In a study of severe, decompensated liver failure, we tried to find a correlation between hemorrhage and parameters of hemostasis and fibrinolysis. Three groups of patients were studied: alcoholic cirrhosis; nonalcoholic cirrhosis, and acute liver failure without known prior liver disease. The two cirrhotic groups did not differ significantly from each other in coagulation or in fibrinolytic parameters, although liver function was more impaired in nonalcoholic cirrhosis. The levels of clotting factors, antithrombin III, prekallikrein, plasminogen and alpha 2-antiplasmin were significantly lower in the third group. Mean values of fibrinolytic activity (fibrin plate method) were slightly reduced as compared to normal in all three groups. Tissue plasminogen activator-related antigen tended to be elevated especially in alcoholic cirrhosis. The free fast-acting plasminogen activator inhibitor showed extremely high and extremely low levels in some patients among all three groups. Nonvariceal, capillary-type bleeding, including mucosal bleeding, hematomas and bleeding from puncture sites correlated with low thrombotest and normotest levels (p less than 0.01), low fibrinogen concentration (p less than 0.05) and with a high quotient of fibrinolytic activity (square root of lysis area) and normotest (p less than 0.001). The ratio between fibrin formation and dissolution appears to be an important parameter of hemorrhagic tendency in liver disease. Variceal bleeding appeared not to be related to impairment of hemostasis or fibrinolysis.
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http://dx.doi.org/10.1002/hep.1840060115 | DOI Listing |
Transfusion
January 2025
Department of Surgery, Temerty Faculty of Medicine, University of Toronto, Toronto, Ontario, Canada.
Background: Effective hemorrhage protocols prioritize immediate hemostatic resuscitation to manage hemorrhagic shock. Prehospital resuscitation using blood products, such as whole blood or alternatively dried plasma in its absence, has the potential to improve outcomes in hemorrhagic shock patients. However, integrating blood products into prehospital care poses substantial logistical challenges due to issues with storage, transport, and administration in field environments.
View Article and Find Full Text PDFMicrobiol Spectr
January 2025
Department of Biological Sciences, University of Notre Dame, Notre Dame, Indiana, USA.
Unlabelled: Group A (GAS) is a major human pathogen that causes several invasive diseases including necrotizing fasciitis. The host coagulation cascade initiates fibrin clots to sequester bacteria to prevent dissemination into deeper tissues. GAS, especially skin-tropic bacterial strains, utilize specific virulence factors, plasminogen binding M-protein (PAM) and streptokinase (SK), to manipulate hemostasis and activate plasminogen to cause fibrinolysis and fibrin clot escape.
View Article and Find Full Text PDFInt J Mol Sci
December 2024
Institute of Experimental Hematology and Transfusion Medicine, University Hospital Bonn, 53127 Bonn, Germany.
Splanchnic vein thrombosis (SVT), which is particularly prevalent in myeloproliferative neoplasms (MPNs), has a multifactorial pathomechanism involving the anticoagulant protein C (PC) pathway. To better characterize the hypercoagulable state in SVT we assessed its key enzymes thrombin and activated PC (APC). The study population included 73 patients with SVT, thereof 36 MPN+, confirmed by bone marrow biopsy, 37 MPN-, and 30 healthy controls.
View Article and Find Full Text PDFJ Thromb Haemost
January 2025
Discovery and Translational Science Department, Leeds Institute of Cardiovascular and Metabolic Medicine, University of Leeds, Leeds, UK.
Background: Blood clot formation, triggered by vascular injury, is crucial for haemostasis and thrombosis. Blood clots are composed mainly of fibrin fibres, platelets and red blood cells (RBCs). Recent studies show that clot surface also develops a fibrin film, which provides protection against wound infection and retains components such as RBCs within the clot.
View Article and Find Full Text PDFSci Rep
January 2025
Department of Emergency Medicine, Medical University of Vienna, Waehringer Guertel 18-20, 1090, Vienna, Austria.
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