title: Decreased tissue factor and tissue-plasminogen activator antigen in relapsed acute promyelocytic leukemia.
abstract: This study evaluated hemostatic data in 28 patients with newly diagnosed acute promyelocytic leukemia (APL) and 15 patients with relapsed APL. Activated partial thromboplastin time and prothrombin time were prolonged at initial onset of APL. Plasma level of fibrinogen was significantly decreased in patients with initial disease of APL, but it was not decreased significantly during the relapse of APL. Plasma fibrin and fibrinogen degradation products levels were significantly increased and platelet counts significantly decreased in both groups. Plasma levels of antiplasmin significantly decreased at initial onset but not during relapse. Plasma levels of antithrombin were within normal range in patients with initial disease but significantly decreased in those with relapse. Plasma levels of D-dimer, soluble fibrin monomer (sFM), plasmin-plasmin inhibitor complex (PPIC), and thrombin antithrombin complex (TAT) levels were significantly high in both groups. Plasma levels of PPIC, sFM, and D-dimer were significantly higher at initial onset of APL than during relapse. However, there was no significant difference in DIC score between patients with initial onset and those with relapse; plasma levels of tissue factor (TF) significantly increased in both groups, but they were significantly higher at initial onset of APL than during relapse. TF and tissue type plasminogen activator (t-PA) antigen levels in leukemic cell lysate were significantly increased in both groups, and they were significantly lower during relapse than at initial onset. Hemostatic abnormalities occurring in patients with relapsed APL might be the result of the decrease of TF and t-PA in leukemic cells. These findings suggest that DIC in APL patients with relapse might not be caused only by TF and t-PA and thus should be treated with different therapy from patients with initial onset of APL.
authors.affiliation: Second Department of Internal Medicine, Mie University School of Medicine, Mie-ken, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Nakasaki
authors.forename: H
authors.initials: H
authors.lastname: Wada
authors.forename: Y
authors.initials: Y
authors.lastname: Mori
authors.forename: Y
authors.initials: Y
authors.lastname: Okugawa
authors.forename: R
authors.initials: R
authors.lastname: Watanabe
authors.forename: M
authors.initials: M
authors.lastname: Nishikawa
authors.forename: E C
authors.initials: EC
authors.lastname: Gabazza
authors.forename: M
authors.initials: M
authors.lastname: Masuya
authors.forename: S
authors.initials: S
authors.lastname: Kageyama
authors.forename: K
authors.initials: K
authors.lastname: Kumeda
authors.forename: H
authors.initials: H
authors.lastname: Kato
authors.forename: H
authors.initials: H
authors.lastname: Shiku
mesh_terms: D000293:Adolescent; D000328:Adult; D000941:Antigens / Q000097:blood; D005260:Female; D005340:Fibrinogen / Q000032:analysis; D006487:Hemostasis; D006801:Humans; D015473:Leukemia, Promyelocytic, Acute / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D012008:Recurrence; D013925:Thromboplastin / Q000378:metabolism*; D010959:Tissue Plasminogen Activator / Q000276:immunology*
chemical_list: D000941:Antigens; D005340:Fibrinogen; D013925:Thromboplastin; D010959:Tissue Plasminogen Activator