Abstract
To study the coagulation and fibrinolytic state in lung cancer, molecular markers for coagulation and fibrinolysis, i. e. plasma fibrinopeptide A (FPA), fibrinopeptide Bβ1-42 (Bβ1-42), fibrinopeptide Bβ15-42 (Bβ15-42), tissue-type plasminogen activator antigen (t-PA antigen) and activity (t-PA activity), plasminogen activator inhibitor (PAI), D-dimer, plasminogen, α2-plasmin inhivitor (α2PI) α2PI-plasmin-complex (PIC), thrombin-antithronbinIII-complex (TAT), ATIII and serum FDP-E levels were assayed in 31 patients with lung cancer. And we also discussed the pathophysiology of coagulation and fibrinolysis according to the histological classification and the clinical staging of lung cancer.All these molecular markers except PAI changed significantly compared with the value in normal subjects. As for coagulation, hypercoagulable state was observed because both FPA and TAT increased and showed positive correlation each other. As for fibrinolytic state, increase of fibrinolysis was observed because of increment of PIC, D-dimer, FDP-E, Bβ1-42, Bβ15-42, t-PA antigen, and activity levels and decrease in plasminogen and α2PI levels. In addition, these changes might be induced through secondary fibrinolysis because the levels of D-dimer and FDP-E were well correlated with the levels of TAT. But compared with the changes in lung cancers with DIC, the grade of these changes were slight. There was no difference of molecular marker levels among the histological classifications and the clinical stagings.These results indicated that these patients with lung cancer might be at the risk of thromboembolic complication because of dynamic changes of coagulation and fibrinolysis.
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