The fibrinolytic system comprises a series of serine proteases that interact to cleave fibrin into fibrin degradation products. Although all key components of the fibrinolytic system are present at birth, important age-dependent, quantitative and qualitative differences are present during childhood as compared to adults. These differences include decreased plasma concentrations of plasminogen, tissue-type plasminogen activator and alpha2-antiplasmin, increased plasma concentrations of plasminogen activator inhibitor-1, as well as a decrease in both plasmin generation and overall fibrinolytic activity. Increasing evidence suggests that these age-dependent differences may contribute to the development of specific childhood diseases and influence the course of fibrinolytic therapy, particularly in newborns. This review aims to summarize the available information on the age-dependent features of the fibrinolytic system in newborns and children in healthy and disease states and the impact of these features on fibrinolytic therapy.
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"Most components of the haemostatic system vary in quantity in premature and full-term infants compared to adults (Parmar et al., 2006; Andrew et al., 1992; Maureen et al., 2000). Differences related to platelets have also been shown. "
[Show abstract][Hide abstract] ABSTRACT: Platelets play a vital role in the coagulation, yet the potential for differences in platelet function, between adults and children, remains underexplored. This is despite the age-related variation in haemostatic proteins, that is encompassed by the term Developmental Haemostasis. Hemotoxins found in the venoms of Australian snakes mimic human blood coagulation factors. The effects of Australian snake venoms on platelets, as well as the possible differential response in adults and children were subject of this study.
[Show abstract][Hide abstract] ABSTRACT: During the past few decades, great progress has been made toward a better understanding of the development of the hemostatic system. It is now clear that the physiology of hemostasis in pediatric patients differs widely from that in adults, supporting the hypothesis that children might have natural protective mechanisms that justify such variations. However, the correct interpretation of hemostasis test results in young patients, along with a deep understanding of the normal postnatal development in the human coagulation system, are essential prerequisites to the proper investigation of thrombotic and hemorrhagic problems in pediatric patients. Because the hemostatic system is not fully mature by 3 to 6 months of age, it is important to recognize that interpretation of laboratory data in pediatric patients must be accompanied by appropriate age-dependent reference ranges, which should also be specific for the testing system used, to prevent misclassification of children as having defects of factors and inhibitors of the coagulation system.
Full-text · Article · Dec 2007 · Seminars in Thrombosis and Hemostasis
[Show abstract][Hide abstract] 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.