View clinical trials related to Pre-eclampsia.
Filter by:This project is being undertaken to test the hypothesis that implementing a community based package of care for women with hypertensive disorders of pregnancy will result in overall improvement in maternal and neonatal outcomes. This is based on the premise that there are three main modifiable reasons why women (and their fetuses/newborns) die due to pregnancy complications: 1) delays by the woman herself in recognizing the seriousness of her condition; 2) delays in her being assessed and then transported to a center capable of providing effective and life-saving interventions; and 3) delays in the health facility in providing those interventions. The treatments for pre-eclampsia that are poorly accessed in LMIC are 1) magnesium sulfate (MgSO4) for prevention and treatment of the grand mal seizures of eclampsia; 2) oral antihypertensive medication to lower maternal BP to reduce the risk of stroke. The CLIP pilot and definitive cRCT will investigate whether the community level intervention including implementation of the CLIP package (oral antihypertensive therapy when indicated, intramuscular (i.m.) MgSO4 when indicated; and appropriate referral to an CEmOC facility when indicated) of care will reduce the incidence of all-cause maternal morbidity and mortality.
The aim of this study is to explore a mechanism that could potentially explain why women with a pregnancy complicated by pre-eclampsia are described as having an increased risk of cardiovascular disease later in life. If the hypothesis of this study turns out to be true, that is to say that women with pre-eclampsia have a higher level of oxidative stress than women with a normal pregnancy and that this difference persists after the delivery (6 months), a controlled randomized interventional study aiming to evaluate either therapeutic supplementation with antioxidant vitamins (Vit C and E) or modifications in diet could be envisaged.
Background and project rationale: Preeclampsia is a common complication of pregnancy, affecting 6-8% of all pregnancies and constitutes a leading cause of maternal morbidity and mortality. Preeclampsia is liable to endanger the lives of both the gravida and the fetus, particularly if treatment is initiated inappropriately or in an untimely fashion. Diagnosis of preeclampsia is dependent on the finding of proteinuria, determined as being over 300mg of protein in a 24 hours urine sample. However, urine collection spanning 24 hours sometimes constitutes a "bottleneck", extending the time to diagnosis of preeclampsia. Additionally, the collection of urine for 24 hours entails a degree of discomfort, requiring that the woman be in proximity to for collection vessel, and increases the length of her hospital admission. The use of an abbreviated test may permit diagnosis and treatment in a more timely fashion. Similarly, the ability to exclude the diagnosis more rapidly could reduce length of hospital stay and consumption of the health system's limited resources. Further, a shorter test may reduce the discomfort associated with the 24-hour test and thus increase compliance. Previous research has suggested that briefer tests correlate with the traditional 24 hour urine collection, however these studies were based on small study populations. Research Objective: To validate a brief and rapid test for the diagnosis of urinary protein excretion. To assess whether, in women with suspected preeclampsia, a difference exists between protein excretion during the daytime and at night. Methods: Urine collection will be performed on pregnant women admitted for investigation of suspected preeclampsia, with volumes recorded and samples taken at 6, 12 and 24 hour intervals for assessment of urinary protein content. As such, a comparison will be made between the protein excretion after 6 and 12 hours with that over a full 24 hour period; in addition, comparison will be made between daytime and nighttime urinary protein excretion. The results will allow for assessment of whether a shorter test can substitute the full 24 hour collection in the diagnosis of preeclampsia; results of women who are shown to not suffer from preeclampsia will be used to assess whether a short test can rule out the disease. Additionally a urine sample for protein/creatinine ratio will be examined and correlated with results of the different collection periods.
Cardiovascular diseases are the principal cause of death in women in developed and developing countries and are importantly promoted by hypertension. Salt sensitivity of the blood pressure is considered as an important cardiovascular risk factor at any blood pressure level. Severe preeclampsia is a hypertensive disorder of the pregnancy that also arises as a risk factor for cardiovascular and renal diseases. The major aim of this study is to examine the salt sensitivity of the ambulatory blood pressure in women with a history of severe preeclampsia (< 34 weeks gestation) compared with women with no history of pregnancy-related hypertensive complications. We plan to recruit 20 non-menopausal women with a history of severe preeclampsia, and 20 age, parity, race- matched premenopausal women as controls. The study has a case control randomized design. The salt sensitivity of the ambulatory blood pressure is defined as an increase of ≥4 mmHg in 24h ambulatory blood pressure on a high sodium diet. The high sodium diet is obtained by adding capsules of 6gr of NaCl/ day in the usual diet. The participants are identified as women discharged from the Maternity of University Hospital of Geneva between 1999 and 2001 with a preeclampsia coding. Fetal and maternal data will be carefully recovered from hospital records to identify severe preeclampsia (PE), based on International Society for the Study of Hypertension in Pregnancy criteria. These criteria are systolic blood pressure ≥160mmHg and/or diastolic blood pressure ≥110 mmHg with severe proteinuria (≥ 5g /24h or 3+ dipstick) and one or more signs of multisystem disease developing after 20 weeks of gestation in previously normotensive women. Severe preeclampsia was also defined as occurring before 34wk of gestation. Women with a history of hypertension, diabetes mellitus, renal or cardiac impairment, polycystic ovary syndrome will be excluded. Other exclusion criteria are anti-inflammatory drugs, diuretics, aspirin, oral contraceptives and hormonal replacement therapy. The protocol is approved by the University Hospital Ethical Committee and written informed consent will be obtained from each individual in accordance with the declaration of Helsinki. The study is conducted between 2009 and 2012 at the University Hospitals of Geneva, Switzerland.
Hypertensive disorders of pregnancy happen in 5% of pregnancies. Being aware of symptoms and complications may help women to present early and preserve their own and their baby's health. The proposed research aims to evaluate the impact of educational tools in pregnant women from an ambulatory population. These tools include a detailed pamphlet (including a graphic-based summary), a magnet summarizing symptoms and appropriate action, and a video. Level of knowledge will be evaluated after one month with a validated questionnaire. We will also evaluate if getting more information about preeclampsia increases patient anxiety as well as satisfaction about the tools.
there is a standard magnesium sulphate protocol and newer protocols for pre-eclampsia, we need to make a trial to find the best protocol
Preeclampsia (PE) is a common disorder of pregnancy that complicates 4-7% of all pregnancies. It is a serious condition with acute proteinuria and hypertension and varying degrees of edema after 20 weeks of gestation. PE leads to a severe risk of low birth weight because of prematurity with inherent complications. The pathogenesis is unknown but is assumed to involve placental ischemia.The primary placental disorder results in renal glomerular injury. Established PE is associated with paradoxical suppression of the renin-angiotensin-aldosterone system, RAAS. Despite suppressed RAAS, patients with PE retain NaCl(sodium chloride) after an intravenous isotonic NaCl overload compared to healthy pregnant women on a low NaCl diet. The investigators believe to have data that provide a possible explanation for the overall relationship between proteinuria, NaCl retension, suppression of RAAS, hypertension and underdevelopment of placenta. Earlier data, which the investigators have confirmed, shows abnormal glomerular loss of the enzyme plasmin/plasminogen from plasma to the urine in PE. Active plasmin in urine from patients with nephrotic syndrome and PE activates the epithelial sodium channel ( ENaC ) in renal collecting duct cells. The investigators hypothesize that loss of plasmin/plasminogen are shared for the diseases with proteinuria, including PE, and that plasmin- driven ENaC (epithelial sodium channel) activation is a causal factor in the pathophysiology of established PE. Hyperactive ENaC causes primary renal sodium retention with secondary suppression of the renin-angiotensin-aldosterone system. Aldosterone is recently established as a placental growth factor. Plasma-aldosterone levels are significant higher in normal pregnant women. PE is characterized by low aldosterone levels (a discovery the investigators have also confirmed) and by placental underdevelopment. Study Aim: To test specific hypothesis regarding established PE´s pathophysiological mechanisms. Study Hypothesis: 1. Excretion of urine proteases (plasmin/plasminogen) in PE leads to an activation of ENaC and hence RAAS is less NaCl sensitive while the blood pressure is more NaCl sensitive compared to healthy pregnant women. 2. The degree of aldosterone suppression in PE determines placental development
A tonic active epithelial Na+ channel (ENaC) in pre-eclampsia (PE) escaped normal hormonal control may offer an attractive explanatory model for the pathophysiology of established PE. The channel is activated by plasmin. Microalbuminuria predicts the development of pre-eclampsia in pregnant patients with pregestational diabetes type 1. The investigators hypothesize that urine-plasmin excreted in the kidneys, when proteinuria occurs, could be the cause. The investigators want to test the correlation between measurable plasmin/plasminogen in the urine early in pregnancy and the development of preeclampsia in pregnant patients with type 1 diabetes.
Between 40,000 and 80,000 pregnant women die annually from pre-eclampsia and eclampsia. Magnesium sulphate and anti-hypertensive therapies can reduce the morbidity associated with pre-eclampsia. The only cure, however, comes with delivery. Prompt delivery of the baby, preferably by vaginal route, is vital in order to achieve good maternal and neonatal outcomes. Induction of labour is therefore a critical intervention in order to prevent morbidity to both mother and baby. Two low cost interventions - oral misoprostol tablets and transcervical Foley catheterization - are already used by some in low resource settings, but their relative risks and benefits are not known. These interventions could optimize the care pathway for women needing induction of labour. This is especially important in low resource settings where improvement is most needed and the potential to reduce the maternal and neonatal mortality and morbidity is the greatest. The ideal induction agent would result in a relatively short induction to delivery interval without risk to fetus and with low rates of emergency caesarean section. The induction to delivery interval is especially important in pre-eclampsia and eclampsia where the condition may deteriorate rapidly until delivery. Inductions with prostaglandins, including misoprostol, are sometimes associated with uterine hyperstimulation and consequent fetal hypoxia, whilst the effectiveness and safety of Foley catheter as an induction agent has been persistently questioned. This study will identify the risk, benefits and trade-offs in efficacy, safety, acceptability and cost of these two low cost induction methods.
Preeclampsia is a pregnancy-specific, multisystem disorder that complicates approximately 5 % of pregnancies. Tracheal intubation in the women with severe pre-eclampsia is usually associated with exaggerated transient increases in blood pressure, heart rate and maternal plasma catecholamine concentrations. These changes may lead to maternal cerebral oedema, haemorrhage, left ventricular failure, pulmonary oedema or mortality, and reduce uterine blood flow which may adversely affect the neonatal wellbeing. Therefore, the attenuation of the haemodynamic responses to tracheal intubation in this unique group of patients is demanding for the best of both mother and foetus. The use of single remifentanil boluses of 0.5 to 1 µg/kg reduces effectively the haemodynamic and catecholamine responses to laryngoscopy and tracheal intubation in severe pre-eclamptics during Cesarean delivery under general anesthesia. Unfortunately, the use of 1 µg/kg doses are associated with more maternal hypotension and neonatal respiratory depression requiring resuscitation. Moreover, the use of preinduction remifentanil bolus of 0.5 µg/kg followed by a continuous infusion at 0.15-0.2 µg/kg/min is associated with significant attenuation of the maternal stress response to tracheal intubation with variable degree of neonatal depression in non-pre-eclamptic women. Whereas, the use of infusion rates of 0.1 µg/kg/min or less is less likely to produce neonatal depression. In our previous study, we demonstrated that the preoperative administration of dexmedetomidine 0.4 and 0.6 µg/kg/h, a specific alpha 2-adrenoceptor agonist, blunts the maternal haemodynamic and hormonal responses to Caesarean delivery under sevoflurane anaesthesia without adverse neonatal effects. However the use of 0.6 µg/kg/h doses is associated with higher postoperative sedation scores.