View clinical trials related to Coagulation Factor Deficiency.
Filter by:The goal of this observational study is to learn about the changes in coagulation factor VIII and IX levels in patients undergoing liver transplantation to help guide future management of coagulation factor replacement in patients with hemophilia and liver disease. The question we aim to answer is: should the recommendations for factor replacement in patients with hereditary bleeding disorders be altered in the setting of end stage liver cirrhosis? Participants will be asked to provide two blood samples, one at the beginning of their liver transplant, and one after their liver transplant.
Critically ill patients with spontaneously prolonged pro-thrombin time, where administration of intravenous administration of phytomenadione (vitamin K) has been ordered by the treating physician will be identified. After signed informed consent baseline samples will be collected. Phytomenadione will be given and 24 hours after administration new blood samples will be collected. Several different advanced coagulation and vitamin K-assays will be performed before and 24 hours after vitamin K administration.
Hemorrhagic and thromboembolic complications are common in Veno-venous ECMO therapy. The aim of this study is to provide a detailed analysis of the activity of different coagulation factors and changes in functional coagulation measurements as in rotational thrombelastometry and multiple electrode aggregometry in the course of ECMO therapy.
Coagulation factor XIII (FXIII), a plasma transglutaminase, is known as the final enzyme of the coagulation cascade, responsible for a cross-linking of fibrin to strengthen blood clot. It also minimizes fibrin degradation by its cross-linking it with alfa2-antiplasmin molecules. It has been found that similar to plasma fibrinogen level, FXIII activity can be reduced in the early phase of severe trauma. Therefore, its immediate substitution is of potential therapeutic interest in trauma-induced coagulopathy. However, unlike plasma fibrinogen level evaluation, measurement of the FXIII activity is not routinely available. Therefore, targeted substitution of FXIII is practically impossible. The plasma fibrinogen level is routinely measured in severe trauma patients. Based on pathophysiologic assumptions and a limited number of published data we hypothesize that the FXIII activity correlates with fibrinogen level. In such case, indirect FXIII activity prediction by fibrinogen level measurement would be a convenient approach to enable FXIII targeted substitution. Therefore we decided to perform a prospective observational clinical trial to determine whether the low plasma fibrinogen level in severe trauma correlates with decreased FXIII activity.
Blood coagulation is a complex mechanism that is required for the rapid establishment of a stable fibrin clot. A series of interdependent enzyme-mediated reactions translate the molecular signals that initiate blood coagulation into the formation of the fibrin clot. Congenital coagulopathies result when there is a deficiency of protein co factors and enzymes implicated in blood coagulation