2012
DOI: 10.1515/cclm-2012-0387
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Laboratory hemostasis: milestones in Clinical Chemistry and Laboratory Medicine

Abstract: Hemostasis is a delicate, dynamic and intricate system, in which pro-and anti-coagulant forces cooperate for either maintaining blood fluidity under normal conditions, or else will prompt blood clot generation to limit the bleeding when the integrity of blood vessels is jeopardized. Excessive prevalence of anticoagulant forces leads to hemorrhage, whereas excessive activation of procoagulant forces triggers excessive coagulation and thrombosis. The hemostasis laboratory performs a variety of first, second and … Show more

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Cited by 27 publications
(26 citation statements)
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“…This is confirmed by the fact that blood coagulation is prevalently activated by the TF-FVIIa pathway and that patients with even severe FXII deficiencies do not exhibit a clinically relevant bleeding phenotype [17]. The entire blood coagulation pathway is modulated at various stages by the activity of a number of physiological inhibitors, which mainly include tissue factor pathway inhibitor, the protein C and S system and antithrombin [16]. After conversion of fibrinogen to fibrin by thrombinmediated cleavage of fibrinopeptides A and B, the soluble fibrin monomers are then converted into an insoluble fibrin gel by covalent cross-linking catalyzed by FXIIIa, and this fibrin gel ultimately stabilizes the original platelet plug.…”
Section: Introduction To Physiological Hemostasismentioning
confidence: 93%
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“…This is confirmed by the fact that blood coagulation is prevalently activated by the TF-FVIIa pathway and that patients with even severe FXII deficiencies do not exhibit a clinically relevant bleeding phenotype [17]. The entire blood coagulation pathway is modulated at various stages by the activity of a number of physiological inhibitors, which mainly include tissue factor pathway inhibitor, the protein C and S system and antithrombin [16]. After conversion of fibrinogen to fibrin by thrombinmediated cleavage of fibrinopeptides A and B, the soluble fibrin monomers are then converted into an insoluble fibrin gel by covalent cross-linking catalyzed by FXIIIa, and this fibrin gel ultimately stabilizes the original platelet plug.…”
Section: Introduction To Physiological Hemostasismentioning
confidence: 93%
“…The complex between activated factor IX and its co-factor FVIII converges into the common pathway, and is hence effective to activate FX to FXa. Interestingly, the amount of thrombin generated by these pathways is relatively modest, lower than 5% of the total amount required for the effective fibrin generation that would be sufficient for successful stabilization of the platelet plug [16]. It is exactly at this point that the factors of the intrinsic (contact) pathway come into play, according to a model conventionally known as the 'thrombin burst'.…”
Section: Introduction To Physiological Hemostasismentioning
confidence: 99%
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“…Pathological derangements of the delicate hemostatic balance may alternatively expose the patient to ineffective coagulation and bleeding (i.e., hypofunction), or excess clotting and thrombosis (i.e., hyperfunction) [3]. Along with mounting evidences that shortened values of APTT may reflect a prothrombotic state [4], prolonged values have been historically associated with a potential hemorrhagic risk.…”
Section: Prolonged Activated Partial Thromboplastin Time and Bleedingmentioning
confidence: 99%
“…Indeed, the coagulation laboratory has an enormous potential for investigation of patients with VTE [7], but all these weapons must be used with moderation and intelligence. In the general perspective of values-based reimbursement and accountability of laboratory performance, there is general consensus that a diagnostic test is only useful when it has an influence on clinical management, when it improves the outcome or, preferably, reverses an adverse outcome.…”
mentioning
confidence: 99%