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Necrotizing Enterocolitis Risk From a Maternal-Fetal Medicine Perspective
Published in David J. Hackam, Necrotizing Enterocolitis, 2021
Mark L. Kovler, Savannah Ireland, Angie C. Jelin, Eric B. Jelin
Preeclampsia and NEC share potential common mechanistic pathways, which could explain the increased risk of NEC with preeclampsia. As mentioned, the pathophysiology of NEC is generally accepted to involve inflammation in the premature intestine and some degree of ischemia (6). Preeclampsia has similarly been linked to both fetal ischemia and a proinflammatory state. The events leading to preeclampsia occur early in pregnancy with abnormal spiral artery remodeling leading to poor placental perfusion (50). This low-flow state has been implicated in the initiation of a placental inflammatory response through up-regulation of the proinflammatory hypoxia-inducible factor 1-alpha and a predilection for proinflammatory Th17 T cells (52, 53). A quite similar cascade has been elegantly described in NEC and may help explain the link between intrauterine inflammation and postnatal NEC development (54).
Immunology of pre-eclampsia
Published in Pankaj Desai, Pre-eclampsia, 2020
This entire process of trophoblastic generation, growth and proliferation, which ultimately results in the generation of a healthy placenta needs dialogue for crosstalk between the blastocyst and the decidua. Burton and Jauniaux rightly called it “a fascinating paradigm”.2 It is well-established now that the maternal immune system and the placenta are involved in the highly choreographed crosstalk that causes adequate spiral artery remodelling, which is required for uteroplacental perfusion and the free flow of nutrients to the foetus.13
Anti-Phospholipid Antibodies and Fetal Loss-Proposed Mechanisms
Published in E. Nigel Harris, Thomas Exner, Graham R. V. Hughes, Ronald A. Asherson, Phospholipid-Binding Antibodies, 2020
Between 14 and 20 weeks of pregnancy a further wave of invasion occurs with intravascular cytotrophoblast moving down the spiral arteries in a retrograde fashion to reach their inner intramyometrial segments. Again there is destruction of maternal endothelium and of the musculo-elastic tissue of the media and deposition of fibrinoid material. The spiral arteries become funnel shaped (Figure 1) and the peripheral resistance is reduced to a minimum with a fall in diastolic BP of 70 mmHg on the radial to 10 mmHg in the spiral artery. The fall in pressure results in a reduced flow rate into the intervillous space and optimizes feto-maternal exchange.
Comparison of uterine, endometrial and subendometrial blood flows in predicting pregnancy outcomes between fresh and frozen-thawed embryo transfer after GnRH antagonist protocol: a retrospective cohort study
Published in Journal of Obstetrics and Gynaecology, 2023
Jianmei Yu, Bo Li, Haiyan Li, Qing Li, Zhen Nai, Bo Deng, Yunxiu Li
To the best of our knowledge, the radial artery is the branch of the uterine artery, which divides after passing through the myometrial–endometrial junction to form the basal arteries, supplying the basal portion of the endometrium, and the spiral arterioles that continue up toward the endometrial surface. As the spiral artery is challenging to examine, the spiral artery in the endometrium could be examined instead of the uterine artery. In the present study, uterine artery RI and endometrial thickness were significantly lower in the frozen-thawed ET group; however, in the logistic regression analysis, there was no association between endometrial thickness and uterine arterial RI between pregnancy outcomes. Prasad et al. also argued that uterine artery PSV values, S/D values, and RI could not predict pregnancy outcomes (Prasad et al.2017). Similarly, we suggest that uterine artery S/D, RI and PI could not be used alone to predict endometrial receptivity.
Advance in placenta drug delivery: concern for placenta-originated disease therapy
Published in Drug Delivery, 2023
Miao Tang, Xiao Zhang, Weidong Fei, Yu Xin, Meng Zhang, Yao Yao, Yunchun Zhao, Caihong Zheng, Dongli Sun
Special physiological conditions during pregnancy help nanodrugs to be trapped in the placenta (Valero et al., 2018). For one thing, the blood flow of the uterine artery increases sharply during pregnancy, and the resistance of flow in the blood vessel is reduced due to the distal segment expansion of the spiral artery. For another, due to the hemodynamic adjustment, maternal blood circulation volume and cardiac output increase (Burton et al., 2009). When nanodrugs were administered intravenously, high placental blood flow increased the transportation of the nanodrugs into the placenta. The nanodrugs reach the placental intervillous space through the spiral artery. The blood flow velocity in the intervillous space decreases rapidly to 10 times lower than that in the uterine artery, prolonging the contact time between the nanodrugs and the chorionic villi, as well as the SCT (Burton et al., 2009). The outer side of the apical membrane of the SCT is a brush-like structure with a large surface area, increasing the possibilities of nanodrugs internalization and local drug release (Arumugasaamy et al., 2020). Furthermore, transport proteins in the apical membrane, such as ATP-binding cassette (ABC) and solute carrier protein (SLC) transport proteins, might be utilized as efficient tools for the delivery or efflux of nanodrugs (Figure 2B) (Arumugasaamy et al., 2020). Overall, the nanodrugs may take advantages of the placental structure, the placental hemodynamics as well as the transporters for placenta-originated disease therapy.
Triggering receptor expressed on myeloid cells (TREM) like transcript-1 (TLT-1) reveals platelet activation in preeclampsia
Published in Platelets, 2022
Linyan He, Yawen Zhang, Chunqi Hou, Ziling Zhu, Qi He, Qin Huang, Shundong Ji
The pathogenesis of preeclampsia is not fully elucidated but tremendous progress has been made over the past decade. The placenta has always been a critical figure in the etiology of preeclampsia because the removal of the placenta is necessary for symptoms to regress [4]. The abnormal spiral artery remodeling has been documented to be the central pathogenic factor in pregnancies complicated by intrauterine growth restriction, gestational hypertension, and preeclampsia [5]. Placental endotheliopathy is the root cause of preeclampsia and disseminates systemically to the maternal circulation. The shift has been made to view preeclampsia as a systemic disease with widespread endothelial damage and the potential to affect future cardiovascular diseases rather than a self-limited occurrence [6].