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Most Used Journals
Category Archives: Semin Thromb Hemost
Extrahemostatic Functions of Platelets and Coagulation Factors.
Semin Thromb Hemost. 2018 Mar;44(2):89-90
Authors: Preston RJS, Lisman T
PMID: 29471579 [PubMed – in process]
Platelets as Modulators of Liver Diseases.
Semin Thromb Hemost. 2017 Sep 12;:
Authors: Lisman T, Luyendyk JP
PMID: 28898899 [PubMed – as supplied by publisher]
Hemostatic Complications in Hepatobiliary Surgery.
Semin Thromb Hemost. 2017 Jun 13;:
Authors: Bos S, Bernal W, Porte R, Lisman T
PMID: 28609799 [PubMed – as supplied by publisher]
Decreased Plasma Fibrinolytic Potential As a Risk for Venous and Arterial Thrombosis.
Semin Thromb Hemost. 2016 Jul 29;
Authors: Lisman T
It has been well established that inherited or acquired hypercoagulability is a risk factor for venous thrombosis. In addition, hypercoagulability may contribute to the risk of arterial events. Much less is known regarding the role of the fibrinolytic system in the risk of thrombotic disease, which partly relates to the lack of validated assays. A plasma-based global fibrinolysis assay, which is sensitive to plasma levels of plasminogen, regulators of fibrinolysis, and proteins involved in coagulation, has been used in large epidemiological studies to assess the role of fibrinolysis in thrombosis. It has been demonstrated that a hypofibrinolytic state increases the risk of a first venous thrombosis, but not of a recurrence. This increased risk of venous thrombosis associated with plasma hypofibrinolysis appears primarily driven by elevated plasma levels of thrombin-activatable fibrinolysis inhibitor and plasminogen activator inhibitor type 1. The combination of hypercoagulability and hypofibrinolysis synergistically enhances the risk of a first venous event. Plasma hypofibrinolysis may constitute a risk factor for the postthrombotic syndrome. Decreased fibrinolytic potential is also associated with an increased risk of arterial thrombosis, but only in individuals younger than 55 years. The association between hypofibrinolysis and myocardial infarction appears primarily driven by elevated levels of α2-antiplasmin. Although recent studies have clearly demonstrated a role of the fibrinolytic system in thrombotic disease, the clinical utility of plasma-based clot lysis assays is probably limited.
PMID: 27472427 [PubMed – as supplied by publisher]
Hemostatic Dysfunction in Liver Diseases.
Semin Thromb Hemost. 2015 Jul;41(5):445-446
Authors: Lisman T, Kwaan HC
PMID: 26126004 [PubMed – as supplied by publisher]
Rebalanced Hemostasis in Patients with Acute Liver Failure.
Semin Thromb Hemost. 2015 Jun 6;
Authors: Lisman T, Stravitz RT
Patients with acute liver failure (ALF) have substantial alterations in their hemostatic system. Since an international normalized ratio of ≥ 1.5 is part of the definition of the syndrome, it has long been believed that patients with ALF had a hemostasis-related bleeding tendency. Recent data, however, show that spontaneous bleeding in ALF is rare. In addition, thrombotic complications may be more common than spontaneous bleeding complications. Laboratory studies have suggested that patients with ALF may be in hemostatic balance as a result of a commensurate decline in pro- and anti-hemostatic factors. The unstable nature of the hemostatic balance in ALF may explain the occurrence of both bleeding and thrombotic complications. The hemostatic profile of patients with ALF includes hypercoagulable features, including von Willebrand factor/a disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13 unbalance, elevated levels of highly procoagulant, platelet-derived microparticles, and a profound hypofibrinolytic status. These hypercoagulable features may contribute to systemic thrombotic complications, but may also drive intrahepatic clot formation. Studies in experimental animal models of ALF have demonstrated that intrahepatic clot formation contributes to disease progression. The clinical consequences of these new insights in the hemostatic system of patients with ALF will be discussed in this review.
PMID: 26049071 [PubMed – as supplied by publisher]
Vascular Disease in Patients with Nonalcoholic Fatty Liver Disease.
Semin Thromb Hemost. 2015 Jun 6;
Authors: Potze W, Siddiqui MS, Sanyal AJ
Nonalcoholic fatty liver disease (NAFLD) is incre… Continue reading