Seminars in thrombosis and hemostasis
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Semin. Thromb. Hemost. · Jan 1998
Review Clinical Trial Controlled Clinical TrialHyperhomocysteinemia and venous thrombosis.
In recent years hyperhomocysteinemia has been established as a new risk factor for neural tube defects, arterial cardiovascular disease, and venous thrombosis. Concerning vascular problems, it first became clear that hyperhomocysteinemia might be (though not proven) a risk factor for arterial disease as observed in case-control studies, as well as in prospective analysis. More recently, the subject of hyperhomocysteinemia and venous thrombosis has received much attention. ⋯ Briefly, the possible mechanisms of how hyperhomocysteinemia can lead to venous thrombosis are discussed. The article ends with therapeutic options to treat hyperhomocysteinemia (hyperhomocysteinemia can easily be treated with vitamins) and the description of a study that is presently being undertaken in an international multicenter design. This placebo-controlled study might resolve the question of whether lowering of homocysteine levels is of any clinical relevance in preventing recurrent venous thrombosis.
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Semin. Thromb. Hemost. · Jan 1998
ReviewRapid D-dimer assays to exclude deep venous thrombosis and pulmonary embolism: current status and new developments.
Studies measuring the fibrin degradation product D-Dimer (DD) using enzyme-linked immunosorbent assays (ELISA) in patients suspected of deep venous thrombosis (DVT) or pulmonary embolism (PE) suggest that it is possible to exclude DVT/PE when the DD level is below a certain cut-off value. However, ELISA methods are time-consuming, bare high costs, and are only available in experienced laboratories. For this reason several rapid and less costly DD assays have been recently developed. ⋯ As for standard ELISA, increased DD concentrations are of no use because of the low specificity of the assays. Future studies should assess the clinical usefulness of both assays in management trials under routine conditions, in the frame of clinical decision-making diagnostic processes to prove that withholding further noninvasive testing and/or anticoagulants in patients with a low or negative DD is safe. Strategies to identify patients with false-negative results should be developed.
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Semin. Thromb. Hemost. · Jan 1998
ReviewClinical experience with antithrombin III concentrates in critically ill patients with sepsis and multiple organ failure.
Despite improvements in critical care medicine and the development and aggressive use of potent broad-spectrum anti-microbial agents, mortality due to severe sepsis has not changed during the recent years and still comes to 35% to 45%. For quite a long time our understanding of the pathophysiology of sepsis was mainly focused on endotoxin and proinflammatory cytokines like tumor necrosis factor or interleukin-1. Now it is generally accepted that many signs and symptoms of sepsis are not directly mediated by cytokines but are transmitted through other mediator systems. ⋯ Antithrombin III is an important inhibitor of the intrinsic, extrinsic and common pathway of coagulation. Recently, evidence has been accumulating that there is an additional anti-inflammatory potential of the drug. Currently there are several clinical trials ongoing to investigate whether this effect is of clinical relevance in the treatment of patients with severe sepsis.
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When the need for surgery arises, temporary interruption of long-term anticoagulation exposes patients to additional thrombotic risk. There is no consensus as to how perioperative anticoagulation should be managed in this setting. Based on an individual assessment of risk factors for arterial or venous thromboembolism and the risk of postoperative bleeding, this review outlines an approach to the perioperative management of anticoagulation that is designed to optimize patient safety and efficient delivery of health care. ⋯ In the postoperative period, this approach is generally reserved for patients with an episode of venous thromboembolism in the preceding 3 months, and patients with an episode of arterial embolism in the preceding month who have a low risk of bleeding. Differences in the approach to management of anticoagulation before and after surgery relate to the fact that surgery is an important risk factor for venous, but not arterial, thromboembolism, and that recent surgery greatly increases the risk of anticoagulant-induced bleeding. Subcutaneous unfractionated or low-molecular-weight heparin, in doses recommended to prevent venous thromboembolism in high-risk surgical patients, should be administered to in-patients who have a lesser risk of thromboembolism until oral anticoagulation is reestablished.
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Semin. Thromb. Hemost. · Jan 1998
ReviewDerangements of coagulation and fibrinolysis in critically ill patients with sepsis and septic shock.
In patients with sepsis and septic shock, both coagulation and fibrinolysis are activated frequently leading to the syndrome of diffuse intravascular coagulation (DIC). The different mechanisms leading to abnormalities in coagulation and fibrinolysis are discussed in detail. The coagulation and fibrinolytic system appear to be influenced by the septic process largely independently, leading to a procoagulant imbalance between these systems. ⋯ Although levels of plasminogen activator antigen are increased, its activity is almost completely inhibited by PAI-1. The resulting effects predispose to a procoagulant state, with widespread fibrin deposition, which may be an important mechanism contributing to multiple organ failure. A thorough understanding of the pathophysiological mechanisms underlying the DIC-syndrome is a prerequisite for a rational approach and future therapy for this severe complication of sepsis.