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Antepartum haemorrhage
Published in David M. Luesley, Mark D. Kilby, Obstetrics & Gynaecology, 2016
Disseminated intravascular coagulation represents a cascade of events which can vary in severity, and range from a compensated state with only laboratory evidence of increased coagulation and fibrinolytic factor turnover, through to massive uncontrollable haemorrhage with very low concentrations of plasma fibrinogen, raised fibrin degradation products (FDPs) and thrombocytopenia. The evolution of events leading to DIC is shown in Fig. 46.2. End-organ damage is caused by hypotension, fibrin-platelet clump deposition in small vessels, and persisting endothelial damage leading to increased vascular permeability.
Evidence for an enhanced procoagulant state in remitted major depression
Published in The World Journal of Biological Psychiatry, 2020
Roland von Känel, Franziska Merz, Hildegard Pfister, Tanja Brückl, Petra Zimmermann, Manfred Uhr, Florian Holsboer, Nina Höhne, Marcus Ising
To elucidate the role of haemostatic function in the link between depression and CHD further, studies must take into account a complex network of pathophysiologic processes, which include platelet, coagulation, anticoagulation and fibrinolysis pathways (Borissoff et al. 2011). Specifically, an enhanced procoagulant state due to platelet hyperactivity, coagulation activation, hypofibrinolysis and decreased endothelium anticoagulant function plays a key role in the initiation and progression of atherothrombotic cardiovascular disease (CVD) (Borissoff et al. 2010, 2011; Abbate et al. 2012; Loeffen et al. 2012). Fibrinogen, D-dimer, von Willebrand factor (VWF) and plasminogen activator inhibitor (PAI)-1, the major endogenous anti-fibrinolytic factor, are critically involved in the pathophysiology of CVD (Kaplan et al. 1990; Vaughan 2005; Wu et al. 2017). Elevated circulating levels of these haemostatic factors have shown to be associated with an increased risk of incident CHD and MI, independent of traditional cardiovascular risk factors (Willeit et al. 2013; Fibrinogen Studies Collaboration 2015; Jung et al. 2018). Increased levels of fibrinogen (Maes et al. 1997; Wium-Andersen et al. 2013), D-dimer (Dentino et al. 1999), VWF (Bot et al. 2015; Lopez-Vilchez et al. 2016) and PAI-1 (Eskandari et al. 2005; Lahlou-Laforet et al. 2006), as well as excessive platelet activation (Dietrich-Muszalska and Wachowicz 2017), have been shown in patients with current MDD compared to controls, and in relation to the severity of depressive symptoms.
NF-κB p65 Knock-down inhibits TF, PAI-1 and promotes activated protein C production in lipopolysaccharide-stimulated alveolar epithelial cells type II
Published in Experimental Lung Research, 2018
Bo Liu, Yanqi Wu, Yahui Wang, Yumei Cheng, Ling Yao, Yuqin Liu, Hong Qian, Huilin Yang, Feng Shen
To further evaluate the effects of p65 gene-silencing on secretions of coagulation and fibrinolytic factor in AECII, we measure TF, PAI-1 and APC concentrations in cell-supernatant using enzyme-linked immunosorbent assay (ELISA). After 24 hrs of LPS stimulation, rat AECII released substantial TF and PAI-1 proteins and little APC production. Intervention with p65 siRNA transfection obviously reversed these three protein levels in supernatant induced by LPS treatment (Figure 3).
The critically low levels of vitamin D predicts the resolution of the ST-segment elevation after the primary percutaneous coronary intervention
Published in Acta Cardiologica, 2023
Hassan Javadzadegan, Ahmad Separham, Aidin Farokhi, Camille Applegate, Nader D. Nader
Moreover, there was an inverse relationship between serum vitamin D level and serum levels of PAI-1 and tpA. PAI-1 is a crucial anti-fibrinolytic factor in the coagulation system. The serum tpA rate is an index of endothelial dysfunction rather than an indicator of fibrinolytic activity [31].