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pubmed-article:15118525pubmed:abstractTextCoagulation activation is part of the acute innate host response to infection that, when uncontrolled, may contribute to organ dysfunction and death. Activated protein C limits excessive coagulation activation by inactivating factors Va and VIIIa. The factor V Leiden mutation (R506Q), a prothrombotic gene polymorphism, disrupts the activity of this natural anticoagulant by rendering factor Va partially resistant to inactivation by activated protein C. Previous findings in the mouse factor V Leiden endotoxemia model and in patients with severe sepsis suggest that factor V Leiden constitutes a rare example of a balanced gene polymorphism that may provide a survival advantage for heterozygous carriers with severe sepsis. We sought to confirm that carriers of this prothrombotic factor V Leiden mutation do not have an increased risk of developing severe sepsis and that carriers with severe sepsis derive similar treatment benefit from recombinant human activated protein C (drotrecogin alfa [activated]) as non-factor V Leiden carriers.lld:pubmed
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pubmed-article:15118525pubmed:articleTitleEffect of factor V Leiden polymorphism in severe sepsis and on treatment with recombinant human activated protein C.lld:pubmed
pubmed-article:15118525pubmed:affiliationLilly Research Laboratories, Indianapolis, IN, USA.lld:pubmed
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