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Impaired fibrinolysis in the pathogenesis of dengue hemorrhagic fever.

By E. van Gorp, T.E. Setiati, A.T. Mairuhu, C. Suharti, H.H. Cate, W.M.V. Dolmans, J.W.M. van der Meer, C.E. Hack and D.P. Brandjes

Abstract

Item does not contain fulltextThe mechanisms contributing to bleeding complications in dengue hemorrhagic fever were studied by investigating the pattern of activation of the coagulation and fibrinolytic systems in 50 children with severe dengue hemorrhagic fever. Thirteen patients (26%) died, and activation of coagulation was most pronounced in the deceased group. Fibrinolysis was also activated, but this activation was relatively weak compared with that of coagulation as a result of persistently high plasminogen activator inhibitor levels. Plasminogen activator inhibitor also prevented a switch from the procoagulant to the profibrinolytic state in lethal dengue hemorrhagic fever, which was further enhanced by an acquired protein C deficiency. The present study is the first to demonstrate such a mechanism in a viral infection. This imbalance between coagulation and fibrinolysis may be used as a prognostic marker, but it may also be a target for future therapeutic intervention

Topics: The role of cytokines in the pathophysiology of febrile illnesses and in host defense against infections, De rol van cytokinen in de pathofysiologie van koortsende ziekten en in de afweer tegen infecties
Publisher: 'Wiley'
Year: 2002
DOI identifier: 10.1002/jmv.10137
OAI identifier: oai:repository.ubn.ru.nl:2066/185362
Provided by: Radboud Repository
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