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Changes in plasma levels of tissue‐plasminogen activator/inhibitor complex and active plasminogen activator inhibitor in patients with disseminated intravascular coagulation
Author(s) -
Asakura Hidesaku,
Jokaji Hiroshi,
Saito Masanori,
Uotani Chika,
Kumabashiri Ichiro,
Morishita Eriko,
Yamazaki Masahide,
Matsuda Tamotsu
Publication year - 1991
Publication title -
american journal of hematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.456
H-Index - 105
eISSN - 1096-8652
pISSN - 0361-8609
DOI - 10.1002/ajh.2830360304
Subject(s) - disseminated intravascular coagulation , plasminogen activator , plasminogen activator inhibitor 1 , acute promyelocytic leukemia , sepsis , medicine , fibrinolysis , tissue plasminogen activator , complication , leukemia , coagulation , immunology , chemotherapy , gastroenterology , cancer research , chemistry , biochemistry , retinoic acid , gene
Plasma levels of tissue‐plasminogen activator · plasminogen activator inhibitor (t‐PA · PAI) complex and active PAI were assayed in 58 cases of disseminated intravas‐cular coagulation (DIC). A significant elevation of both parameters was observed in most cases of DIC, especially in patients with non‐Hodgkin lymphoma, sepsis, or some patients with acute leukemia, but no such elevation was observed in patients with acute promyelocytic leukemia (APL). The levels of both parameters were higher in cases of DIC with multiple organ failure (MOF) than in those without MOF. Since no elevation of t‐PA · PAI complex was observed in most cases of APL, t‐PA did not seem to play an important role in the activation of fibrinolytic system in APL. Active PAI, which reflects the inhibitory regulation in fibrinolytic system, was considered to play a role in the progression of MOF. Plasma levels of active PAI were low in the cases of APL, which had no complication of MOF.