China
Africa
Explore chapters and articles related to this topic
Pregnancy
Published in T. Yee Khong, Annie N. Y. Cheung, Wenxin Zheng, Richard Wing-Cheuk Wong, Hao Chen, Diagnostic Endometrial Pathology, 2019
T. Yee Khong, Annie N. Y. Cheung, Wenxin Zheng
Prior to the arrival of the endovascular trophoblast, the spiral arteries become dilated and there is swelling and loosening of the media and endothelium. It is thought that this change is effected by the uterine natural killer cells.3 From the period when the spiral arteries can definitely be seen to communicate with the intervillous space, the endovascular cytotrophoblast is seen within their lumina. These endovascular trophoblastic plugs restrict the flow of red blood cells into the developing placenta and the relative hypoxemia protects the conceptus from oxidative damage from free radicals. The endovascular trophoblastic cells replace the endothelium and cause much damage to the vessel wall such that the muscular and elastic tissues within the arterial walls are replaced by fibrinoid material. Eventually, the endovascular trophoblastic plugs disappear as the cells are embedded within this fibrinoid material (Figures 3.3 and 3.4); this permits a true uteroplacental circulation, and the oxygen level in the intervillous space rises considerably at the end of the first trimester. This also corresponds to the approximate time when the conceptus switches from histiotrophic to hematotrophic nutrition.
Great obstetrical syndromes
Published in Moshe Hod, Vincenzo Berghella, Mary E. D'Alton, Gian Carlo Di Renzo, Eduard Gratacós, Vassilios Fanos, New Technologies and Perinatal Medicine, 2019
Inadequate spiral artery remodeling may be the result of both shallow invasion and a reduced number of invaded trophoblasts. This assumption is based on numerous histological surveys on hysterectomy and postmortem specimens of uteri with in situ placentas as well as placental bed biopsies, consisting of both decidual and myometrial tissue. Among such studies, severely impaired trophoblast invasion has been shown in full-thickness uterine wall samples obtained from early onset preeclamptic pregnancies combined with intrauterine growth restriction (17). However, the detailed underlying mechanisms, regulating EVT invasion in vivo and how EVTs enable the extensive remodeling of the, in total, approximately 30–60 spiral arteries of the placental bed, remain largely unknown. In recent years, maternal immune cells such as uterine natural killer cells and macrophages have been suggested as key regulators of both EVT invasion and spiral artery remodeling in the placental bed (18,19). A plethora of soluble factors, including cytokines, chemokines, and growth factors, is secreted from decidual macrophages and stromal cells, as well as uterine natural killer cells and even uterine glandular epithelial cells. A balanced cocktail of these factors may drive initial proliferation of trophoblast cell columns and subsequent detachment and invasion of EVTs into the placental bed (20). Moreover, these factors could regulate recruitment of macrophages and natural killer cells as well as other less abundant immune cells into the placental bed. At the same time, decidual stroma cells are suggested to secrete some anti-invasive factors that might be essential to counteract the effects of invasion-promoting factors and restrain exaggerated invasion. Thus, the decidua may provide a timely, balanced production of invasion promoting and inhibiting factors enabling a well-coordinated EVT invasion (21).
Unresponsiveness to oxytocin due to an extremely thin uterine wall in a pregnant woman with systemic lupus erythematosus and Sjögren’s syndrome
Published in Journal of Obstetrics and Gynaecology, 2018
Takuji Tomimatsu, Yukiko Hazama, Makoto Takeuchi, Tadashi Kimura, Koichiro Shimoya
Pregnancy requires a sophisticated immunological response through which the mother’s immune system maintains the maternal–foetal interface by developing decidua and remodelling the spiral arteries. Maternal autoantibody-mediated immune complex diseases like SLE are associated with an increased risk of adverse pregnancy outcomes, which have been partly attributed to several alterations observed at the maternal–foetal interface in these women (Magid et al. 1998; Ilekis et al. 2016). In addition, prednisolone treatment has been demonstrated to reduce the number of uterine natural killer cells (Henderson et al. 2003; Quenby et al. 2005), which are considered to play a significant role in maintaining the maternal–foetal interface (Erlebacher 2013; Moffett and Colucci 2014). Furthermore, prednisolone treatment has been reported to impair spiral artery maturation in the process of placentation (Lash et al. 2011).
T lymphocytes in the third trimester decidua in preeclampsia
Published in Hypertension in Pregnancy, 2019
Jelena Milosevic-Stevanovic, Miljan Krstic, Milan Stefanovic, Radomir Zivadinovic, Predrag Vukomanovic, Sonja Pop Trajkovic-Dinic, Slavica Stojnev
Factors affecting decidual tissue remodeling can be categorized into cellular, microenvironmental, and genetic factors. From the immunological point of view, it has long been thought that preeclampsia could be a form of maternal immune rejection of genetically foreign fetus. During implantation, invasive cytotrophoblasts express a unique combination of human leukocyte antigen (HLA) and uterine natural killer cells (u-NK) which express an unusual set of receptors that can interact with the unique combination of HLA (6). It seems that the u-NK cell and macrophage dysfunction are involved in some form of immune recognition in preeclampsia (7,8).
Are we managing women with Recurrent Miscarriage appropriately? A snapshot survey of clinical practice within the United Kingdom
Published in Journal of Obstetrics and Gynaecology, 2021
Rashmi Manning, Janani Iyer, Judith N Bulmer, Abha Maheshwari, Meenakshi Choudhary
While only a minority of the clinicians offered immune factor testing, it is crucial to emphasise that there is no clear evidence that altered peripheral blood or uterine natural killer cell levels are related to RM (Rai et al. 2005; Wold and Arici, 2005; Tuckerman et al. 2007). Additionally, offering parental peripheral blood karyotyping for all without translocation noted in miscarried tissue seems an inefficient use of NHS resources without patient benefit.