Blood Coagulation, Inflammation, and Malaria
Identifieur interne : 003416 ( Main/Exploration ); précédent : 003415; suivant : 003417Blood Coagulation, Inflammation, and Malaria
Auteurs : Ivo M. B. Francischetti [États-Unis] ; Karl B. Seydel [États-Unis] ; Robson Q. Monteiro [Brésil]Source :
- Microcirculation [ 1073-9688 ] ; 2008-02.
English descriptors
- Teeft :
- Acad, Activates, Activation, Activator, Adhesion, Adhesion molecules, African children, Anticoagulant, Apoptosis, Baboon, Biol, Biol chem, Blood cells, Blood coagulation, Blood coagulation cascade, Cascade, Cerebral malaria, Clin, Clinical features, Coagulation, Coagulation cascade, Coagulation complexes, Coagulation disorder, Coagulation factor, Coagulation factors, Coagulation studies, Coagulopathy, Coli, Coma, Crit, Crit care, Cytoadherence, Cytokine, Disease pathogenesis, Disease severity, Dysfunction, Elastase, Endothelial, Endothelial cells, Endothelium, Erythrocyte, Falciparum, Falciparum infection, Falciparum malaria, Falciparum malaria pathogenesis, Fibrin, Fibrinolysis, Fibrinolytic, Fibrinolytic system, Francischetti, Grau, Haemost, Hematol, Hemmer, Hemostatic, Hemozoin, Heparin, High levels, Immune, Immunol, Inflammation, Inflammatory, Inhibitor, Intercellular, Intravascular, Intravascular coagulation, Intrinsic xnase, Lancet, Leukocyte, Looareesuwan, Macrophage, Malaria, Malaria pathogenesis, Malaria patients, Microcirculation, Microparticles, Microvascular, Molyneux, Monocyte, Multiorgan, Multiorgan dysfunction, Natl, Neutrophil, Organ dysfunction, Other words, Parasite, Parasitemia, Parasitized, Parasitol, Pathogenesis, Pathol, Pathway, Permeability, Placenta, Plasma levels, Plasmin, Plasminogen, Plasmodium, Plasmodium erythrocytes, Plasmodium falciparum, Plasmodium falciparum malaria, Platelet, Platelet aggregation, Polymorphism, Potential role, Prbc, Prbcs, Proc, Proc natl acad, Procoagulant, Proinflammatory, Receptor, Rogerson, Sepsis, Sequestration, Sequestration sites, Serum levels, Severe cases, Severe falciparum malaria, Severe malaria, Supplementary material, Tfpi, Thromb, Thromb haemost, Thrombin, Thrombin generation, Thrombocytopenia, Thrombomodulin, Tissue factor, Tissue factor expression, Tissue factor pathway inhibitor, Trans, Tumor necrosis factor, Uncomplicated, Uncomplicated malaria, Vascular, Vascular permeability, Vivax, Vivax malaria.
Abstract
Malaria remains a highly prevalent disease in more than 90 countries and accounts for at least 1 million deaths every year. Plasmodium falciparum infection is often associated with a procoagulant tonus characterized by thrombocytopenia and activation of the coagulation cascade and fibrinolytic system; however, bleeding and hemorrhage are uncommon events, suggesting that a compensated state of blood coagulation activation occurs in malaria. This article (i) reviews the literature related to blood coagulation and malaria in a historic perspective, (ii) describes basic mechanisms of coagulation, anticoagulation, and fibrinolysis, (iii) explains the laboratory changes in acute and compensated disseminated intravascular coagulation (DIC), (iv) discusses the implications of tissue factor (TF) expression in the endothelium of P. falciparum infected patients, and (v) emphasizes the procoagulant role of parasitized red blood cells (RBCs) and activated platelets in the pathogenesis of malaria. This article also presents the Tissue Factor Model (TFM) for malaria pathogenesis, which places TF as the interface between sequestration, endothelial cell (EC) activation, blood coagulation disorder, and inflammation often associated with the disease. The relevance of the coagulation‐inflammation cycle for the multiorgan dysfunction and coma is discussed in the context of malaria pathogenesis. [Supplementary materials are available for this article. Go to the publisher's online edition of Microcirculation to access this free supplemental resource]
Url:
DOI: 10.1080/10739680701451516
Affiliations:
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Le document en format XML
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<term>Activates</term>
<term>Activation</term>
<term>Activator</term>
<term>Adhesion</term>
<term>Adhesion molecules</term>
<term>African children</term>
<term>Anticoagulant</term>
<term>Apoptosis</term>
<term>Baboon</term>
<term>Biol</term>
<term>Biol chem</term>
<term>Blood cells</term>
<term>Blood coagulation</term>
<term>Blood coagulation cascade</term>
<term>Cascade</term>
<term>Cerebral malaria</term>
<term>Clin</term>
<term>Clinical features</term>
<term>Coagulation</term>
<term>Coagulation cascade</term>
<term>Coagulation complexes</term>
<term>Coagulation disorder</term>
<term>Coagulation factor</term>
<term>Coagulation factors</term>
<term>Coagulation studies</term>
<term>Coagulopathy</term>
<term>Coli</term>
<term>Coma</term>
<term>Crit</term>
<term>Crit care</term>
<term>Cytoadherence</term>
<term>Cytokine</term>
<term>Disease pathogenesis</term>
<term>Disease severity</term>
<term>Dysfunction</term>
<term>Elastase</term>
<term>Endothelial</term>
<term>Endothelial cells</term>
<term>Endothelium</term>
<term>Erythrocyte</term>
<term>Falciparum</term>
<term>Falciparum infection</term>
<term>Falciparum malaria</term>
<term>Falciparum malaria pathogenesis</term>
<term>Fibrin</term>
<term>Fibrinolysis</term>
<term>Fibrinolytic</term>
<term>Fibrinolytic system</term>
<term>Francischetti</term>
<term>Grau</term>
<term>Haemost</term>
<term>Hematol</term>
<term>Hemmer</term>
<term>Hemostatic</term>
<term>Hemozoin</term>
<term>Heparin</term>
<term>High levels</term>
<term>Immune</term>
<term>Immunol</term>
<term>Inflammation</term>
<term>Inflammatory</term>
<term>Inhibitor</term>
<term>Intercellular</term>
<term>Intravascular</term>
<term>Intravascular coagulation</term>
<term>Intrinsic xnase</term>
<term>Lancet</term>
<term>Leukocyte</term>
<term>Looareesuwan</term>
<term>Macrophage</term>
<term>Malaria</term>
<term>Malaria pathogenesis</term>
<term>Malaria patients</term>
<term>Microcirculation</term>
<term>Microparticles</term>
<term>Microvascular</term>
<term>Molyneux</term>
<term>Monocyte</term>
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<term>Multiorgan dysfunction</term>
<term>Natl</term>
<term>Neutrophil</term>
<term>Organ dysfunction</term>
<term>Other words</term>
<term>Parasite</term>
<term>Parasitemia</term>
<term>Parasitized</term>
<term>Parasitol</term>
<term>Pathogenesis</term>
<term>Pathol</term>
<term>Pathway</term>
<term>Permeability</term>
<term>Placenta</term>
<term>Plasma levels</term>
<term>Plasmin</term>
<term>Plasminogen</term>
<term>Plasmodium</term>
<term>Plasmodium erythrocytes</term>
<term>Plasmodium falciparum</term>
<term>Plasmodium falciparum malaria</term>
<term>Platelet</term>
<term>Platelet aggregation</term>
<term>Polymorphism</term>
<term>Potential role</term>
<term>Prbc</term>
<term>Prbcs</term>
<term>Proc</term>
<term>Proc natl acad</term>
<term>Procoagulant</term>
<term>Proinflammatory</term>
<term>Receptor</term>
<term>Rogerson</term>
<term>Sepsis</term>
<term>Sequestration</term>
<term>Sequestration sites</term>
<term>Serum levels</term>
<term>Severe cases</term>
<term>Severe falciparum malaria</term>
<term>Severe malaria</term>
<term>Supplementary material</term>
<term>Tfpi</term>
<term>Thromb</term>
<term>Thromb haemost</term>
<term>Thrombin</term>
<term>Thrombin generation</term>
<term>Thrombocytopenia</term>
<term>Thrombomodulin</term>
<term>Tissue factor</term>
<term>Tissue factor expression</term>
<term>Tissue factor pathway inhibitor</term>
<term>Trans</term>
<term>Tumor necrosis factor</term>
<term>Uncomplicated</term>
<term>Uncomplicated malaria</term>
<term>Vascular</term>
<term>Vascular permeability</term>
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<front><div type="abstract" xml:lang="en">Malaria remains a highly prevalent disease in more than 90 countries and accounts for at least 1 million deaths every year. Plasmodium falciparum infection is often associated with a procoagulant tonus characterized by thrombocytopenia and activation of the coagulation cascade and fibrinolytic system; however, bleeding and hemorrhage are uncommon events, suggesting that a compensated state of blood coagulation activation occurs in malaria. This article (i) reviews the literature related to blood coagulation and malaria in a historic perspective, (ii) describes basic mechanisms of coagulation, anticoagulation, and fibrinolysis, (iii) explains the laboratory changes in acute and compensated disseminated intravascular coagulation (DIC), (iv) discusses the implications of tissue factor (TF) expression in the endothelium of P. falciparum infected patients, and (v) emphasizes the procoagulant role of parasitized red blood cells (RBCs) and activated platelets in the pathogenesis of malaria. This article also presents the Tissue Factor Model (TFM) for malaria pathogenesis, which places TF as the interface between sequestration, endothelial cell (EC) activation, blood coagulation disorder, and inflammation often associated with the disease. The relevance of the coagulation‐inflammation cycle for the multiorgan dysfunction and coma is discussed in the context of malaria pathogenesis. [Supplementary materials are available for this article. Go to the publisher's online edition of Microcirculation to access this free supplemental resource]</div>
</front>
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