scholarly journals Bleeding Disorders in Primary Fibrinolysis

2021 ◽  
Vol 22 (13) ◽  
pp. 7027
Author(s):  
Massimo Franchini ◽  
Marco Zaffanello ◽  
Pier Mannuccio Mannucci
Keyword(s):  
Narrative Review ◽  
Fibrinolytic System ◽  
Bleeding Disorders ◽  
Enzymatic Process ◽  
Blood Clots ◽  
Adults And Children ◽  
Vascular Occlusions

Fibrinolysis is a complex enzymatic process aimed at dissolving blood clots to prevent vascular occlusions. The fibrinolytic system is composed of a number of cofactors that, by regulating fibrin degradation, maintain the hemostatic balance. A dysregulation of fibrinolysis is associated with various pathological processes that result, depending on the type of abnormality, in prothrombotic or hemorrhagic states. This narrative review is focused on the congenital and acquired disorders of primary fibrinolysis in both adults and children characterized by a hyperfibrinolytic state with a bleeding phenotype.

What drives “fibrinolysis”?

2015 ◽  
Vol 35 (04) ◽  
pp. 303-310 ◽  
Author(s):  
R. L. Medcalf
Keyword(s):  
Binding Sites ◽  
Fibrinolytic System ◽  
Tissue Type ◽  
Plasminogen Activation ◽  
Enzymatic Process ◽  
Type Plasminogen Activator ◽  
Blood Clots ◽  
Lysine Residues ◽  
The Brain

SummaryThe timely removal of blood clots and fibrin deposits is essential in the regulation of haemostasis. This is achieved by the fibrinolytic system, an enzymatic process that regulates the activation of plasminogen into its proteolytic form, plasmin. This is a self-regulated event as the very presence of fibrin initiates plasminogen activation on the fibrin surface due to the presentation of exposed C-terminal lysine residues in fibrin that allow plasminogen to position itself via its lysine binding sites and to be more efficiently cleaved by tissue-type plasminogen activator (t-PA). Hence fibrin, the ultimate substrate of plasmin during fibrinolysis, is indeed an essential cofactor in the cascade. What has now come to light is that the fibrinolytic system is not solely designed to eliminate fibrin. Indeed, it is a broad acting system that processes a variety of proteins, including many in the brain where there is no fibrin. So what drives t-PA-mediated plasminogen activation when fibrin is not available?This review will describe the broadening role of the fibrinolytic system highlighting the importance of fibrin and other key proteins as facilitators during t-PA-mediated plasminogen activation.

Coagulation (Hemostasis and Thrombosis)

2012 ◽  
Author(s):  
Rajiv K. Pruthi
Keyword(s):  
Risk Factors ◽  
Platelet Activation ◽  
Coagulation Factors ◽  
Fibrin Clot ◽  
Coagulation System ◽  
Bleeding Disorders ◽  
Hemostatic System ◽  
Blood Clots ◽  
Anticoagulant System ◽  
Plug Formation

The coagulation system has 2 essential functions: to maintain hemostasis and to prevent and limit thrombosis. The procoagulant component of the hemostatic system prevents and controls hemorrhage. Vascular injury results in activation of hemostasis, which consists of vasospasm, platelet plug formation (platelet activation, adhesion, and aggregation), and fibrin clot formation (by activation of coagulation factors in the procoagulant system). The anticoagulant system prevents excessive formation of blood clots, and the fibrinolytic system breaks down and remodels blood clots. Quantitative abnormalities (deficiencies) and qualitative abnormalities of platelets and coagulation factors lead to bleeding disorders, whereas deficiencies of the anticoagulant system are risk factors for thrombosis. Common disorders of hemostasis and thrombosis are reviewed.

scholarly journals A Narrative Review on Evaluation of Hypercoagulability State in Severe COVID-19 Patients with Background Risk Factors

2020 ◽  
Author(s):  
Minoosh Moghimi ◽  
Kasra Khodadadi ◽  
Yousef Mortazavi
Keyword(s):  
Risk Factors ◽  
Cause Of Death ◽  
Background Risk ◽  
Narrative Review ◽  
Fibrinolytic System ◽  
High Rate ◽  
Thromboembolic Events ◽  
Cytokine Storm ◽  
System A

COVID-19 induces coagulopathy at the base of SIC (sepsis-induced coagulopathy) and it is an important cause of death in the patients. Cytokine storm causes imbalance in coagulation and fibrinolytic system. A combination of hypercoagulability state, decrease or inhibition of fibrinolytic and endothelialopathy causes thromboembolic events. Underlined disease with a high rate of mortality in COVID-19 like diabetes, hypertension and some conditions like aging and obesity are the main disorders with hemostatic disturbance and increase of coagulopathy. Therefore, it seems that the combination of COVID-19 infection and these risk factors increase the risk of thromboembolic all together.

scholarly journals Narrative Review of Hydration and Selected Health Outcomes in the General Population

Nutrients ◽  
2019 ◽  
Vol 11 (1) ◽  
pp. 70 ◽  
Author(s):  
DeAnn Liska ◽  
Eunice Mah ◽  
Tristin Brisbois ◽  
Pamela L. Barrios ◽  
Lindsay B. Baker ◽  
...  
Keyword(s):  
General Population ◽  
Health Outcomes ◽  
Randomized Trials ◽  
Narrative Review ◽  
Hydration Status ◽  
Healthy Population ◽  
Adequate Hydration ◽  
Adults And Children ◽  
State Of The Science

Although adequate hydration is essential for health, little attention has been paid to the effects of hydration among the generally healthy population. This narrative review presents the state of the science on the role of hydration in health in the general population, specifically in skin health, neurological function (i.e., cognition, mood, and headache), gastrointestinal and renal functions, and body weight and composition. There is a growing body of evidence that supports the importance of adequate hydration in maintaining proper health, especially with regard to cognition, kidney stone risk, and weight management. However, the evidence is largely associative and lacks consistency, and the number of randomized trials is limited. Additionally, there are major gaps in knowledge related to health outcomes due to small variations in hydration status, the influence of sex and sex hormones, and age, especially in older adults and children.

Fibrinolysis and the Immune Response in Trauma

2020 ◽  
Vol 46 (02) ◽  
pp. 176-182
Author(s):  
Robert L. Medcalf ◽  
Charithani B. Keragala ◽  
Dominik F. Draxler
Keyword(s):  
Immune Response ◽  
Traumatic Event ◽  
Optimal Recovery ◽  
Innate Immune ◽  
Fibrinolytic System ◽  
Post Injury ◽  
Antifibrinolytic Agents ◽  
Blood Clots ◽  
Injured Patients

AbstractIt has long been known that the fibrinolytic system becomes activated following trauma. At first glance, this is not at all surprising and would appear to be in response to coagulation and the apparent need to remove blood clots and restore blood flow. However, in a bleeding patient, the opposite is what is actually needed. Therefore, one may ask why the fibrinolytic system gets activated in the first place or is there another purpose? Or is it that the waxing and waning of hemostasis in such severely injured patients creates a “moving target” such that the fibrinolytic system itself is constantly responding to changing circumstances? Depending on the injury modalities and the time point post injury, the fibrinolytic system could be either turned on or off. Various theories now abound that offer new insights into the turmoil and paradoxes associated with the fibrinolytic system in this unique setting and the use of antifibrinolytic agents. While this presents one conundrum, there is also another dimension to add to this discussion that has nothing to do with hemostasis per se but rather with the modulation of other critical processes that are also essential for optimal recovery following severe injury. Indeed, overwhelming data are now supporting an important role of the fibrinolytic system in the removal of necrotic tissue (mortolysis) and as a modulator of the innate immune response. Therefore, what is really going on when the fibrinolytic system decides to go into overdrive and generate plasmin, albeit even briefly after a traumatic event? Moreover, what other consequence may occur when antifibrinolytic agents are administered? This review will address this developing story and will outline a hypothesis that places the fibrinolytic system as a gateway to a myriad of processes that are not only linked to fibrin removal but are also broader players in the modulation of innate immunity.

The Influence of Transport Parameters and Enzyme Kinetics of the Fibrinolytic System on Thrombolysis: Mathematical Modelling of Two Idealised Cases

1991 ◽  
Vol 65 (05) ◽  
pp. 553-559 ◽  
Author(s):  
A Zidanšek ◽  
A Blinc
Keyword(s):  
Mathematical Models ◽  
Plasminogen Activator ◽  
Fibrinolytic System ◽  
Transport Parameters ◽  
Fibrin Network ◽  
Blood Clots ◽  
Lag Period ◽  
Dissolution In Vitro

SummaryExperimental data obtained by magnetic resonance imaging and photographing clot dissolution in vitro have shown that whole blood clots dissolve almost two orders of magnitude faster when urokinase is introduced into the clot by pressure induced permeation than when its access is limited to diffusion. In view of these findings, two mathematical models have been developed that quantitatively link the enzymatic and transport properties of the fibrinolytic system to the velocity of thrombolysis. Without a pressure gradient across the thrombus, the plasminogen activator molecules diffuse into the thrombus through the blood-thrombus boundary plane. The blood-thrombus boundary slowly moves inwards due to thrombolysis that is spatially restricted to a relatively narrow zone. The velocity of thrombolysis is primarily limited by the diffusion constants of the plasminogen activator and plasmin. In contrast, when plasminogen activator is rapidly distributed along the thrombus by pressure induced bulk flow, lysis occurs at each segment of the thrombus after a lag period that is due to plasmin activation and sufficient fibrin degradation. The lag time is determined primarily by the catalytical properties of the plasminogen activator and plasmin. The mathematical models with the observations of the clot boundaries during lysis permit the characterization of plasmin action on the fibrin network.

scholarly journals Thrombin Activatable Fibrinolysis Inhibitor (TAFI): An Updated Narrative Review

2021 ◽  
Vol 22 (7) ◽  
pp. 3670
Author(s):  
Machteld Sillen ◽  
Paul J. Declerck
Keyword(s):  
Potential Role ◽  
Biochemical Properties ◽  
Narrative Review ◽  
Fibrinolytic System ◽  
Thrombin Activatable Fibrinolysis Inhibitor ◽  
General Overview ◽  
Physiologic Function ◽  
Fibrinolysis Inhibitor ◽  
Thrombotic Diseases ◽  
Coagulation And Fibrinolysis

Thrombin activatable fibrinolysis inhibitor (TAFI), a proenzyme, is converted to a potent attenuator of the fibrinolytic system upon activation by thrombin, plasmin, or the thrombin/thrombomodulin complex. Since TAFI forms a molecular link between coagulation and fibrinolysis and plays a potential role in venous and arterial thrombotic diseases, much interest has been tied to the development of molecules that antagonize its function. This review aims at providing a general overview on the biochemical properties of TAFI, its (patho)physiologic function, and various strategies to stimulate the fibrinolytic system by interfering with (activated) TAFI functionality.

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