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Dense and dangerous: The tissue plasminogen activator-resistant fibrinolysis shutdown phenotype is due to abnormal fibrin polymerization
Author(s) -
Nathan Dow,
Julia R. Coleman,
Hunter B. Moore,
Zachary T Osborn,
Adrian M Sackheim,
Grant W. Hennig,
Saulius Butenas,
Mark T. Nelson,
Ernest E. Moore,
Kalev Freeman
Publication year - 2019
Publication title -
the journal of trauma and acute care surgery
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.25
H-Index - 187
eISSN - 2163-0763
pISSN - 2163-0755
DOI - 10.1097/ta.0000000000002554
Subject(s) - fibrinolysis , fibrin , hyperfibrinolysis , shutdown , fibrinogen , medicine , plasminogen activator , pathology , chemistry , immunology , nuclear chemistry
Both hyperfibrinolysis and fibrinolysis shutdown can occur after severe trauma. The subgroup of trauma patients with fibrinolysis shutdown resistant to tissue plasminogen activator (t-PA)-mediated fibrinolysis have increased mortality. Fibrin polymerization and structure may influence fibrinolysis subgroups in trauma, but fibrin architecture has not been characterized in acutely injured subjects. We hypothesized that fibrin polymerization measured in situ will correlate with fibrinolysis subgroups.

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