Preeclampsia Syndrome Research Articles

A CASE-CONTROL STUDY ABOUT HEMATOLOGICAL PROFILE AND MORBIDITY OF NEWBORNS AT BIRTH, BORN TO MOTHERS WITH HYPERTENSION IN PREGNANCY.

Background: Hypertensive disorders of pregnancy complicate about 8% of all gestations. Hypertensive disorders are responsible for significant maternal and perinatal morbidity and mortality.
 AIMS: To determine the hematological parameters and morbidity in neonates born to mothers with gestational hypertension, pre-eclampsia or eclampsia syndrome and in neonates born to normotensive mothers without any maternal complications or medical illness with special reference to platelet count and neutrophil count.
 Methods and Material: The study was a prospective study conducted on neonates born to pregnant women complicated with gestational hypertension, pre-eclampsia or eclampsia syndrome and neonates born to normotensive mothers recruited at Neonatal Intensive Care Unit and Post natal wards who were delivered at Ananta Hospital and AIMS & RC, Rajsamand (Raj.) from October 2018 to September 2019 and the hematological parameters of these babies were studied.
 Results: In our study we observed that the mean value of platelet count were significantly lower in study group compared to control group which was highly Statistical significant (p<0.001). The mean value of PT, aPTT, Bleeding Time and Clotting time were significantly higher in study group, as compared to control group. The statistical analytic differences were highly significant in all parameters i.e. PT, aPTT, Bleeding Time and Clotting time (P<0.001).
 Conclusion: To conclude early hematological screening of babies are recommended to facilitate early detection and management of serious neonatal complications describes above, to decrease morbidity and improved growth, development and survival.
 Keywords: Pre-eclampsia, Eclampsia, Gestational Hypertension, Newborns.

Angiogenic profiling in HELLP syndrome cases with or without hypertension and proteinuria

ObjectivesAngiogenic profiling with the use of sFlt-1/PlGF ratio (soluble fms-like tyrosine kinase-1/placental growth factor) can be helpful to characterize women with signs of impending preeclampsia (PE). However, little is known about the angiogenic profile of pregnancies complicated by HELLP syndrome. The aim of this study was to examine the relationship of angiogenic profiles in cases of HELLP syndrome with and without classical signs of preeclampsia. Study designThe angiogenic profile of pregnant women with singleton gestation and isolated PE (group 1), PE associated with HELLP syndrome (group 2), and isolated HELLP syndrome (group 3) from 01/2011 to 03/2018, were compared. To overcome gestational age dependent angiogenic behavior, cases (group 3) were matched 1:2 with cases from group 1 and 2. Matching criteria was gestational age (±1 week). PE and HELLP syndrome were defined according to the international Society for the Study of Hypertension in Pregnancy (ISSHP) statement 2014. ResultsDuring the observational period, 244 women could be included in the study. Of those, 237 (97.1%) were diagnosed with PE. In 42 cases (17.2%) PE was associated with HELLP syndrome while 7 (2.9%) patients were diagnosed with isolated HELLP syndrome. Angiogenic profiles in terms of sFlt-1/PlGF ratios differed significantly between the three groups, showing highest levels in group 2 (PE/HELLP) while cases with isolated HELLP demonstrated the lowest ratios and sFlt-1 values (p = 0.01). ConclusionWe conclude that isolated HELLP syndrome is rare and seems to be a particular entity expressing a different angiogenic behaviour compared to classical PE or PE associated with HELLP syndrome.

Fulminant severe HELLP syndrome in early onset preeclampsia: A case report

Fulminant severe HELLP syndrome in early onset preeclampsia: A case report

P5359Pulmonary artery pressure is elevated three month after delivery in patients with preeclampsia and antiphospholipid syndrome

Abstract Introduction Preeclampsia (PE) is a multisystem disease affecting 2–8% of all pregnancies. Recently we found that the prevalence of antiphospholipid syndrome (APS) in PE patients at 13.9%. APS can be the cause of thromboembolic pulmonary hypertension. However, data on heart function and pulmonary pressure in PE and in PE with APS are sparse. Purpose We sought to investigate cardiac hemodynamics in this population. Method Between July 2016 and December 2018, we performed echocardiography in patients who had suffered from PE alone (n=102, age=32.6±4.8 y) or PE with APS (n=21, age=32.1±4.2 y) 3 months after delivery. APS was diagnosed according to the Sapporo criteria. Results The overall prevalence of APS was 17%. Right ventricular to right atrial pressure (RV/RA) gradient was significantly higher in PE + APS patients than in patients who had PE only (21.1±3.8 vs. 17.9±4.6mmHg, p=0.04, PE+APS vs. PE). The indexed volume of the left atrium (LA: 20.3±4.4 vs 23.5±5.5ml/m2, p=0.01, PE+APS vs. PE) and the birthweight of the newborn (1379.8±759.1 vs 1848.1±879.6.1g, p=0.02, PE+APS vs. PE) were lower in APS patients. Conclusion In patients with preeclampsia and APS, three month after delivery, pulmonary artery pressure was higher and the left atrium size smaller than in patients who had PE only. Conceivably this may reflects multiple subclinical clots in the pulmonary vessels in APS patients and may put these patients at an elevated risk of pulmonary hypertension later in life.

Hypertension Editors' Picks Preeclampsia.

Hypertension Editors' Picks Preeclampsia.

Proteomic identification of membrane-associated placental protein 4 (MP4) as perlecan and characterization of its placental expression in normal and pathologic pregnancies.

BackgroundMore than 50 human placental proteins were isolated and physico-chemically characterized in the 70–80s by Hans Bohn and co-workers. Many of these proteins turned to have important role in placental functions and diagnostic significance in pregnancy complications. Among these proteins was membrane-associated placental protein 4 (MP4), for which identity or function has not been identified yet. Our aim was to analyze the sequence and placental expression of this protein in normal and complicated pregnancies including miscarriage, preeclampsia and HELLP syndrome.MethodsLyophilized MP4 protein and frozen healthy placental tissue were analyzed using HPLC-MS/MS. Placental tissue samples were obtained from women with elective termination of pregnancy (first trimester controls, n = 31), early pregnancy loss (EPL) (n = 13), early preeclampsia without HELLP syndrome (n = 7) and with HELLP syndrome (n = 8), late preeclampsia (n = 8), third trimester early controls (n = 5) and third trimester late controls (n = 9). Tissue microarrays were constructed from paraffin-embedded placentas (n = 81). Slides were immunostained with monoclonal perlecan antibody and evaluated using light microscopy and virtual microscopy. Perlecan was also analyzed for its expression in placentas from normal pregnancies using microarray data.ResultsMass spectrometry-based proteomics of MP4 resulted in the identification of basement membrane-specific heparan sulfate proteoglycan core protein also known as perlecan. Immunohistochemistry showed cytoplasmic perlecan localization in syncytiotrophoblast and cytotrophoblasts of the villi. Perlecan immunoscore decreased with gestational age in the placenta. Perlecan immunoscores were higher in EPL compared to controls. Perlecan immunoscores were higher in early preeclampsia without and with HELLP syndrome and lower in late preeclampsia than in respective controls. Among patients with preeclampsia, placental perlecan expression positively correlated with maternal vascular malperfusion and negatively correlated with placental weight.ConclusionOur findings suggest that an increased placental perlecan expression may be associated with hypoxic ischaemic injury of the placenta in miscarriages and in early preeclampsia with or without HELLP syndrome.

Distribution of Polymorphisms of the Renin-Angiotensin System Genes (ACE, AGT, and AGTR1), ITGB3, and FTO in Pregnant Patients with Hypertensive Disorders.

The study included pregnant women aged 23-41 years with preeclampsia and gestation-associated arterial hypertension at weeks 27-40 and patients with essential arterial hypertension developing under conditions of the metabolic syndrome and without it. Frequency analysis of polymorphisms of the renin-angiotensin system genes (ACE, AGT, and AGTR1), ITGB3, FTO and their associations confirmed the syndrome nature of hypertensive disorders in pregnancy. The presence allele T of AGT gene and/or allele C of AGTR1 gene in the genotype of patients with preeclampsia was associated with higher BP and pressure load over 24 h. Allele D of ACE gene was also essential for BP parameters (pressure load) in patients with preeclampsia and gestation-associated arterial hypertension. Due to high genetic heterogeneity of the preeclampsia syndrome and genetic differences in the incidence of the studied gene polymorphisms in preeclampsia and gestation-associated arterial hypertension, no direct associations between these gestation disorders and polymorphic markers of the renin-angiotensin system genes can be established. However, polymorphisms of the renin-angiotensin system genes are essential for the 24-h dynamics of BP and pressure load under conditions of hypertensive disorders in pregnancy.

Profound Decrease in Glomerular Arginine Transport by CAT (Cationic Amino Acid Transporter)-1 Contributes to the FLT-1 (FMS-Like Tyrosine Kinase 1) Induced Preeclampsia in the Pregnant Mice.

Endothelial dysfunction because of nitric oxide inactivation has been suggested to play a role in the pathogenesis of preeclampsia. During pregnancy, L-arginine transport by CAT-1 (cationic amino acid transporter 1), the only transporter for eNOS (endothelial nitric oxide synthase) is inhibited. We hypothesize that maternal arginine deficiency contributes to the development of preeclampsia. Adenovirus-mediated overexpression of sFlt-1 (soluble fms-like tyrosine kinase 1) in virgin and pregnant mice resulted in glomerular endotheliosis, hypertension, and albuminuria. L-arginine prevented the increase in blood pressure and albuminuria in Flt-1 pregnant but not in Flt-1 virgin mice. Flt-1 augmented arginine transport in pregnant but not in virgin dames. Ex vivo inhibition of CAT-2 leaving exclusively CAT-1 activity, decreased arginine transport velocities in Flt-1 animals more prominently in pregnant dames. Phosphorylated CAT-1/CAT-1 increased in pregnant, sFlt-1-pregnant, and sFlt-1 virgin mice. CAT-2 increased in Flt-1-pregnant and Flt-1-virgin dames. L-arginine augmented arginine transport in pregnant and Flt-pregnant mice and prevented the increase in pCAT-1 and CAT-2 expression. Glomerular cGMP (cyclic guanosine monophosphate) generation as a measure of eNOS activity was decreased in all Flt-1 treated animals. L-arginine abolished the decrease in cGMP levels only in Flt-1-pregnant mice. In conclusion, glomerular endothelial NO generation is compromised in Flt-1-pregnant mice because of CAT-1 inhibition induced by a combined effect of pregnancy and preeclampsia which involves: phosphorylation of CAT-1 and induction of CAT-2. These processes contribute to the clinical syndrome of preeclampsia in mice and are prevented by L-arginine.

Intrapartum Sildenafil Therapy Reprograms Susceptibility to Hypertension in Offspring of Dahl S Rats

Up to 15 million people in the United States are offspring of preeclamptic pregnancies. These offspring have increased blood pressure (BP) during childhood as well as nearly double the risk of stroke later in life. The Developmental Origins of Health and Disease (DOHAD) hypothesis proposes that the adverse intrauterine environment created by preeclampsia programs fetal tissues and organs to develop high BP from early childhood. Sildenafil citrate (SLD, a PDE‐5 inhibitor) improves the maternal syndrome of preeclampsia in the Dahl S rat, and we have shown that offspring of dams treated with SLD during gestation exhibit significantly decreased systolic BP at 11 weeks of age compared to age‐matched offspring of vehicle‐fed dams. The objective of this study was to test the hypothesis that intrapartum SLD would attenuate the BP programming effects on offspring of preeclamptic pregnancies in this model. Female Dahl S rats on a 0.3% salt diet, a previously characterized spontaneous model of superimposed preeclampsia, were mated and treated orally with SLD (50 mg/kg/day), labetalol (LAB, currently used to manage hypertension in preeclamptic patients, 10 mg/kg/day), or vehicle (VEH) from gestational day 10 to delivery. Dams were placed on normal rat chow at delivery throughout weaning at four weeks of age. To determine if SLD could attenuate the susceptibility to hypertensive stimuli, groups of offspring were exposed to one of two secondary hits: high‐salt diet (2% NaCl, Harlan Teklad, four weeks), or subpressor angiotensin II infusion (200 ng/kg/min, Alzet 2002 pump, two weeks). In both experiments, rats were implanted with telemetry devices (DSI, HD‐S10) via the femoral artery at ten weeks of age and allowed to recover for ten days before administration of high‐salt diet ad libitum or implantation of osmotic minipumps containing angiotensin II. On a high‐salt diet, mean arterial pressure (MAP) increased in all animals as expected; however, male offspring of SLD‐treated dams exhibited a significant attenuation of this increase after four weeks high salt (n=3–7/group). Although female offspring show no differences between groups, this could be due to a lower number of animals present in the female VEH group. On exposure to angiotensin II, all animals exhibited an increase in MAP (n=4/group), with a smaller rise in females as expected. No difference was seen between female groups by study completion. However, male offspring of SLD‐treated dams exhibited a significantly lower plateau than did male offspring of VEH‐fed or LAB‐treated dams. These data indicate that sildenafil citrate not only improves the maternal phenotype of superimposed preeclampsia in the Dahl S rat, but also acts to reprogram hypertension and response to secondary hits in the offspring of preeclamptic pregnancies.Support or Funding InformationThis work was supported by the National Institutes of Health (F30DK118864 [HRT], R01HL137673 [MRG], and R01HL134711 [JMS]).This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Preeclampsia: Pathophysiology, Challenges, and Perspectives

Hypertensive disorders of pregnancy-chronic hypertension, gestational hypertension, and preeclampsia-are uniquely challenging as the pathology and its therapeutic management simultaneously affect mother and fetus, sometimes putting their well-being at odds with each other. Preeclampsia, in particular, is one of the most feared complications of pregnancy. Often presenting as new-onset hypertension and proteinuria during the third trimester, preeclampsia can progress rapidly to serious complications, including death of both mother and fetus. While the cause of preeclampsia is still debated, clinical and pathological studies suggest that the placenta is central to the pathogenesis of this syndrome. In this review, we will discuss the current evidence for the role of abnormal placentation and the role of placental factors such as the antiangiogenic factor, sFLT1 (soluble fms-like tyrosine kinase 1) in the pathogenesis of the maternal syndrome of preeclampsia. We will discuss angiogenic biomarker assays for disease-risk stratification and for the development of therapeutic strategies targeting the angiogenic pathway. Finally, we will review the substantial long-term cardiovascular and metabolic risks to mothers and children associated with gestational hypertensive disorders, in particular, preterm preeclampsia, and the need for an increased focus on interventional studies during the asymptomatic phase to delay the onset of cardiovascular disease in women.

Superimposed Preeclampsia Exacerbates Postpartum Renal Injury Despite Lack of Long-Term Blood Pressure Difference in the Dahl Salt-Sensitive Rat.

Preeclampsia results in increased susceptibility to hypertension and chronic kidney disease postpartum; however, the mechanisms responsible for disease progression in these women remain unknown. The purpose of this study was to test the hypothesis that 2 mechanisms contribute to the link between the maternal syndrome of preeclampsia and the increased postpartum risk of cardiovascular and renal disease: (1) increased T cells in the kidney and (2) a decreased NO:ET-1 (endothelin-1) ratio. Dahl S rats (a previously characterized model of preeclampsia superimposed on chronic hypertension) who experienced 2 pregnancies and virgin littermate controls were studied at 6 months of age. Mean arterial pressure was measured via telemetry, and renal injury was assessed through both histological analysis and measurement of urinary markers including nephrin, podocalyxin, and KIM-1 (kidney injury marker 1). Contributing mechanisms were assessed through flow cytometric analysis of renal T cells, quantification of plasma TNF-α (tumor necrosis factor-α) and IL-10 (interleukin-10), and quantification of urinary concentrations of NO metabolites and ET-1. Although prior pregnancy did not exacerbate the hypertension at 6 months, this group showed greater renal injury compared with virgin littermates. Flow cytometric analyses revealed an increase in renal T cells after pregnancy, and cytokine analysis revealed a systemic proinflammatory shift. Finally, the NO:ET-1 ratio was reduced. These results demonstrate that the link between the maternal syndrome of superimposed preeclampsia and postpartum risk of chronic kidney disease could involve both immune system activation and dysregulation of the NO:ET-1 balance.

Progress in non-invasive prenatal testing failure due to less cell-free fetal DNA

Non-invasive prenatal testing (NIPT) has been extensively applied in fetal chromosomal aneuploidy screening with high sensitivity and specificity. The concentration of cell-free fetal DNA (cffDNA) is an important factor related to the accuracy of NIPT. When cffDNA concentration is lower than 4%, accurate results are often unavailable, resulting in failure of NIPT. The factors influencing cffDNA concentration in maternal blood were reviewed and it was found that the concentration of cffDNA was positively correlated with the gestational week at the time of sampling, but negatively correlated with the maternal weight/body mass index. Moreover, gestational complications (such as preeclampsia and polycystic ovary syndrome), maternal age, results of serological screening for Down's syndrome in second trimester, fetal chromosomal karyotype and nuchal translucency thickness were also potential influencing factors. Analysis of the influencing factors of cffDNA concentration helps to improve the NIPT specifications, which is significant for prenatal genetic counselling. Key words: Aneuploidy; Prenatal diagnosis; Cell-free system; DNA; Fetus

A successful conservative management of ruptured subcapsular hepatic hematoma with pre-eclampsia

Ruptured subcapsular hematoma of the liver is a rare complication of pregnancy, commonly associated with pre-eclampsia or HELLP syndrome (Hemolysis, Elevated Liver Enzymes, and Low Platelets Syndrome). We report a case of a 32-year-old woman, with no particular antecedents, admitted to our emergency department at 32 weeks of amenorrhea, for pre-eclampsia with epigastralgia. The liver ultrasound performed at admission was normal. In the presence of acute fetal distress, a caesarean section with midline vertical incision was performed urgently. The surgical exploration revealed massive haemoperitoneum with ruptured subcapsular hepatic hematoma. The management consisted of hepatic packing with massive transfusion. Removal of packing was performed on the fourth day after stabilization and regression of hepatic encephalopathy. Fortunately, the evolution was favorable and the patient was discharged after 4 weeks of hospital stay in stable condition. The ruptured subcapsular hematoma of the liver remains a very challenging situation and potentially life-threatening condition.

Biology of preeclampsia: Combined actions of angiogenic factors, their receptors and placental proteins

Although massive efforts have been undertaken to elucidate the etiology of the pregnancy syndrome preeclampsia, its developmental origin remains a mystery. Most efforts of the last decade have focused on biomarkers to predict and/or diagnose preeclampsia, including the anti-angiogenic factor sFlt-1 (soluble fms-like tyrosin kinase-1), the angiogenic factor PGF (placental growth factor) and PP13 (placental protein 13). The origins of these marker proteins are still under debate, and so far their actions have only been describe separate from each other. This study will focus on the origins and actions of all three markers during pregnancy and outside pregnancy and will describe a scenario where all three markers act synergistically to rescue the mother from the deleterious effects of the debris that is released from the placenta during preeclampsia. This more holistic approach may open new avenues to think about maternal-fetal interactions and putative therapies.

447. Paternal consequences of preeclampsia

Women experiencing pre-eclampsia or HELLP syndrome are known to be at increased risk of developing mental health conditions such as posttraumatic stress disorder (PTSD) and postpartum depression. While the role of fathers in the etiology and pathophysiology of pre-eclampsia becomes increasingly clear, the effects of pre-eclampsia on the mental wellbeing of fathers is scarcely researched. A recent meta-analysis on the mental health of fathers demonstrate that 8% of fathers suffers from depression, which is twice the rate of depression in the adult male population. Postpartum posttraumatic stress disorder (PTSD) may also occur in partners. Particularly stressful for fathers in case of severe preeclampsia with preterm birth appears to be the separation from and between mother and child, and starting fatherhood facing existential issues. Research into the paternal consequences of preeclampsia is scarce and warrants further evaluation. In the meantime, qualitative studies point out the important of supporting partners of women with pre-eclampsia during pregnancy and in the postpartum period: by actively involving fathers during the hospitalization and in postnatal care; by normalizing the mental health impact of potentially life-threatening conditions such as pre-eclampsia and HELLP syndrome, also on partners; by monitoring the wellbeing of fathers postpartum, especially in case of preterm birth and in partners with a history of mental disorders; by informing partners of possible mental health consequences; and by validating fathers if they report mental health issues or psychiatric symptoms.

205. Elecsys® and Kryptor immunoassays for the measurement of sFlt-1 and PlGF to aid preeclampsia diagnosis: Are they comparable?

Introduction In pregnant women with suspected preeclampsia, the soluble Fms-like tyrosine-kinase 1 (sFlt-1)/placental growth factor (PlGF) ratio is used as a biomarker to aid diagnosis. sFlt-1 and PlGF levels are measured using Elecsys® (Roche) or Kryptor (BRAHMS) immunoassays; Elecsys® sFlt-1/PlGF ratio cut-offs 85 and 110 may indicate preeclampsia. Objectives To perform method comparisons between the Elecsys® versus Kryptor immunoassays for sFlt-1 and PlGF measurement, and assess diagnostic performance for preeclampsia/HELLP syndrome in a large cohort. Methods Analyses included 396 serum samples from a case-control study in 113 pregnant women with preeclampsia or HELLP syndrome and 270 controls. sFlt-1 and PlGF were determined using Elecsys® and Kryptor sFlt-1 and PlGF immunoassays, and gestation-specific cut-offs 85 for early-onset preeclampsia (eoPE; 20 + 0–33 + 6 weeks) and 110 for late-onset preeclampsia (loPE; ⩾34 + 0 weeks) were assessed. Method comparisons were based on Passing-Bablok regression, and Bland–Altman plots (CLSI EP09-A3). ROC analysis was performed for all sFlt-1/PlGF cut-offs. Results Mean (±2 SD) differences between Elecsys® and Kryptor values were: sFlt-1, 173.13 pg/mL (6237.66, −5891.40); PlGF, 102.71 pg/mL (186.06, −391.48); and sFlt-1/PlGF ratio, 151.74 (1085.11, −781.63). Elecsys® and Kryptor immunoassays showed high correlation: Pearson’s correlation coefficient (r), 0.913; slope, 1.06; intercept, −358.19 pg/mL (sFlt-1), and Pearson’s r, 0.945; slope, 0.79; intercept, −17.89 pg/mL (PlGF), resulting in ∼20% lower values for PlGF. Sensitivities and specificities using the sFlt-1/PlGF 85 cut-off (eoPE) were 88.0%/100.0% (Elecsys®) and 90.4%/96.2% (Kryptor), and using a sFlt-1/PlGF 110 cut-off (loPE) were 51.3%/96.5% (Elecsys®) and 78.9%/90.1% (Kryptor). Using Elecsys® and Kryptor sFlt-1/PlGF ratios, 0% and 3.8% of women were falsely ruled-in for eoPE, and 3.5% and 9.9% for loPE. Discussion Despite high correlation between Elecsys® and Kryptor immunoassays, substantial differences were observed between Elecsys® and Kryptor sFlt-1/PlGF and PlGF. sFlt-1/PlGF cut-offs 85 and 110 showed lower specificity on Kryptor versus Elecsys®, resulting in more false-positive preeclampsia diagnoses.

162. Progression from isolated proteinuria to severe preeclampsia – Does severity of proteinuria matter?

Introduction The majority of women with preeclampsia have increased proteinuria. However, the 2013 Task Force on Hypertension in Pregnancy suggested that the degree of proteinuria is no longer a severe feature of preeclampsia due to a minimal correlation between proteinuria levels and pregnancy outcome. This change has brought about even more uncertainty regarding the clinical significance of isolated proteinuria in the development of pre-eclampsia. Objective To investigate the association between the severity of isolated proteinuria and later development of severe preeclampsia and other placental mediated complications. Methods Pregnant women with new onset proteinuria levels exceeding 300 mg in 24-h urine collection, who were referred to our institution between 2014 and 2017 were approached. Exclusion criteria included immediate diagnosis of preeclampsia, chronic renal disease or chronic hypertension. 104 women met inclusion criteria and were followed throughout pregnancy and until after delivery. Results Overall, 29 of 104 (28%) women developed severe preeclampsia. The rate of severe preeclampsia was significantly higher in women with proteinuria ⩾3 g⧹24 h (57.1%) compared to women with proteinuria ± 2 for women with ⩾3 g ⧹ 24 h, versus 36.4 ± 1 for women with 3 g ⧹ 24 h, (p 0.01). The median time interval (days) between the diagnosis of proteinuria and presentation of severe preeclampsia was not significantly different between women with ⩾ 3 g ⧹ 24 h (15) and 3 g ⧹ 24 h (17). Discussion Isolated proteinuria > 3 g ⧹ 24h is a significant risk factor for severe preeclampsia and HELLP syndrome with a rapid and earlier progression to clinical disease.

250. ‘It was my body. It was happening to me. I should have known.’ Women’s knowledge and information needs in pregnancies complicated by pre eclampsia

Introduction Raised blood pressure (BP) is a common problem in pregnancy which can lead to significant morbidity and mortality for mother and child, particularly when accompanied by proteinuria or other metabolic changes (pre-eclampsia). Consequently, blood pressure and urinary protein are monitored by health professionals throughout pregnancy. There is little research on the psychological consequences of experiencing pre-eclampsia, although women’s perceptions and experiences suggest they are physically and emotionally distressed (Furuta 2014). Women’s knowledge about hypertension in pregnancy and pre-eclampsia, and their information needs during and after pregnancy, are largely unknown. Methods In depth semi-structured interviews were carried out with women in the UK who had experienced pre-eclampsia or HELLP syndrome about their experiences of pregnancy and its complications. Interviews were audio recorded and transcribed for analysis. Thematic analysis was undertaken based using constant comparison. Results 17 women were interviewed. Women often didn’t know how serious blood pressure problems in pregnancy could be, and described knowledge journeys from largely ignorance to becoming experts. Women often struggled to understand and make sense of information they were given, especially while they were ill. They described pinch points when information was particularly important: on receiving diagnosis, admission to hospital, during labour and at discharge. Although women and their relatives could go online, information and communication from health professionals was key. In the absence of verbal explanations, sometimes women interpreted body language and glanced looks. Discussion Our analysis highlights the lack of knowledge that women have about hypertension in pregnancy and its risks. If they develop complications their learning curve is steep and often frightening. The need for clear communication from health professionals and more reliable information about the risks and reality of pre-eclampsia are needed.

15. Preeclampsia and hellp syndrome – Obstetric prognosis

We are selected 185 pregnant women with HELLP syndrome and severe preeclampsia. The physical examination of patients the blood, function of liver, ultrasound. Patient with HELLP syndrome is a microangiopathic hemolytic anemia. Red blood cells become fragmented as they pass through small blood vessels with endothelial damage and fibrin deposits. The peripheral smear may reveal spherocytes, schistocytes, triangular cells and burr cells. increase in Bilirubin and lactic dehydrogenase levels. The elevated liver enzyme levels in the syndrome are thought to be secondary to obstruction of hepatic blood flow by fibrin deposits in the sinusoids. This obstruction leads to periportal necrosis and, in severe cases, intrahepatic hemorrhage, subcapsular hematoma formation or hepatic rupture. The thrombocytopenia has been attributed to increased consumption and/or destruction of platelets. Our results of clinical presentation: 90% of patients present with generalized malaise, 65% with epigastric pain, 30% with nausea and vomiting, 31% with headache. Because of the variable nature of the clinical presentation, the diagnosis of HELLP syndrome is generally delayed for an average of eight days. Only two of 14 patients entered the hospital with the correct diagnosis. Because early diagnosis of this syndrome is critical, any pregnant woman who presents with malaise or a viral-type illness in the third trimester should be evaluated with a complete blood cell count and liver function tests. However, there is obviously still a lack of consensus on the laboratory parameters and their cutoff values used to diagnose. We are examination laboratory diagnostic criteria for HELLP syndrome. Clinical utility of strict diagnostic criteria for the HELLP the use of strict diagnostic criteria in the definition of the HELLP syndrome allows for greater prediction of complication rates. and define the cases that are Eligible to conservative management.

ELABELA plasma concentrations are increased in women with late-onset preeclampsia

Objective: ELABELA is a newly discovered peptide hormone that appears to be implicated in the mechanisms leading to preeclampsia, independently of angiogenic factors. The aim of the current study was to investigate whether women with early- or late-onset preeclampsia have altered ELABELA plasma concentrations compared to gestational-age-matched normal pregnant women.Methods: This retrospective cross-sectional study focused on the maternal plasma samples collected from 232 women with a singleton pregnancy who were allocated into the following groups: (1) early-onset preeclampsia (<34 weeks of gestation, N = 56); (2) late-onset preeclampsia (≥34 weeks of gestation, N = 57); and (3) gestational-age-matched controls with a normal pregnancy [(<34 weeks of gestation, N = 59); (≥34 weeks of gestation, N = 60)]. ELABELA plasma concentrations were determined using a validated enzyme immunoassay.Results: (1) ELABELA plasma concentrations are higher in patients with late-onset preeclampsia compared with those from gestational-age-matched controls with a normal pregnancy [median: 7.99 ng/mL (IQR, 5.3–13.95 ng/mL) versus median: 4.17 ng/mL (IQR, 3–11.19 ng/mL), p =.001]; (2) ELABELA plasma concentrations in patients with early-onset preeclampsia do not differ from those of normal pregnant women [median: 6.09 ng/mL (IQR, 2.8–10.66 ng/mL) versus median: 4.02 ng/mL (IQR, 3.26–7.49), p = .32]; and (3) ELABELA plasma concentrations are higher in patients with late-onset preeclampsia compared to those with early-onset preeclampsia [median: 7.99 ng/mL (IQR, 5.3–13.95 ng/mL) versus median: 6.09 ng/mL (IQR, 2.8–10.66 ng/mL), p = .01].Conclusion: ELABELA plasma concentrations are higher in patients with late-onset preeclampsia than in those with a normal pregnancy. However, women with early-onset preeclampsia have similar ELABELA plasma concentrations to those with a normal pregnancy. These findings provide insight into the ELABELA axis during the human syndrome of preeclampsia. In addition, these data support the concept that different pathophysiologic mechanisms are implicated in early- and late-onset preeclampsia.