Active clinical trials for "Pre-Eclampsia"

The investigators conduct a study to evaluate the underlying causes of preeclampsia in oocyte-donation pregnancies.

This study will recruit women with post partum pre-eclampsia and match them to controls without postpartum pre-eclampsia to identify an epigenetic signature that is specific to women with post partum pre-eclampsia to help characterize the underlying pathophysiology of post partum pre-eclampsia.

Studying the ultrastructural and immunohistochemical characteristics of Telocytes from umbilical cord vessels wall in PE patients compared to control and its relation to severity of disease whether controlled or uncontrolled.

Investigation of cardiovascular risk 5-15 years after early or late-onset preeclampsia by adenosine stress Magnetic Resonance Imaging and non-invasive methods like retinal vessel analysis, skin measurement of advanced glycation end products, flow-mediated dilation or pulse wave analysis in comparison to women after healthy pregnancies.

This study will investigate the interplay of different immune cells and placental cells as well as their potential for the development of pregnancy complications. In particular, the translation of the uteroplacental syndrome into a maternal syndrome, considered in the multifactorial pregnancy disorder preeclampsia, will be investigated. Immune cell subtypes are causally involved in the formation and translation of preeclampsia by inducing an endothelial dysfunction which leads to cardiovascular damage.

Identifying modifiable factors that contribute to preeclampsia risk associated with assisted reproduction can improve maternal health. Recent studies have shown an increased risk for hypertensive disorders of pregnancy after in vitro fertilization, particularly for pregnancies occurring during a hormone replacement therapy such a donor egg recipient and a frozen embryo transfer. This risk may be partly attributable to the degree by which the assisted reproductive treatment affects the maternal hormonal environment, when the corpus luteum is a major source of reproductive hormones. On the other hand, cryopreserved embryos are usually thawed and replaced in in a natural or hormonally manipulated cycle; on this point, frozen embryo transfer is associated with better perinatal outcome regarding preterm birth and low birth weight yet higher risk of large for gestational age and macrosomia compared to fresh transfer. The objective of our study is to investigate whether the absence of corpus luteum adversely affects pregnancy and to analyse if there are differences in the perinatal outcomes due to differences in the endometrial preparation protocol for a frozen embryo transfer.

Despite advances in obstetric care, preeclampsia (PE) remains the leading cause of maternal death and disability in both developed and developing countries, contributing to over 70,000 maternal and 500,000 fetal deaths annually worldwide. PULSE was designed using a preventative medicine approach, focusing on improving early detection of PE as opposed to managing symptoms after onset. The study aims to uncover the earliest possible signs of PE using a combination of novel clinical tools and established diagnostic techniques to better identify, track, and manage high risk pregnant women. Specifically, PULSE will be examining the incorporation of a non-invasive test for the measurement of arterial stiffness, which has been shown to be predictive of hypertensive disorders. This test, in combination with a wide range of blood biomarkers, detailed ultrasound imaging, and a comprehensive battery of physical and mental health questionnaires, represents the largest, most comprehensive preventative PE study to date. The results of this work has the potential to revolutionize the way PE and other hypertensive disorders of pregnancy are managed and treated and can serve to inform the design of future preventative clinical research studies.

It is known that if there isn't an efficient exposure to the paternal antigens before conception, there is an increased risk for the pre-eclampsia (PE) cascade and other pregnancy complications to take place. It is possible that maternal immune system that doesn't develop tolerance to the paternal antigens that the seminal fluid carries, doesn't developed an adequate immune tolerance to the trophoblast cells and due to that, they are being under greater attack during placentation. Thus, the cells don't go through a normal differentiation, don't perform normal pseudo-vasculogenesis and the PE cascade is more likely to be carried out. Both the maternal immune system and the paternal alloantigens have a role in the development of PE. Although the specific etiology remains unclear and can be only hypothesized. In this study the investigators aim is to try and prove that there is a difference in the immunological reactions to semen prior to conception and that these changes are related to PE and/or other obstetric complications. Hence the investigators aim to study the immune response to semen of women that will be exposed to the culprit semen for the first time compare to women that have been exposed to a culprit semen more than once previously (namely more than 1 insemination prior to the time of evaluation). After that, in a prospective cohort study the investigators would follow those women through their pregnancies and check for different pregnancy outcomes. In this manner, the investigators are hoping to create a screening tool that will help to predict pregnancy and fetal complications before conception related to maternal immune responses of paternal antigens.

major objective This multicenter, prospective cohort study aims at evaluating the predictive value of microbiome ,proteomics and serum markers in preeclampsia. secondary objective to evaluate the value of microbiome,proteomics and serum markers in assessing pregnancy outcome (complications during pregnancy and delivery, delivery) and neonatal prognosis.

Preeclampsia is a multi-system progressive disorder characterized by the new onset of hypertension and proteinuria, or hypertension and significant end-organ dysfunction with or without proteinuria, in the last half of pregnancy or postpartum. The genesis of the disease is laid down in early pregnancy and is characterized anatomically by abnormal remodeling of the maternal spiral arteries at the placental site.