Literature DB >> 16961586

Prothrombotic factors enhance heparin-induced thrombocytopenia and thrombosis in vivo in a mouse model.

M P Reilly1, S M Taylor, C Franklin, B S Sachais, D B Cines, K J Williams, S E McKenzie.   

Abstract

BACKGROUND: Heparin-induced thrombocytopenia/thrombosis (HIT/T) is a common cause of life- and limb-threatening thrombosis. The development of antibodies that react with complexes of heparin and platelet factor 4 (PF4) is fundamental to the development of the disease. However, anti-PF4/heparin antibodies are far more common than is HIT/T and there is less understanding of the factors that contribute to thrombosis in only a subset of patients.
OBJECTIVES: Both qualitative and quantitative differences in multiple factors (e.g. antibodies, heparin and platelets) may influence the clinical course of patients who develop anti-PF4/heparin antibodies. We examined the hypothesis that host-specific factors, such as comorbid prothrombotic conditions, would exacerbate the pathologic effects of anti-PF4/heparin antibodies. METHODS AND
RESULTS: A mouse model transgenic for human Fcgamma RIIa and PF4 and null for mouse PF4 was used to study the influence of prothrombotic conditions on the effects of anti-PF4/heparin antibodies in vivo. To simulate a prothrombotic milieu, mice were fed a hypercholesterolemic diet (HD). HD-fed mice had elevated plasma cholesterol, increased platelet reactivity and increased endothelial activation relative to mice fed a standard diet (SD). Age- and sex-matched mice from each diet group were treated with an anti-PF4/heparin antibody and heparin. HD-fed mice developed more severe thrombocytopenia than similarly treated SD-fed mice. Mice with moderate to severe thrombocytopenia had elevated plasma levels of thrombin-antithrombin complexes, indicative of increased thrombin generation in vivo. Platelet-fibrin thrombi were observed in multiple organs of HD-fed mice that developed severe thrombocytopenia.
CONCLUSIONS: Host-specific factors, such as prothrombotic changes in platelet reactivity and/or endothelial activation, may influence the development of thrombosis in a subset of patients who develop anti-PF4/heparin antibodies.

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Year:  2006        PMID: 16961586     DOI: 10.1111/j.1538-7836.2006.02201.x

Source DB:  PubMed          Journal:  J Thromb Haemost        ISSN: 1538-7836            Impact factor:   5.824


  4 in total

1.  CalDAG-GEFI deficiency protects mice in a novel model of Fcγ RIIA-mediated thrombosis and thrombocytopenia.

Authors:  Moritz Stolla; Lucia Stefanini; Pierrette André; Timothy D Ouellette; Michael P Reilly; Steven E McKenzie; Wolfgang Bergmeier
Journal:  Blood       Date:  2011-06-07       Impact factor: 22.113

2.  PRT-060318, a novel Syk inhibitor, prevents heparin-induced thrombocytopenia and thrombosis in a transgenic mouse model.

Authors:  Michael P Reilly; Uma Sinha; Pierrette André; Scott M Taylor; Yvonne Pak; Francis R Deguzman; Nisha Nanda; Anjali Pandey; Moritz Stolla; Wolfgang Bergmeier; Steven E McKenzie
Journal:  Blood       Date:  2010-11-18       Impact factor: 22.113

3.  Cholesterol enrichment of human monocyte/macrophages induces surface exposure of phosphatidylserine and the release of biologically-active tissue factor-positive microvesicles.

Authors:  Ming-Lin Liu; Michael P Reilly; Peter Casasanto; Steven E McKenzie; Kevin Jon Williams
Journal:  Arterioscler Thromb Vasc Biol       Date:  2006-12-07       Impact factor: 8.311

4.  Confusing combination of thrombocytopenia and thrombosis after heparin therapy in a patient with cardiac leiomyosarcoma; a nephrologist viewpoint.

Authors:  Mohammad-Reza Ardalan
Journal:  J Nephropharmacol       Date:  2014-07-01
  4 in total

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