Decreased tissue factor and tissue-plasminogen activator antigen in relapsed acute promyelocytic leukemia

Citation
T. Nakasaki et al., Decreased tissue factor and tissue-plasminogen activator antigen in relapsed acute promyelocytic leukemia, AM J HEMAT, 64(3), 2000, pp. 145-150
Citations number
28
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Hematology,"Cardiovascular & Hematology Research
Journal title
AMERICAN JOURNAL OF HEMATOLOGY
ISSN journal
0361-8609 → ACNP
Volume
64
Issue
3
Year of publication
2000
Pages
145 - 150
Database
ISI
SICI code
0361-8609(200007)64:3<145:DTFATA>2.0.ZU;2-Y
Abstract
This study evaluated hemostatic data in 28 patients with newly diagnosed ac ute promyelocytic leukemia (APL) and 15 patients with relapsed APL. Activat ed partial thromboplastin time and prothrombin time were prolonged at initi al onset of APL, Plasma level of fibrinogen was significantly decreased in patients with initial disease of APL, but it was not decreased significantl y during the relapse of APL, Plasma fibrin and fibrinogen degradation produ cts levels were significantly increased and platelet counts significantly d ecreased in both groups, Plasma levels of antiplasmin significantly decreas ed at initial onset but not during relapse. Plasma levels of antithrombin w ere within normal range in patients with initial disease but significantly decreased in those with relapse. Plasma levels of D-dimer, soluble fibrin m onomer (sFM), plasmin-plasmin inhibitor complex (PPIC), and thrombin antith rombin 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 i n DIC score between patients with initial onset and those with relapse; pla sma levels of tissue factor (TF) significantly increased in both groups, bu t they were significantly higher at initial onset of APL than during relaps e. TF and tissue type plasminogen activator (t-PA) antigen levels in leukem ic cell lysate were significantly increased in both groups, and they were s ignificantly lower during relapse than at initial onset. Hemostatic abnorma lities occurring in patients with relapsed APL might be the result of the d ecrease of TF and t-PA in leukemic cells. These findings suggest that DIC i n APL patients with relapse might not be caused only by TF and t-PA and thu s should be treated with different therapy from patients with initial onset of APL. (C) 2000 Wiley-Liss, Inc.