A Short History of Thrombosis and Hemostasis: Part I (40th Year Celebratory Issue)

Favaloro, Emmanuel J.

doi:10.1055/s-0034-1384768

Cited by 12 publications

(19 citation statements)

References 20 publications

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“…The discovery of the anti-haemophilic globulin (AHG) in the middle of the 20 th century led to the production of cryoprecipitate and FVII and FIX concentrates. [4] Eric Adolf von Willebrand in 1924 investigated a family suffering from a bleeding disorder named (VWD) which was apparently different from haemophilia. By the end of 1960 vWD was accepted as a combined deficiency of FVIII and platelet adhesion factor, Jerry Koults provided evidence that both are linked but separate molecules.…”

Section: Introductionmentioning

confidence: 99%

“…VWF is responsible for collagen binding, platelet glycoprotein 1b binding, and FVIII binding. [4] Patient's with Glanzmann thrombasthenia were found by Alan Nurden in the 1960's to lack two major platelet surface glycoprotein's (GP's) which mediates platelet adhesion and aggregation Subsequent studies by Alan defined the function of the GpIIb -IIIa complex, known as integrin alphaIIb beta3, in binding fibrinogen and other adhesive proteins on activated platelets and formation of the protein bridges that joins platelets together in the platelet aggregate. [4] Also patients with Bernard-Soulier Syndrome has macro thrombocytopenia and absence of Gp1b; which interacts with VWF and mediates platelet attachment to injured sites in the vessel wall.…”

Section: Introductionmentioning

confidence: 99%

“…[4] Patient's with Glanzmann thrombasthenia were found by Alan Nurden in the 1960's to lack two major platelet surface glycoprotein's (GP's) which mediates platelet adhesion and aggregation Subsequent studies by Alan defined the function of the GpIIb -IIIa complex, known as integrin alphaIIb beta3, in binding fibrinogen and other adhesive proteins on activated platelets and formation of the protein bridges that joins platelets together in the platelet aggregate. [4] Also patients with Bernard-Soulier Syndrome has macro thrombocytopenia and absence of Gp1b; which interacts with VWF and mediates platelet attachment to injured sites in the vessel wall. [4] The plasminogen-plasmin (fibrinolytic) system consists of several serine proteases and their inhibitors involved in fibrinolysis, embryogenesis, cell migration, wound healing and pathogenesis of many diseases including atherosclerosis, obesity, cancer, autoimmune disorders and neuronal degeneration.…”

Section: Introductionmentioning

confidence: 99%

“…[4] Also patients with Bernard-Soulier Syndrome has macro thrombocytopenia and absence of Gp1b; which interacts with VWF and mediates platelet attachment to injured sites in the vessel wall. [4] The plasminogen-plasmin (fibrinolytic) system consists of several serine proteases and their inhibitors involved in fibrinolysis, embryogenesis, cell migration, wound healing and pathogenesis of many diseases including atherosclerosis, obesity, cancer, autoimmune disorders and neuronal degeneration. [2,4] …”

Section: Introductionmentioning

confidence: 99%

“…[4] The plasminogen-plasmin (fibrinolytic) system consists of several serine proteases and their inhibitors involved in fibrinolysis, embryogenesis, cell migration, wound healing and pathogenesis of many diseases including atherosclerosis, obesity, cancer, autoimmune disorders and neuronal degeneration. [2,4] …”

Section: Introductionmentioning

confidence: 99%

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Perioperative Coagulopathy and the Clinical Implications

Orilonise¹

2016

AIMDR

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Perioperative bleeding as conceived in this review refers to the clinical scenario whereby there is impairment of blood coagulation leading to prolonged or excessive bleeding, accompanying trauma or surgical exposure. Aetiology of bleeding disorders could be classified under the following subheadings: vascular disorders, Thrombocytopenia, Platelet function defects, Coagulation factors disorder(s). Primary haemostasis is initiated or triggered by the release of tissue factor at the site of injury leading to generation of small quantity thrombin, sufficient to activate platelets leading to the formation of prothrombin complex. The ability of FXa to activate FVII creates a link between the extrinsic and intrinsic coagulation pathways; leading to the generation of sufficient thrombin to convert fibrinogen to fibrin which organizes platelet plug to indissoluble clots (Secondary haemostasis) or thrombus formation. A balance is required between haemostasis, thrombosis and fibrinolysis to prevent perioperative coagulopathy. Whenever positive findings in the history and physical examination suggests an increased risk of significant bleeding, then it is more cost effective to carry out routine screening tests of coagulation. Specific coagulation tests used routinely has longer turnaround times and is not appropriate in the perioperative setting. Current recommendations for the prevention of massive bleeding in the perioperative setting; requires communication of appropriate treatment plans in a multidisciplinary setting, intraoperative monitoring, the treatment of underlying disorder, and replacement therapy with blood products. As point-of-care diagnostics becomes available in emergency areas, timely targeted intervention for haemorrhage control will result in better patient outcomes and reduced demand for blood products.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%