Changes of hemostatic factors in children with acute lymphoblastic leukemia receiving combined chemotherapy including high dose methylprednisolone and L-asparaginase

Citation
Af. Oner et al., Changes of hemostatic factors in children with acute lymphoblastic leukemia receiving combined chemotherapy including high dose methylprednisolone and L-asparaginase, LEUK LYMPH, 33(3-4), 1999, pp. 361-364
Citations number
14
Categorie Soggetti
Hematology,"Onconogenesis & Cancer Research
Journal title
LEUKEMIA & LYMPHOMA
ISSN journal
10428194 → ACNP
Volume
33
Issue
3-4
Year of publication
1999
Pages
361 - 364
Database
ISI
SICI code
1042-8194(199904)33:3-4<361:COHFIC>2.0.ZU;2-H
Abstract
In this study, protein C (PC), protein S (PS), heparin cofactor TI (HCFII), prothrombin fragment 1+2 (PF 1,2), thrombin-antithrombin III complex (TAT) , von Willebrand factor (VWF) and thrombomodulin (TM) were investigated in 19 patients with acute lymphoblastic leukemia, (ALL) receiving combined che motherapy including L-asparaginase (L-ASP) and high dose methylprednisolone (HDMP). HDMP was administered in doses of 30 mg/kg/day for 7 days, and 20 mg/kg/day for another 7 days. In order to evaluate the effect of HDMP on th e hemostatic system, the 8 patients studied here received HDMP (30 mg/kg/da y) therapy for 4 days before the combined chemotherapy. These parameters we re also studied in 12 healthy children as a control group. PC levels were n ormal in the patients while PS levels were decreased both before and after combined chemotherapies. Patients with ALL have laboratory signs of coagula tion activation such as PF 1,2, TAT prior to initiation of chemotherapy. Wi th combined chemotherapy, TAT levels were found to be normal while PF1,2 we re not. TM levels were found to be increased both before and after therapie s whereas HCFII and VWF levels were not different from those of the control group. The short course of HDMP therapy did not prominently influence thes e hemostatic parameters. These results indicate that both the malignant process and the drugs used i n combined chemotherapy cause a decrease in natural inhibitors and an incre ase in procoagulant activity and endothelial injury. These hemostatic chang es may contribute to a thrombotic tendency in the patients with ALL.