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      Oxidative stress and endothelial function in normal pregnancy versus pre-eclampsia, a combined longitudinal and case control study

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          Abstract

          Background

          Pre-eclampsia (PE) is related to an impaired endothelial function. Endothelial dysfunction accounts for altered vascular reactivity, activation of the coagulation cascade and loss of vascular integrity. Impaired endothelial function originates from production of inflammatory and cytotoxic factors by the ischemic placenta and results in systemic oxidative stress (OS) and an altered bioavailability of nitric oxide (•NO). The free radical •NO, is an endogenous endothelium-derived relaxing factor influencing endothelial function. In placental circulation, endothelial release of •NO dilates the fetal placental vascular bed, ensuring feto-maternal exchange. The Endopreg study was designed to evaluate in vivo endothelial function and to quantify in vitro OS in normal and pre-eclamptic pregnancies.

          Methods/design

          The study is divided into two arms, a prospective longitudinal study and a matched case control study. In the longitudinal study, pregnant patients ≥18 years old with a singleton pregnancy will be followed throughout pregnancy and until 6 months post-partum. In the case control study, cases with PE will be compared to matched normotensive pregnant women. Maternal blood concentration of superoxide (O 2•) and placental concentration of •NO will be determined using EPR (electron paramagnetic resonance). Endothelial function and arterial stiffness will be evaluated using respectively Peripheral Arterial Tonometry (PAT), Flow-Mediated Dilatation (FMD) and applanation tonometry. Placental expression of eNOS (endothelial NOS) will be determined using immune-histochemical staining. Target recruitment will be 110 patients for the longitudinal study and 90 patients in the case-control study.

          Discussion

          The results of Endopreg will provide longitudinal information on in vivo endothelial function and in vitro OS during normal pregnancy and PE. Adoption of these vascular tests in clinical practice potentially predicts patients at risk to develop cardiovascular events later in life after PE pregnancies. •NO, O 2 and eNOS measurements provide further inside in the pathophysiology of PE.

          Trial registration

          This trial has been registered on clinicaltrials.gov. ClinicalTrials.gov Identifier: NCT02603913. Registered October 2015.

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          Most cited references40

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          Cardiovascular sequelae of preeclampsia/eclampsia: a systematic review and meta-analyses.

          Preeclampsia affects 3% to 5% of gestations and eclampsia 0.05% to 0.93%, but their subsequent cardiovascular sequelae are unclear. The aim of this study was to determine if women with a history of preeclampsia/eclampsia are at increased risk of long-term cardiovascular sequelae. From Medline and Embase searches, we included case-control and cohort studies that examined cardiac, cerebrovascular or peripheral arterial disease, or cardiovascular mortality>6 weeks postpartum, in women with and without a history of preeclampsia/eclampsia and that controlled for or matched for confounders. Two independent reviewers determined study eligibility and extracted data. Five case-control and 10 cohort studies met eligibility criteria, with a total of 116,175 women with and 2,259,576 women without preeclampsia/eclampsia. Most studies focused on women<56 years of age. Relative to women with uncomplicated pregnancies, women with a history of preeclampsia/eclampsia had an increased risk of subsequent cardiac disease in both the case-control studies (odds ratio 2.47, 95% CI 1.22-5.01) and the cohort studies (relative risk [RR] 2.33, 1.95-2.78), as well as an increased risk of cerebrovascular disease (RR 2.03, 1.54-2.67), peripheral arterial disease (RR 1.87, 0.94-3.73), and cardiovascular mortality (RR 2.29, 1.73-3.04). Meta-regression revealed a graded relationship between the severity of preeclampsia/eclampsia and the risk of cardiac disease (mild: RR 2.00, 1.83-2.19, moderate: RR 2.99, 2.51-3.58, severe: RR 5.36, 3.96-7.27, P<.0001). Women with a history of preeclampsia/eclampsia have approximately double the risk of early cardiac, cerebrovascular, and peripheral arterial disease, and cardiovascular mortality. Further research is needed to determine the mechanisms underlying these associations and to identify effective prevention strategies.
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            Endothelial dysfunction and preeclampsia: role of oxidative stress

            Preeclampsia (PE) is an often fatal pathology characterized by hypertension and proteinuria at the 20th week of gestation that affects 5–10% of the pregnancies. The problem is particularly important in developing countries in where the incidence of hypertensive disorders of pregnancy is higher and maternal mortality rates are 20 times higher than those reported in developed countries. Risk factors for the development of PE include obesity, insulin resistance and hyperlipidemia that stimulate inflammatory cytokine release and oxidative stress leading to endothelial dysfunction (ED). However, how all these clinical manifestations concur to develop PE is still not very well understood. The related poor trophoblast invasion and uteroplacental artery remodeling described in PE, increases reactive oxygen species (ROS), hypoxia and ED. Here we aim to review current literature from research showing the interplay between oxidative stress, ED and PE to the outcomes of current clinical trials aiming to prevent PE with antioxidant supplementation.
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              Uterine artery Doppler at 11 + 0 to 13 + 6 weeks in the prediction of pre-eclampsia.

              To determine the performance of screening for pre-eclampsia (PET) by maternal characteristics and uterine artery pulsatility index (PI) at 11 + 0 to 13 + 6 weeks' gestation. In women with singleton pregnancies attending for routine care at 11 + 0 to 13 + 6 weeks' gestation we recorded maternal variables and measured the uterine artery PI. We identified 107 cases that subsequently developed PET and 5041 that were unaffected by PET, gestational hypertension or delivery of newborns with birth weight below the 10(th) centile. A multivariate Gaussian model was fitted to the distribution of log multiples of the median (MoM) PI in the PET and unaffected groups. Likelihood ratios for log MoM PI were computed and used together with maternal variables to produce patient-specific risks for each case. Predicted detection rates (DR) and false-positive rates (FPR) were calculated by taking the proportions with risks above a given risk threshold. In the unaffected group log MoM PI was influenced by maternal ethnic origin, body mass index, previous history of PET and fetal crown-rump length. In the prediction of PET significant contributions were provided by log MoM PI, ethnic origin, body mass index and previous and family history of PET. For an FPR of 10% the DRs of all PET and PET leading to delivery before 34 weeks' gestation by log MoM PI and maternal variables were 61.7% and 81.8%, respectively. Maternal variables together with uterine artery PI at 11 + 0 to 13 + 6 weeks' gestation provide sensitive prediction of the development of PET, especially of severe early-onset PET. Copyright (c) 2007 ISUOG
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                Author and article information

                Contributors
                dominique.mannaerts@uantwerpen.be
                ellen.faes@uantwerpen.be
                jangielis@live.be
                emeline.vancraenebroeck@uantwerpen.be
                paul.cos@uantwerpen.be
                marc.spaanderman@mumc.nl
                wilfried.gyselaers@zol.be
                j.cornette@erasmusmc.nl
                yves.jacquemyn@uza.be
                Journal
                BMC Pregnancy Childbirth
                BMC Pregnancy Childbirth
                BMC Pregnancy and Childbirth
                BioMed Central (London )
                1471-2393
                27 February 2018
                27 February 2018
                2018
                : 18
                : 60
                Affiliations
                [1 ]ISNI 0000 0004 0626 3418, GRID grid.411414.5, Departement of Obstetrics and Gynaecology, , Antwerp University Hospital, ; Antwerp, Belgium
                [2 ]ISNI 0000 0001 0790 3681, GRID grid.5284.b, ASTARC, Antwerp Surgical Training, Anatomy and Research Centre, , University of Antwerp, ; Antwerp, Belgium
                [3 ]ISNI 0000 0004 0626 3418, GRID grid.411414.5, Laboratory for Cellular and Molecular Cardiology and Department of Cardiology, , Antwerp University Hospital, ; Edegem, Belgium
                [4 ]ISNI 0000 0001 0790 3681, GRID grid.5284.b, Research Group Cardiovascular Diseases, Translational Pathophysiological Research, , University of Antwerp, ; Antwerp, Belgium
                [5 ]ISNI 0000 0001 0790 3681, GRID grid.5284.b, Laboratory for Microbiology, Parasitology and Hygiene (LMPH), , University of Antwerp, ; Antwerp, Belgium
                [6 ]ISNI 0000 0004 0480 1382, GRID grid.412966.e, Departement of Obstetrics and Gynecology, , Maastricht University Medical Center, ; Maastricht, The Netherlands
                [7 ]ISNI 0000 0004 0612 7379, GRID grid.470040.7, Departement of Obstetrics and Gynecology, , Ziekenhuis-Oost-Limburg (ZOL), ; Genk, Belgium
                [8 ]ISNI 000000040459992X, GRID grid.5645.2, Departement of Obstetrics and Gynecology, , Erasmus Medical Center, ; Rotterdam, The Netherlands
                [9 ]ISNI 0000 0001 0790 3681, GRID grid.5284.b, Department of Obstetrics and Gynaecology, Antwerp Surgical Training and Anatomy Research Centre (ASTARC), , Antwerp University/Antwerp University Hospital, ; Antwerp, Belgium
                Author information
                http://orcid.org/0000-0003-3172-5672
                Article
                1685
                10.1186/s12884-018-1685-5
                5827979
                29482567
                e0348235-2f4c-4324-b970-c65b37c960fd
                © The Author(s). 2018

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                : 6 January 2017
                : 12 February 2018
                Funding
                Funded by: Fund for scientific research-Flanders (FWO) as senior clinical investigator.
                Categories
                Study Protocol
                Custom metadata
                © The Author(s) 2018

                Obstetrics & Gynecology
                pre-eclampsia,endothelial (dys) function,oxidative stress,electron paramagnetic resonance,nitric oxide,maternal outcome

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