View clinical trials related to Coagulation.
Filter by:The understanding of haemostasis and inflammation cross-talk has gained considerable knowledge during the past decade in the field of arterial and venous thrombosis. Complex and delicately balanced interaction between coagulation and inflammation involve all cellular and humoral components. Elements of the coagulation system such as activated thrombin, fibrinogen or factor Xa may increase inflammation by promoting the production of proinflammatory cytokines, chemokines, growth factors and adhesion molecules that lead to a procoagulant state amplifying the pathological process. Recent evidence supports inflammation as a common pathogenic contributor to both arterial and venous thrombosis, giving rise to the concept of inflammation induced thrombosis. Patients with infection of COVID-19 and severe pneumoniae seem to have higher risk of thromboembolism. The purpose of this project is to analyze hemostasis and coagulation of every hospitalized patient with infection of COVID-19. Blood sample for coagulation and hemostasis analysis will be collected on every patient hospitalized in Amiens hospital for COVID-19 infection. Thrombin time, factors V and II, fibrin/fibrinogen degradation products, antithrombin will be assessed every week. Anticardiolipin, anti-beta2 glycoprotein I and anti-annexin A2 antibodies IgG and IgM at day of admission and at fourth week after admission will be assessed. SARS-CoV2 viral load and serodiagnosis will be performed at the same time. At the same time venous ultrasound to diagnose thrombosis will be performed.
The understanding of haemostasis and inflammation cross-talk has gained considerable knowledge during the past decade in the field of arterial and venous thrombosis. Complex and delicately balanced interaction between coagulation and inflammation involve all cellular and humoral components. Elements of the coagulation system such as activated thrombin, fibrinogen or factor Xa may increase inflammation by promoting the production of pro-inflammatory cytokines, chemokines, growth factors and adhesion molecules that lead to a procoagulant state amplifying the pathological process. Recent evidence supports inflammation as a common pathogenic contributor to both arterial and venous thrombosis, giving rise to the concept of inflammation-induced thrombosis. Patients with infection of COVID-19 and severe pneumoniae seem to have higher risk of thromboembolism. Very few data are available regarding the biological disorders of coagulation in these patients. Th purpose of this project is to analyze hemostasis and coagulation of patients with infection of COVID-19 and severe pneumonia.
The goal of this proposal is to prospectively collect data from a series of 100 patients (all ages) undergoing complex cardiac surgical procedures involving cardiopulmonary bypass (CPB) to: 1. Measure the number of blood activated circulating monocytes before, during and after cardiac surgery and serum GABA and pro-inflammatory cytokine levels 2. Understand the correlation between GABA and inflammatory cytokines (and/or activated monocytes) and 3. Assess the correlation between thrombosis and monocyte activation in patients undergoing cardiac surgery under CPB and at risk of thrombosis.
Coagulation within the dialyzer membrane fibres is an obvious biological sign of bio-incompatibility. To avoid clotting during extracorporeal treatment, an anticoagulant is added to the circuit, resulting in an increased risk for bleeding complications. In addition, there is evidence that a substantial number of fibers can become blocked before this is reflected in routinely observed parameters, or in termination of the dialysis session. Little is known about the impact of such subclinical clotting on dialyzer performance in terms of solute clearance. Membrane clogging due to deposition of proteins and red blood cells on the dialysis membrane may influence both the diffusive and convective transport characteristics of the dialyzer membrane before leading to complete dialyzer clotting. In 2018, the invesitgators described a method to objectively count the number of blocked fibres inside a dialyzer using a micro-CT scanning technique. In the present trial, the investigators use this method to assess the resistance of the dialyzer to clotting, and to evaluate the impact of subclinical fibre blocking on solute removal and thus performance of a dialyzer during a dialysis session. The aim of this randomized cross-over study is to objectively quantify the performance of different dialyzer membranes: ATA™ membrane in the Solacea™ dialyzer, polysulfone membrane in the FX800 dialyzer, and the heparin-coated AN membrane in the Evodial dialyzer, and this with different anticoagulation strategies.
A randomized study is to learn more about how a supplement called DHEA (dehydroepiandrosterone) affects clotting factors in women taking combined oral contraceptive pills. Current research suggests that the progestin hormone in a specific type of birth control pill may increase a woman's blood clot risk. However, it is unknown exactly how the progestin causes the increased risk. This study aims to learn if taking a daily dose of supplemental androgen (dehydroepiandrosterone, or DHEA) in addition to birth control pills containing DRSP affects proteins related to coagulation.
This study aims to evaluate whether dietary supplementation with fish oil can protect against the cardiopulmonary alterations linked to air pollution
This study will establish reference range intervals for the Quantra System, a next-generation diagnostic platform that provides whole blood coagulation testing at the point-of-care.
This study is intended to define the PCM normal laboratory range.
The investigators will define procoagulant properties of packed red blood cells and investigate whether packed red blood cells from certain donor populations are prone to induce procoagulant states.
The purpose of this study is to evaluate the effects of pharmacologic FXa inhibition (via edoxaban 30 mg daily) on inflammation, as reflected in plasma Interleukin-6 levels.