The Experts below are selected from a list of 4195917 Experts worldwide ranked by ideXlab platform
C W G Redman - One of the best experts on this subject based on the ideXlab platform.
-
pre eclampsia pathophysiology and clinical implications
BMJ, 2019Co-Authors: Graham J Burton, C W G Redman, James M Roberts, Ashley MoffettAbstract:Pre-Eclampsia is a common disorder that particularly affects first pregnancies. The clinical presentation is highly variable but hypertension and proteinuria are usually seen. These systemic signs arise from soluble factors released from the placenta as a result of a response to stress of syncytiotrophoblast. There are two sub-types: early and late onset Pre-Eclampsia, with others almost certainly yet to be identified. Early onset Pre-Eclampsia arises owing to defective placentation, whilst late onset Pre-Eclampsia may center around interactions between normal senescence of the placenta and a maternal genetic predisposition to cardiovascular and metabolic disease. The causes, placental and maternal, vary among individuals. Recent research has focused on placental-uterine interactions in early pregnancy. The aim now is to translate these findings into new ways to predict, prevent, and treat Pre-Eclampsia.
-
interleukin 1 family cytokines and their regulatory proteins in normal pregnancy and pre eclampsia
Clinical and Experimental Immunology, 2015Co-Authors: J Southcombe, C W G Redman, I L Sargent, Ingrid GranneAbstract:Maternal systemic inflammation is a feature of Pre-Eclampsia, a condition in pregnancy characterized by hypertension and proteinuria. Pre-Eclampsia is caused by the placenta; many placental factors contribute to the syndrome's progression, and proinflammatory cytokines have been identified previously as one such mediator. The interleukin (IL)-1 family of cytokines are key regulators of the inflammatory network, and two naturally occurring regulatory molecules for IL-1 family cytokines, IL-1RA and sST2, have been found previously to be elevated in maternal blood from women with Pre-Eclampsia. Here we investigate more recently identified IL-1 family cytokines and regulatory molecules, IL-1RAcP, IL-37, IL-18BP, IL-36α/β/γ/Ra and IL-38 in Pre-Eclampsia. Pregnant women have more circulating IL-18BP and IL-36Ra than non-pregnant women, and sIL-1RAcP is elevated from women with Pre-Eclampsia compared to normal pregnancies. The placenta expresses all the molecules, and IL-37 and IL-18BP are up-regulated significantly in Pre-Eclampsia placentas compared to those from normal pregnancies. Together, these changes contribute to the required inhibition of maternal systemic cytotoxic immunity in normal pregnancy; however, in Pre-Eclampsia the same profile is not seen. Interestingly, the increased circulating levels of sIL-1RAcP and increased placental IL-18BP and IL-37, the latter of which we show to be induced by hypoxic damage to the placenta, are all factors which are anti-inflammatory. While the placenta is often held responsible for the damage and clinical symptoms of Pre-Eclampsia by the research community, here we show that the Pre-Eclampsia placenta is also trying to prevent inflammatory damage to the mother.
-
immunology of pre eclampsia
American Journal of Reproductive Immunology, 2010Co-Authors: C W G Redman, I L SargentAbstract:Pre-Eclampsia develops in stages, only the last being the clinical illness. This is generated by a non-specific, systemic (vascular), inflammatory response, secondary to placental oxidative stress and not by reactivity to fetal alloantigens. However, maternal adaptation to fetal (paternal alloantigens) is crucial in the earlier stages. A pre-conceptual phase involves maternal tolerization to paternal antigens by seminal plasma. After conception, regulatory T cells, interacting with indoleamine 2,3-dioxygenase, together with decidual NK cell recognition of fetal HLA-C on extravillous trophoblast may facilitate placental growth by immunoregulation. Complete failure of this mechanism would cause miscarriage, while partial failure would cause poor placentation and dysfunctional uteroplacental perfusion. The first pregnancy preponderance and partner specificity of Pre-Eclampsia can be explained by this model. For the first time, the pathogenesis of Pre-Eclampsia can be related to defined immune mechanisms that are appropriate to the fetomaternal frontier. Now, the challenge is to prove the detail.
-
inflammation and pre eclampsia
Seminars in Fetal & Neonatal Medicine, 2006Co-Authors: Angela M Borzychowski, I L Sargent, C W G RedmanAbstract:Pre-Eclampsia is a common and potentially dangerous disorder of human pregnancy. The maternal syndrome of hypertension, proteinuria and oedema is part of a severe systemic inflammatory response that includes leukocyte and endothelial cell activation. Although the origins of Pre-Eclampsia remain unclear, a major cause is the failure to develop an adequate blood supply to the placenta, leading to placental oxidative stress. This results in the excess release of placental factors, such as syncytiotrophoblast debris or soluble fms-like tyrosine kinase-1 (sFlt-1), the soluble receptor for vascular endothelial growth factor (VEGF), into the maternal circulation, where they trigger an inflammatory response and endothelial dysfunction. Alternatively, Pre-Eclampsia can develop in the presence of a normal placenta in women that are susceptible to systemic inflammation, such as with chronic cardiovascular disease or diabetes. While clinical management of Pre-Eclampsia does not currently include anti-inflammatory agents, current research is focusing on ways to reduce inflammation and oxidative stress.
-
the pre eclampsia community guideline precog how to screen for and detect onset of pre eclampsia in the community
BMJ, 2005Co-Authors: Fiona Milne, C W G Redman, James J Walker, Philip N Baker, Julian Bradley, Carol Cooper, Michael De Swiet, Gillian Fletcher, Mervi Jokinen, Deirdre J MurphyAbstract:Pre-Eclampsia is a major cause of poor outcome in pregnancy: the category “hypertensive diseases of pregnancy” remains a leading cause of direct maternal deaths in the United Kingdom1; pre-eclamptic conditions represent one in three cases of severe obstetric morbidity2; hypertension and/or proteinuria is the leading single identifiable risk factor in pregnancy associated with stillbirth (one in five stillbirths in otherwise viable babies)3; and Pre-Eclampsia is strongly associated with fetal growth restriction, low birth weight, preterm delivery, respiratory distress syndrome, and admission to neonatal intensive care.4 In 46% of maternal deaths1 and 65% of fetal deaths5 due to Pre-Eclampsia reported through the Confidential Enquiries into Maternal Deaths and the Confidential Enquiry into Stillbirths and Deaths in Infancy, different management would reasonably have expected to alter the outcome. There was a failure to identify and act on known risk factors at booking and to recognise and respond to signs and symptoms from 20 weeks' gestation.6 No guidelines exist for the screening and early detection of Pre-Eclampsia in the community, and there is no uniformity in referral thresholds and assessment procedures. We developed the Pre-Eclampsia community guideline (PRECOG) under the auspices of the charity Action on Pre-Eclampsia, following the National Institute for Clinical Excellence's recommendations for the development of guidelines.7 Our guideline is supported by the Royal College of Obstetricians and Gynaecologists, the Royal College of Midwives, the Royal College of General Practitioners, and the National Childbirth Trust. Box 1 lists the definitions used in the guideline; Pre-Eclampsia is defined as new hypertension and proteinuria (see bmj.com for definition of levels of evidence). The Pre-Eclampsia community guideline provides an evidence based risk assessment, with criteria for early referral for specialist input, a two tiered schedule for monitoring women in the community after …
I L Sargent - One of the best experts on this subject based on the ideXlab platform.
-
interleukin 1 family cytokines and their regulatory proteins in normal pregnancy and pre eclampsia
Clinical and Experimental Immunology, 2015Co-Authors: J Southcombe, C W G Redman, I L Sargent, Ingrid GranneAbstract:Maternal systemic inflammation is a feature of Pre-Eclampsia, a condition in pregnancy characterized by hypertension and proteinuria. Pre-Eclampsia is caused by the placenta; many placental factors contribute to the syndrome's progression, and proinflammatory cytokines have been identified previously as one such mediator. The interleukin (IL)-1 family of cytokines are key regulators of the inflammatory network, and two naturally occurring regulatory molecules for IL-1 family cytokines, IL-1RA and sST2, have been found previously to be elevated in maternal blood from women with Pre-Eclampsia. Here we investigate more recently identified IL-1 family cytokines and regulatory molecules, IL-1RAcP, IL-37, IL-18BP, IL-36α/β/γ/Ra and IL-38 in Pre-Eclampsia. Pregnant women have more circulating IL-18BP and IL-36Ra than non-pregnant women, and sIL-1RAcP is elevated from women with Pre-Eclampsia compared to normal pregnancies. The placenta expresses all the molecules, and IL-37 and IL-18BP are up-regulated significantly in Pre-Eclampsia placentas compared to those from normal pregnancies. Together, these changes contribute to the required inhibition of maternal systemic cytotoxic immunity in normal pregnancy; however, in Pre-Eclampsia the same profile is not seen. Interestingly, the increased circulating levels of sIL-1RAcP and increased placental IL-18BP and IL-37, the latter of which we show to be induced by hypoxic damage to the placenta, are all factors which are anti-inflammatory. While the placenta is often held responsible for the damage and clinical symptoms of Pre-Eclampsia by the research community, here we show that the Pre-Eclampsia placenta is also trying to prevent inflammatory damage to the mother.
-
immunology of pre eclampsia
American Journal of Reproductive Immunology, 2010Co-Authors: C W G Redman, I L SargentAbstract:Pre-Eclampsia develops in stages, only the last being the clinical illness. This is generated by a non-specific, systemic (vascular), inflammatory response, secondary to placental oxidative stress and not by reactivity to fetal alloantigens. However, maternal adaptation to fetal (paternal alloantigens) is crucial in the earlier stages. A pre-conceptual phase involves maternal tolerization to paternal antigens by seminal plasma. After conception, regulatory T cells, interacting with indoleamine 2,3-dioxygenase, together with decidual NK cell recognition of fetal HLA-C on extravillous trophoblast may facilitate placental growth by immunoregulation. Complete failure of this mechanism would cause miscarriage, while partial failure would cause poor placentation and dysfunctional uteroplacental perfusion. The first pregnancy preponderance and partner specificity of Pre-Eclampsia can be explained by this model. For the first time, the pathogenesis of Pre-Eclampsia can be related to defined immune mechanisms that are appropriate to the fetomaternal frontier. Now, the challenge is to prove the detail.
-
inflammation and pre eclampsia
Seminars in Fetal & Neonatal Medicine, 2006Co-Authors: Angela M Borzychowski, I L Sargent, C W G RedmanAbstract:Pre-Eclampsia is a common and potentially dangerous disorder of human pregnancy. The maternal syndrome of hypertension, proteinuria and oedema is part of a severe systemic inflammatory response that includes leukocyte and endothelial cell activation. Although the origins of Pre-Eclampsia remain unclear, a major cause is the failure to develop an adequate blood supply to the placenta, leading to placental oxidative stress. This results in the excess release of placental factors, such as syncytiotrophoblast debris or soluble fms-like tyrosine kinase-1 (sFlt-1), the soluble receptor for vascular endothelial growth factor (VEGF), into the maternal circulation, where they trigger an inflammatory response and endothelial dysfunction. Alternatively, Pre-Eclampsia can develop in the presence of a normal placenta in women that are susceptible to systemic inflammation, such as with chronic cardiovascular disease or diabetes. While clinical management of Pre-Eclampsia does not currently include anti-inflammatory agents, current research is focusing on ways to reduce inflammation and oxidative stress.
-
placental debris oxidative stress and pre eclampsia
Placenta, 2000Co-Authors: C W G Redman, I L SargentAbstract:Pre-Eclampsia is a dangerous, common, unpredictable and highly variable complication of the second half of pregnancy, labour or the early puerperium. The presence of a placenta is both necessary and sufficient to cause the disorder. A fetus is not required as Pre-Eclampsia can occur with hydatidiform mole (Chun et al., 1964). A uterus is probably not required because Pre-Eclampsia may develop in abdominal pregnancy (Piering et al., 1993). Central to management, is delivery, which removes the causative organ, namely the placenta. The problem with the placenta is generally considered to be an inadequate uteroplacental circulation leading to placental hypoxia, oxidative stress and, in the most severe cases, infarction. Two abnormalities, affecting the spiral arteries, are known to predispose to the problem: the arteries may be either too small because of deficient placentation, or obstructed because of acute atherosis, or both.
Lelia Duley - One of the best experts on this subject based on the ideXlab platform.
-
clinical pharmacokinetic properties of magnesium sulphate in women with pre eclampsia and eclampsia
British Journal of Obstetrics and Gynaecology, 2016Co-Authors: Babasola O Okusanya, Lelia Duley, Olufemi T Oladapo, Qian Long, Pisake Lumbiganon, Guillermo Carroli, Zahida Qureshi, Joao Paulo Souza, A M GulmezogluAbstract:Background The pharmacokinetic basis of magnesium sulphate (MgSO 4) dosing regimens for eclampsia prophylaxis and treatment is not clearly established.
-
alternative magnesium sulphate regimens for women with pre eclampsia and eclampsia
Cochrane Database of Systematic Reviews, 2010Co-Authors: Lelia Duley, Hosam E Matar, Muhammad Qutayba Almerie, David R HallAbstract:Background Magnesium sulphate remains the drug of choice for both prevention and treatment of women with eclampsia. Regimens for administration of this drug have evolved over the years, but have not yet been formally evaluated. Objectives To assess the comparative effects of alternative regimens for the administration of magnesium sulphate when used for the care of women with Pre-Eclampsia or eclampsia, or both. Search strategy We searched the Cochrane Pregnancy and Childbirth Group's Trials Register (June 2010). Selection criteria Randomised trials comparing different regimens for administration of magnesium sulphate used for the care of women with Pre-Eclampsia or eclampsia, or both. Data collection and analysis All four review authors assessed trial quality and extracted data independently. Main results We identified 17 studies of which six (866 women) met the inclusion criteria: two trials (451 women) compared regimens for women with eclampsia and four (415 women) for women with Pre-Eclampsia.Treatment of eclampsia: one trial compared loading dose alone with loading dose plus maintenance therapy for 24 hours (401 women). There was no clear difference between the groups in the risk ratio (RR) of recurrence of convulsions (RR 1.13, 95% confidence interval (CI) 0.42 to 3.05) or stillbirth (RR 1.13, 95% CI 0.66 to 1.92), and the CIs are wide. One trial compared a low dose regimen with a standard dose regimen over 24 hours (50 women). This study was too small for any reliable conclusions about the comparative effects.Prevention of eclampsia: one trial compared intravenous with intramuscular maintenance regimen for 24 hours (17 women). This trial was too small for any reliable conclusions. Three trials compared short maintenance regimens postpartum with continuing for 24 hours after the birth (398 women), even taken together these trials were too small for any reliable conclusions. Authors' conclusions Although strong evidence supports the use of magnesium sulphate for prevention and treatment of eclampsia, trials comparing alternative treatment regimens are too small for reliable conclusions.
-
the global impact of pre eclampsia and eclampsia
Seminars in Perinatology, 2009Co-Authors: Lelia DuleyAbstract:Over half a million women die each year from pregnancy related causes, 99% in low and middle income countries. In many low income countries, complications of pregnancy and childbirth are the leading cause of death amongst women of reproductive years. The Millennium Development Goals have placed maternal health at the core of the struggle against poverty and inequality, as a matter of human rights. Ten percent of women have high blood pressure during pregnancy, and preeclampsia complicates 2% to 8% of pregnancies. Preeclampsia can lead to problems in the liver, kidneys, brain and the clotting system. Risks for the baby include poor growth and prematurity. Although outcome is often good, preeclampsia can be devastating and life threatening. Overall, 10% to 15% of direct maternal deaths are associated with preeclampsia and eclampsia. Where maternal mortality is high, most of deaths are attributable to eclampsia, rather than preeclampsia. Perinatal mortality is high following preeclampsia, and even higher following eclampsia. In low and middle income countries many public hospitals have limited access to neonatal intensive care, and so the mortality and morbidity is likely to be considerably higher than in settings where such facilities are available. The only interventions shown to prevent preeclampsia are antiplatelet agents, primarily low dose aspirin, and calcium supplementation. Treatment is largely symptomatic. Antihypertensive drugs are mandatory for very high blood pressure. Plasma volume expansion, corticosteroids and antioxidant agents have been suggested for severe preeclampsia, but trials to date have not shown benefit. Optimal timing for delivery of women with severe preeclampsia before 32 to 34 weeks' gestation remains a dilemma. Magnesium sulfate can prevent and control eclamptic seizures. For preeclampsia, it more than halves the risk of eclampsia (number needed to treat 100, 95% confidence interval 50 to 100) and probably reduces the risk of maternal death. A quarter of women have side effects, primarily flushing. With clinical monitoring serious adverse effects are rare. Magnesium sulfate is the anticonvulsant of choice for treating eclampsia; more effective than diazepam, phenytoin, or lytic cocktail. Although it is a low cost effective treatment, magnesium sulfate is not available in all low and middle income countries; scaling up its use for eclampsia and severe preeclampsia will contribute to achieving the Millennium Development Goals.
-
antioxidants for preventing pre eclampsia
Cochrane Database of Systematic Reviews, 2008Co-Authors: Alice R Rumbold, Lelia Duley, Caroline A Crowther, Ross R HaslamAbstract:BACKGROUND Oxidative stress has been proposed as a key factor involved in the development of Pre-Eclampsia. Supplementing women with antioxidants during pregnancy may help to counteract oxidative stress and thereby prevent or delay the onset of Pre-Eclampsia. OBJECTIVES To determine the effectiveness and safety of any antioxidant supplementation during pregnancy and the risk of developing Pre-Eclampsia and its related complications. SEARCH STRATEGY We searched the Cochrane Pregnancy and Childbirth Group Trials Register (June 2004) and the Cochrane Central Register of Controlled Trials (The Cochrane Library, Issue 3, 2004). SELECTION CRITERIA All randomised and quasi-randomised trials comparing one or more antioxidants with either placebo or no antioxidants during pregnancy for the prevention of Pre-Eclampsia, and trials comparing one or more antioxidants with another, or with other interventions. DATA COLLECTION AND ANALYSIS Two review authors independently assessed trials for inclusion, data extraction and trial quality. Data were double-entered into the Review Manager software. MAIN RESULTS Seven trials involving 6082 women are included in this review. The largest trial (5021 women) was quasi-random and only three of the seven included trials were rated high quality. Supplementing women with any antioxidants during pregnancy compared with control or placebo was associated with a 39% reduction in the risk of Pre-Eclampsia (relative risk (RR) 0.61, 95% confidence intervals (CI) 0.50 to 0.75, seven trials, 6082 women). Women receiving antioxidants compared with control or placebo also had a reduced risk of having a small-for-gestational-age infant (RR 0.64, 95% CI 0.47 to 0.87, three trials, 634 women), their infants had a greater mean birthweight (weighted mean difference 91.83 g, 95% CI 11.55 to 172.11, three trials, 451 women), but they were more likely to give birth preterm (RR 1.38, 95% CI 1.04 to 1.82, three trials, 583 women). There were insufficient data for reliable conclusions about possible effects on any other outcomes. AUTHORS' CONCLUSIONS These results should be interpreted with caution, as most of the data come from poor quality studies. Nevertheless, antioxidant supplementation seems to reduce the risk of Pre-Eclampsia. There also appears to be a reduction in the risk of having a small-for-gestational-age baby associated with antioxidants, although there is an increase in the risk of preterm birth. Several large trials are ongoing, and the results of these are needed before antioxidants can be recommended for clinical practice.
-
cost effectiveness of prophylactic magnesium sulphate for 9996 women with pre eclampsia from 33 countries economic evaluation of the magpie trial
British Journal of Obstetrics and Gynaecology, 2006Co-Authors: Judit Simon, Alastair Gray, Lelia DuleyAbstract:Objective To assess the cost-effectiveness of using magnesium sulphate for Pre-Eclampsia to prevent eclampsia. Design Multinational trial-based economic evaluation. Setting Thirty-three countries participating in the Magnesium Sulphate for Prevention of Eclampsia (Magpie) Trial. Population Women (9996) with Pre-Eclampsia from the Magpie Trial. Methods Outcome and hospital resource use data were available for the trial period from the Magpie Trial. Country-specific unit costs (U.S. dollar, year 2001) were obtained subsequently from participating hospitals by questionnaire. Cost-effectiveness was estimated for three categories of countries grouped by gross national income (GNI) into high, middle and low GNI countries using a regression model. Uncertainty was explored in sensitivity analyses. Main outcome measures Eclampsia, hospital care costs and the incremental cost per case of eclampsia prevented. Results The number of women with Pre-Eclampsia who needed to receive magnesium sulphate to prevent one case of eclampsia was 324 [95% confidence interval (CI) 122, ∞] in high, 184 (95% CI 91, 6798) in middle and 43 (95% CI 30, 68) in low GNI countries. The additional hospital care cost per woman receiving magnesium sulphate was $65, $13 and $11, respectively. The incremental cost of preventing one case of eclampsia was $21,202 in high, $2473 in middle and $456 in low GNI countries. Reserving treatment for severe Pre-Eclampsia would lower these estimates to $12,942, $1179 and $263. Conclusions Magnesium sulphate for Pre-Eclampsia costs less and prevents more eclampsia in low GNI than in high GNI countries. Cost-effectiveness substantially improves if it is used only for severe Pre-Eclampsia, or the purchase price is reduced in low GNI countries.
Hannele Laivuori - One of the best experts on this subject based on the ideXlab platform.
-
aspirin in the prevention of pre eclampsia in high risk women a randomised placebo controlled predo trial and a meta analysis of randomised trials
British Journal of Obstetrics and Gynaecology, 2013Co-Authors: Pia M Villa, Eero Kajantie, Katri Raikkonen, Ak Pesonen, Esa Hamalainen, Merja Vainio, Pekka Taipale, Hannele LaivuoriAbstract:Objective To study the effect of aspirin in the prevention of Pre-Eclampsia in high-risk women. Design Randomised, double-blinded, placebo-controlled trial. Setting Maternity clinics in ten Finnish hospitals participating in the PREDO Project. Sample A total of 152 women with risk factors for Pre-Eclampsia and abnormal uterine artery Doppler velocimetry. Methods Participants were randomised to start either aspirin 100 mg/day or placebo at 12 + 0 to 13 + 6 weeks + days of gestation. Because of the limited power of this trial, we also conducted a meta-analysis of randomised controlled trials that included data on 346 women with abnormal uterine artery Doppler flow velocimetry, and aspirin 50–150 mg/day started at or before 16 weeks of gestation. Main outcome measure Pre-Eclampsia, gestational hypertension and birthweight standard deviation (SD) score. Outcome measures for the meta-analysis were Pre-Eclampsia, severe Pre-Eclampsia, preterm (diagnosed <37 + 0 weeks of gestation) and term Pre-Eclampsia. Results From the 152 randomised women, 121 were included in the final analysis. Low-dose aspirin did not reduce the rate of Pre-Eclampsia (relative risk [RR] 0.7, 95% CI 0.3–1.7); gestational hypertension (RR 1.6, 95% CI 0.6–4.2); early-onset Pre-Eclampsia (diagnosed <34 + 0 weeks of gestation) (RR 0.2, 95% CI 0.03–2.1); or severe Pre-Eclampsia (RR 0.4, 95% CI 0.1–1.3); and the results were not statistically significant in an intention-to-treat analysis. However, our meta-analysis, including the current data, suggested that low-dose aspirin initiated before 16 weeks of gestation reduces the risk of Pre-Eclampsia (RR 0.6, 95% CI 0.4–0.8) and severe Pre-Eclampsia (RR 0.3, 95% CI 0.1–0.7). Conclusions Our trial showed no statistically significant effect of aspirin in preventing Pre-Eclampsia in high-risk women. However, our meta-analysis suggested that aspirin may reduce the incidence of Pre-Eclampsia.
-
association of the rs1424954 polymorphism of the acvr2a gene with the risk of pre eclampsia is not replicated in a finnish study population
BMC Research Notes, 2011Co-Authors: Inkeri Lokki, Leena Hiltunen, Miira M Klemetti, Sanna Heino, Seppo Heinonen, Hannele LaivuoriAbstract:Background: Pre-Eclampsia/eclampsia is a common vascular pregnancy disorder associated with high maternal and infant mortality and morbidity worldwide. The role of Activin A and more recently type 2 Activin A receptor (ACVR2A) in the pathogenesis of Pre-Eclampsia has been the subject of genetic and biochemical research with controversial results. Findings: We genotyped a candidate Pre-Eclampsia-associated single nucleotide polymorphism rs1424954 in ACVR2A in three independent study populations of Finnish pre-eclamptic (total N = 485) and non-pre-eclamptic (total N = 449) women using pre-designed TaqMan allele discrimination assay and polymerase chain reaction. The possible association of the alleles and genotypes of interest with Pre-Eclampsia was evaluated using the chi-square test and logistic regression analysis. We found no association of rs1424954 to Pre-Eclampsia in Finnish patients. Conclusions: rs1424954 was not associated to Pre-Eclampsia in the Finnish study population. We hypothesise that while the gene associates to Pre-Eclampsia worldwide, the causative polymorphism in ACVR2A may be unique in genetically differing populations. Further research is needed to characterise the haplotype structure of ACVR2A in order for the causative genetic variant to be identified.
-
blood group ab and factor v leiden as risk factors for pre eclampsia a population based nested case control study
Thrombosis Research, 2009Co-Authors: Leena Hiltunen, Hannele Laivuori, Anna Rautanen, Risto Kaaja, Juha Kere, T Krusius, Mikko Paunio, Vesa RasiAbstract:Abstract Introduction Pre-Eclampsia is an important cause of maternal morbidity and mortality. Its etiology is still unknown. Clinical symptoms correlate with activation of coagulation and inherited thrombophilia has been associated with Pre-Eclampsia. ABO blood group has been associated with thrombotic disorders and Pre-Eclampsia. We assessed ABO blood group, seven thrombophilia associated polymorphisms, and anti-beta2-glycoprotein I antibodies as risk factors for Pre-Eclampsia. Materials and methods We performed a population-based nested case-control study of 100,000 consecutive pregnancies in Finland. Cases and controls were identified by combining national registers and medical records were reviewed. We studied 248 cases fulfilling strict criteria for Pre-Eclampsia and 679 controls. Severe Pre-Eclampsia, early Pre-Eclampsia, and Pre-Eclampsia with intra-uterine growth restriction (IUGR) were analyzed separately. Results Blood group AB increased the risk for Pre-Eclampsia as a whole (OR 2.1, 95% CI 1.3-3.5), and in the three subgroups (OR 2.3, 3.8, 3.4; 95% CI 1.3-3.9, 2.0-7.1, 1.6-7.1). FV Leiden increased the risk as a whole (OR 1.7, 95% CI 0.8-3.9), and in the three subgroups, although not statistically significantly. Anti-beta2-glycoprotein I antibodies were not associated with Pre-Eclampsia. High body mass index, diabetes, first pregnancy, and twin pregnancy increased the risk from 1.5-fold to 8.2-fold. Conclusions Our results confirm and extend the prior observation of blood group AB being a risk factor for Pre-Eclampsia. ABO blood group is known from all pregnant women. The value of blood group as risk factor for Pre-Eclampsia should be further assessed in prospective studies. In this study, FV Leiden was not statistically significant risk factor.
B Thilaganathan - One of the best experts on this subject based on the ideXlab platform.
-
uterine artery doppler screening for pre eclampsia comparison of the lower mean and higher first trimester pulsatility indices
Ultrasound in Obstetrics & Gynecology, 2011Co-Authors: R Napolitano, R Rajakulasingam, A Memmo, A Bhide, B ThilaganathanAbstract:Objectives A previous study suggested that the lower uterine artery pulsatility index (PI) is a better predictor of Pre-Eclampsia than is either the mean or higher indices. The aim of this study was to assess the relative value of these three indices for the prediction of Pre-Eclampsia in the first trimester of pregnancy. Methods This was a prospective study of 6221 singleton pregnancies. Uterine artery PI was obtained at the time of the 11–14-week nuchal translucency scan and receiver–operating characteristics curves for the lower, mean and higher PI value of the two uterine arteries in the prediction of Pre-Eclampsia were calculated. Results There were 178 cases of Pre-Eclampsia. The associations between uterine artery PI and Pre-Eclampsia were stronger for early (requiring delivery < 34 weeks' gestation) and preterm (requiring delivery < 37 weeks) Pre-Eclampsia compared to Pre-Eclampsia at any gestation. There was no significant difference in the strength of the association between lower, mean and higher PI for Pre-Eclampsia at any gestation. Conclusions First-trimester uterine artery PI is strongly associated with the development of early and preterm Pre-Eclampsia. Lower, mean and higher uterine artery PIs are comparable in screening for Pre-Eclampsia. Any differences that exist between the lower, mean and higher uterine artery indices are unlikely to have a significant impact on screening sensitivities. Copyright © 2011 ISUOG. Published by John Wiley & Sons, Ltd.
-
first trimester uterine artery doppler indices in term and preterm pre eclampsia
Ultrasound in Obstetrics & Gynecology, 2008Co-Authors: K Melchiorre, A Bhide, B Wormald, Karin Leslie, B ThilaganathanAbstract:Objectives To assess the relationship between first-trimester uterine artery Doppler measurements and the development of term and preterm Pre-Eclampsia. Methods This prospective study of uterine artery Doppler findings at 11–14 weeks in 3058 singleton pregnancies included 57 and 33 cases of term and preterm Pre-Eclampsia, respectively. Results The first-trimester uterine artery resistance index (RI) was significantly higher in women who subsequently developed preterm Pre-Eclampsia (mean RI, 0.79) than in those with a normal outcome (mean RI, 0.70; P = 0.0001) or those who developed Pre-Eclampsia at term (mean RI, 0.72; P = 0.002). There were no significant differences in first-trimester mean uterine artery RI (P = 0.136) or prevalence of bilateral notches (P = 0.459) between women who had a normal pregnancy outcome and those who developed Pre-Eclampsia at term. The receiver–operating characteristics curves for the prediction of term and preterm Pre-Eclampsia by uterine artery Doppler imaging demonstrated a significant association with development of preterm Pre-Eclampsia (P = 0.0001; area under the curve (AUC), 0.76; 95% CI, 0.66–0.86) but not term Pre-Eclampsia (P = 0.25; AUC, 0.54; 95% CI, 0.46–0.63). Conclusions The uterine artery Doppler data in this study suggest that preterm Pre-Eclampsia is strongly associated with defective invasion of the spiral arteries, in contrast to the findings in term Pre-Eclampsia which may be a consequence of placental deterioration at term. Our study findings support, but do not prove, a rigid separation between the etiology of early- and late-onset Pre-Eclampsia. Although there is a strong relationship between first-trimester uterine artery Doppler indices and the subsequent development of preterm Pre-Eclampsia, our data do not support its routine introduction into clinical practice. Copyright © 2008 ISUOG. Published by John Wiley & Sons, Ltd.
