Journal of thrombosis and haemostasis : JTH
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Tranexamic acid (TXA) reduces blood loss by inhibiting the enzymatic breakdown of fibrin. It is often used in surgery to decrease bleeding and the need for blood transfusion. In 2011, results from a multi-center, randomized, and placebo-controlled trial (CRASH-2 trial) showed that TXA (1 g loading dose over 10 min followed by an infusion of 1 g over 8 h) safely reduces mortality in bleeding trauma patients. ⋯ Because it does not have any serious adverse effects, TXA can be administered to a wide spectrum of bleeding trauma patients. Limiting its use to the most severely injured or those with a diagnosis of 'hyperfibrinolysis' would result in thousands of avoidable deaths. A clinical trial (CRASH-3 trial) of TXA in patients with traumatic brain injury is now in progress.
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J. Thromb. Haemost. · Jun 2015
Comparative StudyQualitative point-of-care D-dimer testing compared with quantitative D-dimer testing in excluding pulmonary embolism in primary care.
General practitioners can safely exclude pulmonary embolism (PE) by using the Wells PE rule combined with D-dimer testing. ⋯ Combined with the Wells PE rule, both tests are safe to use in excluding PE. The quantitative test seemed to be safer than the POC test, albeit not statistically significant. The specificity of the POC test was higher, resulting in more patients in whom PE could be excluded.
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J. Thromb. Haemost. · Jun 2015
Multicenter StudyRecombinant factor VIII Fc fusion protein for the prevention and treatment of bleeding in children with severe hemophilia A.
Prophylactic factor replacement, which prevents hemarthroses and thereby reduces the musculoskeletal disease burden in children with hemophilia A, requires frequent intravenous infusions (three to four times weekly). ⋯ Twice-weekly infusions with rFVIIIFc were well tolerated and yielded low bleeding rates in children with severe hemophilia A.
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J. Thromb. Haemost. · Jun 2015
ReviewDysfibrinogenemia: from molecular anomalies to clinical manifestations and management.
Congenital dysfibrinogenemia is a qualitative congenital fibrinogen disorder characterized by normal antigen levels of a dysfunctional fibrinogen. The diagnosis is usually based on discrepancies between fibrinogen activity and antigen levels, but could require more specialized techniques for the assessment of fibrinogen function, owing to some limitations in routine assays. Molecular abnormalities, which are frequently heterozygous missense mutations localized in exon 2 of FGA and exon 8 of FGG, lead to defects in one or more phases of fibrinogen to fibrin conversion, fibrin network formation, and other important functions of fibrinogen. ⋯ Functional analysis of polymerization and fibrinolysis, structural studies of the fibrin network and the viscoelastic properties of fibrin clot could help to predict the phenotype of congenital dysfibrinogenemia, but have not yet been evaluated in detail. The management is essentially based on personal and family history; however, even individuals who are still asymptomatic and without a family history should be carefully assessed and monitored. Particular situations, such as pregnancy, delivery, and surgery, require a multidisciplinary approach.
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J. Thromb. Haemost. · Jun 2015
ReviewTACTIC: Trans-Agency Consortium for Trauma-Induced Coagulopathy.
Trauma-induced coagulopathy (TIC) includes heterogeneous coagulopathic syndromes with different underlying causes, and treatment is challenged by limited diagnostic tests to discriminate between these entities in the acute setting. We provide an overview of progress in understanding the mechanisms of TIC and the context for several of the hypotheses that will be tested in 'TACTIC'. ⋯ We do anticipate that 'early translation' of promising results will occur. Functions anticipated at this early translational level include: (i) basic science groundwork for future therapeutic candidates; (ii) development of acute coagulopathy scoring systems; (iii) coagulation factor composition-based computational analysis; (iv) characterization of novel analytes including tissue factor, polyphosphates, histones, meizothrombin and α-thrombin-antithrombin complexes, factor XIa, platelet and endothelial markers of activation, signatures of protein C activation and fibrinolysis markers; and (v) assessment of viscoelastic tests and new point-of-care methods.