Akademik Veri Yönetim Sistemi
Journal of Pediatric Hematology/Oncology, cilt.30, sa.1, ss.26-31, 2008 (SCI-Expanded)
Infection has an important role in the pathogenesis of thrombosis and it becomes more prominent in childhood cases, in whom the infection frequency is higher. It has been suggested that patients with high tumor necrosis factor (TNF)-α and interleukin (IL)-6 levels might be at increased risk of developing thrombotic complications owing to the effects of these cytokines on the coagulation pathway. Functional polymorphisms in the promoter regions of the genes coding for TNF-α and IL-6 are associated with increased plasma levels of these cytokines. The aims of this study were to evaluate the serum levels of acute phase reactants, such as C-reactive protein, and of cytokines (TNF-α and IL-6) and to investigate the association between the TNF-α-308 G/A and IL-6-174 G/C polymorphisms in Turkish pediatric patients with thrombosis. Fifty-eight children with thrombosis (group 1) and 89 controls (group 2) were included in the study. Patients who had a history of infection within the 15 days before thrombosis were classified as group 1a and those who had no infection history before thrombosis were classified as group 1b. Serum TNF-α did not differ significantly between the groups. However, the IL-6 level was higher in group 1a than in group 1b (P<0.05). The genotype distribution and allele frequencies of TNF-α G/A polymorphism were significantly higher in the thrombotic children without infection and in the control group than in the thrombotic children with an infection history (P<0.05). The IL-6-174 C/C genotype was significantly higher in thrombotic children with an infection history (P<0.05); there were no differences between the groups in mean allele frequency (). On the basis of our results, patients with a history of infection seem to have higher C-reactive protein and IL-6 levels and IL-6-174 C/C genotype. Furthermore, venous thrombosis is more frequent in this group than arterial thrombosis (P<0.05). © 2008 Lippincott Williams & Wilkins, Inc.