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Platelet activation in hemolytic uremic syndrome
Lunds universitet.
Lunds universitet.
Lunds universitet.
Lunds universitet.
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2006 (Engelska)Ingår i: Seminars in Thrombosis and Hemostasis, ISSN 0094-6176, E-ISSN 1098-9064, Vol. 32, nr 2, s. 128-145Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

Platelet consumption in platelet-fibrin aggregates leading to thrombocytopenia and small vessel obstruction are major features of the hemolytic uremic syndrome (HUS). Although thrombocytopenia has been correlated to poor prognosis, the mechanisms by which thrombocytopenia develops in HUS have not been completely elucidated. However, plausible explanations have been platelet contact with thrombogenic surfaces and/or direct contact with an aggregating agent. This article summarizes several mechanisms of platelet activation, interactions with leukocytes, chemokine release, complement activation, and antimicrobial defense. Specific mechanisms are outlined by which platelets may be activated, leading to thrombocytopenia during HUS. In diarrhea-associated HUS Shiga toxin has been shown to injure the endothelium, thus exposing the subendothelium, releasing tissue factor, and rendering the vessel wall prothrombotic. Shiga toxin also binds to and activates platelets. The toxin may activate endothelial cells and platelets simultaneously. In atypical HUS the alternative complement pathway is activated because of mutations in complement regulatory proteins. Mutated factor H does not bind to endothelium and platelets efficiently, enabling complement activation on these cells. In thrombotic thrombocytopenic purpura, intravascular platelet clotting Occurs due to dysfunction of the von Willebrand factor (VWF)-cleaving protease ADAMTS13. Thrombi are formed by binding of platelets to ultralarge VWF multimers.

Ort, förlag, år, upplaga, sidor
2006. Vol. 32, nr 2, s. 128-145
Nyckelord [en]
Shiga toxin; complement; enterohaemorrhagic Escherichia coli; haemolytic uraemic syndrome; microvesicles
Nationell ämneskategori
Cell- och molekylärbiologi Immunologi inom det medicinska området
Identifikatorer
URN: urn:nbn:se:hkr:diva-12661DOI: 10.1055/s-2006-939769ISI: 000236558600008PubMedID: 27723152OAI: oai:DiVA.org:hkr-12661DiVA, id: diva2:739695
Tillgänglig från: 2014-08-21 Skapad: 2014-08-21 Senast uppdaterad: 2018-01-11Bibliografiskt granskad

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Vaziri-Sani, Fariba

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Seminars in Thrombosis and Hemostasis
Cell- och molekylärbiologiImmunologi inom det medicinska området

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