Preeclampsia As Modulator of Offspring Health (original) (raw)
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Reproductive Sciences, 2007
Development of the National Institutes of Health sponsored a 2-day workshop titled "Preeclampsia-A Pressing Problem." The purpose of the workshop was to bring together leaders in the field to present and discuss their diverse research areas, which ranged from basic science to clinical trials and management, and to identify scientific gaps. This article is a summary of the proceedings of that workshop. Although much progress is being made in understanding the underpinnings of preeclampsia, a number of research gaps are identified that, if filled, would hasten progress in the field. It is the overall consensus that preeclampsia is a multifactorial disease whose pathogenesis is not solely vascular, genetic, immunologic, or environmental but a complex combination of factors. In addition, a number of specific scientific gaps are identified including insufficient multidisciplinary and collaborative research, clinical trials and studies of patient management, and a lack of in-depth mechanistic research. The research community needs to focus on these gaps to better understand the disease, with the ultimate goal of preventing the disorder.
Opinion article Preeclampsia and human reproduction. An essay of a long term reflection
2003
Gestational hypertension/preeclampsia, is a major disease of human reproduction, with 10% of human births being affected. It is due to the failure of extravillous cytotrophoblast to invade the maternal uterine spiral arteries to a sufficient depth at the second physiological invasion around the 14-16th week of gestation, inducing poor vascular exchanges between the mother and the placenta. The rise of blood pressure in the human mother is then a compensatory mechanism to increase the exchanges and try to save the fetus from poor supplies. Indeed, it is only in the late 1970s that a puzzling phenomenon has been described: in human pregnancy, in contrast with other mammals, implantation of the embryo occurs by two physiological invasions of the cytotrophoblast inside the uterine wall: (a) at the beginning of pregnancy after fecundation (like all mammals); (b) then follows an apparent long pause (6-8 weeks) and (c) late at the end of first trimester (14-16th week) of gestation, a second very deep (1/3 of the uterine wall) invasion. This two-wave physiological endovascular trophoblast invasion represents a remarkable immunological placental-maternal interaction. Moreover, preeclampsia which has been considered as 'the disease of primigravidae' during all the XXth century may be in fact associated with new paternity especially in couples conceiving very shortly after the beginning of their sexual relationship. 'Primipaternity', rather than primigravidity, is probably the leading cause of preeclampsia. Comprehension in the near future of the physiological immunological tolerance in normal pregnancies and immunological rejection (preeclampsia) of the second trophoblastic invasion will give the biological clue of this puzzling disease, real plague of human reproduction.
Preeclampsia: Pathophysiology and management
Journal of Gynecology Obstetrics and Human Reproduction, 2020
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Pre-eclampsia has an adverse impact on maternal and fetal health
Translational Research, 2015
Pre-eclampsia (preE) is a multifaceted complication found uniquely in the pregnant patient and one that has puzzled scientists for years. PreE is not a single disorder, but a complex syndrome that is produced by various pathophysiological triggers and mechanisms affecting about 5% of obstetrical patients. PreE is a major cause of premature delivery and maternal and fetal morbidity and mortality. PreE is characterized by de novo development of hypertension and proteinuria after 20 weeks of gestation and affects nearly every organ system, with the most severe consequences being eclampsia, pulmonary edema, intrauterine growth restriction, and thrombocytopenia. PreE alters the intrauterine environment by modulating the pattern of hormonal signals and activating the detrimental cellular signaling that has been transported to the fetus. The fetus has to adapt to this intrauterine environment with detrimental signals. The adaptive changes increase the risk of disease later in life. This review defines the predisposition and causes of preE and the cellular signaling detrimental to maternal health during preE. Moreover, the risk factors for diseases that are transmitted to the offspring have been addressed in this review. The detrimental signaling molecules that have been overexpressed in preE patients raises the possibility that those signals could be therapeutically blocked one day.
Journal of Reproductive Immunology
The 11th workshop on Immunology of preeclampsia in Reunion 2018 celebrated its 20th candle In this paper we try to summarize the main tracks of reflections during these two decades. First, of course, the advances in immunology of reproduction in the field of preeclampsia, which was poorly developed 2 decades ago when we first started in 1998. But, this workshop has not been dedicated only to immunology. Second, one of the main reflections has always been, workshop after workshop: "why does preeclampsia exists in humans?" in an evolutionary view, as we have no established natural animal models in the other some 4500 other mammal species. Third, besides the reflections on the biological plausibility of preeclampsia-disease-of-first-pregnancies-at-a-level-of-a-couple (primipaternity rather than primigravidity), i.e. immunology, paternal-maternal conflict, we had to face an apparent conundrum: the human species should have disappeared (almost 40-50% incidence of hypertensive disorders of pregnancy in couples conceiving within the first 4 months of sexual cohabitation). We report then the dialogues we were obliged to have with zoologists who themselves had no clues on our apparent "extravagant sexuality" and strange reproduction (ridiculous low fertility rate of the human female: 25%). Fourth, debates on the main difference between early onset ("rather immunological") and late onset PE ("rather maternal vascular predispositions"). Further, the debate of why high income countries report 90% of their PE being LOP, while other countries describe epidemiologically very high incidences of EOP. Finally, and always present at all workshops, the physiopathology of the reversible systemic maternal vascular inflammation.
Journal of reproductive immunology, 2015
This workshop had four main objectives: (A) Trying to look at the preeclampsia (PE) problem "from the Space Shuttle": why preeclampsia has emerged in humans (a specific human reproductive feature among 4300 mammal species)? (B) Epidemiology: there are major geographical differences concerning early onset PE and late onset PE throughout the world. (C) Vascular: The very promising use of pravastatin in the treatment of the vascular maternal syndrome (based on the metabolism of carbon monoxide (CO), the role of inositol phosphate glycans P-type (IPG-P), a major role in comprehending the insulin resistance phenotype in preeclampsia. (D) Immunology: the specialty of these workshops since their start in 1998; our understanding of the role of the immune system and the regulation of the deep implantation of the human trophoblast (and the obligatory compromises between the fetal/placental unit and the mother) have reached a kind of "maturity," following the pivotal studie...