancies. Maternal samples were drawn at three points: before LDA initiation (13–26 weeks’ gestation), 24–28 weeks’ gestation (at least two weeks after LDA) and 34–36 weeks’ gestation. 15-epi-LXA4 levels were measured by ELISA. Results Analysis included 82 patients: 63 receiving daily LDA and 29 receiving daily placebo starting between 13 and 25 weeks gestation. Prior to randomization, baseline 15-epi-LXA4 levels were similar between both groups (75.9 pg/mL [IQR; 63.8–114.0] vs 136.2 pg/mL [52.4–476.2]; p = 0.10). Patients receiving daily LDA were noted to have significantly increased levels of 15-epi-LXA4 after LDA administration (136.2 pg/mL [IQR; 52.4–476.2] vs 1758.2 pg/mL [905.4–6638.5]; p Conclusion Daily LDA administration increases 15-epi-LXA4 levels in high-risk pregnancies for PE. In LDA group, pregnancies complicated by PE have lower levels of 15-epi-LXA4 compared to pregnancies without PE.

Background Preeclampsia is associated with increased risk of future heart failure (HF), but the relationship between preeclampsia and HF subtypes are not well-established. Objectives The objective of this analysis was to identify the risk of HF with preserved ejection fraction (HFpEF) following a delivery complicated by preeclampsia/eclampsia. Methods A retrospective cohort study using the New York and Florida state Healthcare Cost and Utilization Project State Inpatient Databases identified delivery hospitalizations between 2006 and 2014 for women with and without preeclampsia/eclampsia. The authors identified women admitted for HF after discharge from index delivery hospitalization until September 30, 2015, using International Classification of Diseases-9th Revision-Clinical Modification diagnosis codes. Patients were followed from discharge to the first instance of primary outcome (HFpEF hospitalization), death, or end of study period. Secondary outcomes included hospitalization for any HF and HF with reduced ejection fraction, separately. The association between preeclampsia/eclampsia and HFpEF was analyzed using Cox proportional hazards models. Results There were 2,532,515 women included in the study: 2,404,486 without and 128,029 with preeclampsia/eclampsia. HFpEF hospitalization was significantly more likely among women with preeclampsia/eclampsia, after adjusting for baseline hypertension and other covariates (aHR: 2.09; 95% CI: 1.80-2.44). Median time to onset of HFpEF was 32.2 months (interquartile range: 0.3-65.0 months), and median age at HFpEF onset was 34.0 years (interquartile range: 29.0-39.0 years). Both traditional (hypertension, diabetes mellitus) and sociodemographic (Black race, rurality, low income) risk factors were also associated with HFpEF and secondary outcomes. Conclusions Preeclampsia/eclampsia is an independent risk factor for future hospitalizations for HFpEF.