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      The effect of antithrombin on the systemic inflammatory response in disseminated intravascular coagulation.

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          Abstract

          Sepsis and major trauma are the two most common causes of disseminated intravascular coagulation (DIC) and are characterized by a sudden increase in inflammatory mediators. In general, the outcome of the patient is determined by the degree of the inflammatory response. In severe cases of sepsis and trauma, cascade systems, such as the coagulation, fibrinolytic and complement systems, are activated beyond the capacity of the autoregulatory mechanisms. During DIC, plasma levels of antithrombin (AT)--a serine protease inhibitor that acts mainly on the serine proteases of the coagulation system--decrease due to the formation and subsequent elimination of complexes between AT and activated coagulation factors. The consumption of AT may start a vicious circle by facilitating further intravascular fibrin formation, followed by ischaemic tissue injury and accelerated activation of blood coagulation. Infusion of AT has an anti-inflammatory effect through its ability to counteract microvascular thrombosis. Furthermore, AT induces the release of prostacyclin from the vessel wall by binding to glycosaminoglycans on the surface of endothelial cells. Prostacyclin has a marked anti-inflammatory effect as a result of its inhibitory effect on neutrophils, monocytes and platelets.

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          Author and article information

          Journal
          Blood Coagul. Fibrinolysis
          Blood coagulation & fibrinolysis : an international journal in haemostasis and thrombosis
          0957-5235
          0957-5235
          Nov 1998
          : 9 Suppl 3
          Affiliations
          [1 ] Coagulation Laboratory and Thrombosis Centre, Copenhagen County Hospital in Gentofte, Hellerup, Denmark. jdn@dadlnet.dk
          Article
          10102494
          5bd6b277-5a58-4d29-8411-33964f43114b
          History

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