This study was undertaken to determine the prevalence of the Factor V 1691 G-A and PT 20210 G-A mutations in Turkish children with leukemia. We genotyped 135 pediatric leukemia patients with for these mutations. Eleven (8%) of the 135 patients were heterozygous for the FV 1691 G-A mutation. Seven (5,1%) of the patients carried the PT 20210 G-A heterozygous mutation. Of the 135 patients, only three had thrombotic event, none of which had these two mutations, which is common in Turkish population. Our findings revealed a controversial compared to the previous reports, which needs further investigation. 1. Introduction The reported incidence of thrombosis ranges from 2.4% to 11.5% and an important complication in pediatric acute lymphoblastic leukaemia (ALL) patients. Its occurrence may complicate the treatment course with a negative prognostic impact [2, 3]. Thromboembolic events (TEs) are thought to result from the interaction of various factors, including effects of disease itself, central venous line, and chemotherapy, catheterization, infections, dehydration, chemotherapeutic agents such as steroids and L-asparaginase (L-Asp), and acquired or inherited prothrombotic defects (IPDs) may influence the occurrence of thromboembolism [4–8]. Various molecular defects of different hemostatic components have been established as risk factors for thromboembolic diseases mainly in adults and pediatric cases such as deficiencies of protein C, protein S, and antithrombin, resistance to activated protein C, mostly due to the factor V (FV) G1691A gene mutation and the prothrombin (PT) G20210A genotype [9]. Chemotherapy can influence the haemostatic system either through the direct effect of the chemotherapeutic agent or through complications such as infections. Corticosteroids activate platelet function, asparaginase reduces the synthesis of natural anticoagulants and in combination they increase the risk of TE in children with ALL. Some studies have shown increased thrombin activation at diagnosis in children with ALL [6, 9]. Factor V gene G-A transition at nucleotide 1691 in exon 10 is the leading cause of constitutional thrombophilia and results in with thrombus formation and creates a protein that is resistant to APC in the majority of affected individuals. The risk of developing thrombotic episodes for persons heterozygous for the FVL mutation is about 5–10 fold and for those homozygous is 80–100-fold higher than the general population.The frequency of FVL is about 8% in our healthy population [10]. The prothrombin 20210？G-A polymorphism is the second most
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