Seminars in thrombosis and hemostasis
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Semin. Thromb. Hemost. · Sep 2014
ReviewAging hemostasis: changes to laboratory markers of hemostasis as we age - a narrative review.
The incidence of venous thromboembolism (VTE) is well recognized to increase with aging. Concurrently, the plasma concentrations of many coagulation factors (e.g., fibrinogen, factor [F] V, FVII, FVIII, and FIX) increase with aging, as does von Willebrand factor (VWF), thrombin generation, and platelet activation. Data are conflicting regarding age-related changes in the natural anticoagulants, including protein C, protein S, and antithrombin. ⋯ A variety of acquired prothrombotic risk factors (e.g., cancer, autoimmune disorders, and diabetes) also gradually develop with aging, some of which may induce profound abnormalities of hemostasis, and confound the age-related changes in hemostasis, as well as their influence on thrombotic risk. In this article, we review the changes in hemostasis markers measurable within many hemostasis laboratories, and consider many of the important implications for clinical and laboratory practice. Apart from representing an increased thrombotic risk, additional considerations entail the potential need (1) to utilize age-adjusted normal ranges (e.g., for D-dimer), (2) to consider the consequence on previous diagnoses (e.g., "mild type 1" von Willebrand disease [VWD], where VWF test results may "normalize" with aging), and (3) to consider the effect of these changes of risk factors on the (perceived) therapeutic efficacy of antithrombotic medications such as aspirin.
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Semin. Thromb. Hemost. · Sep 2014
ReviewA review of the value of D-dimer testing for prediction of recurrent venous thromboembolism with increasing age.
Recurrent thrombosis is a relatively frequent complication of venous thromboembolism (VTE) and represents an important cause of clinical and economic issues for health care systems worldwide. Rates of thrombosis increase with increasing age, with aging recognized to be a risk factor for thrombosis. ⋯ Convincing evidence has now been provided that while D-dimer values may be effectively utilized for predicting the risk of recurrent thrombosis with increasing age, conventional cutoff values are inappropriate for older populations. In summary, analysis of the current scientific literature suggests that the adoption of age-dependent thresholds may increase the diagnostic effectiveness of this biomarker with increasing age.
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Semin. Thromb. Hemost. · Mar 2014
ReviewExternal quality assessment/proficiency testing and internal quality control for the PFA-100 and PFA-200: an update.
Platelet function testing is an essential component of comprehensive hemostasis evaluation within the framework of bleeding and/or bruising investigations, and it may also be performed to evaluate antiplatelet medication effects. Globally, the platelet function analyzer (PFA)-100 (Siemens Healthcare, Marburg, Germany) is the most used primary hemostasis-screening instrument and has also been recently remodeled/upgraded to the PFA-200. The PFA-100 is sensitive to a wide range of associated disorders, including platelet function defects and von Willebrand disease (VWD), as well as to various antiplatelet medications. ⋯ Interpretations are also in general consistent with expectations and test data provided by laboratories. The EQA created material has also been assessed within the context of possible IQC material. In conclusion, EQA and IQC processes for the PFA-100/PFA-200 have been developed that include highly reproducible test challenge processes, not only supporting the concept that EQA/IQC is possible for platelet function testing but also providing a valuable mechanism for monitoring and improving laboratory performance in this area.
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Semin. Thromb. Hemost. · Nov 2013
ReviewIntracerebral bleeding in patients on antithrombotic agents.
Patients treated with oral anticoagulants (OAC) carry a 7- to 10-fold higher risk of intracerebral hemorrhage (ICH) than patients without OAC. ICH related to oral anticoagulation (OAC-ICH) is a particularly severe form of stroke. The overall incidence of OAC-ICH ranges between 2 and 9 per 100,000 population/year and is expected to increase as the number of patients treated with OAC rises. ⋯ Factors that mediate worse outcome in OAC-ICH are more frequent and prolonged secondary hematoma enlargement and intraventricular hemorrhage, The current concept of emergency treatment in OAC-ICH is rapid restoration of effective coagulation using hemostatic factors such as prothrombin complex concentrate, fresh frozen plasma, factor IX concentrates, and recombinant factor VIIa in addition to vitamin K. Emergency management of ICH under treatment with the new direct OAC is a major challenge. In the absence of specific antidotes, prothrombin concentrates are recommended mainly on the basis of preclinical data.
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Polytraumatic injury results in tissue factor (TF) release from damaged cells. The acute coagulopathy of trauma (ACT) occurs early and results from significant tissue injury and tissue hypoperfusion. ACT is augmented by therapies resulting in acidemia, hypothermia, and hemodilution contributing to trauma-induced coagulopathy. ⋯ TBI has also recently been shown to cause platelet dysfunction. Platelet receptor inhibition prevents cellular initiation and amplification of the clotting cascade, limiting thrombin incorporation, and stabilization of clot to stop hemorrhage. Therefore, head injury in the presence of polytrauma does appear to augment ACT and warrants close monitoring and appropriate intervention.