Interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α) levels and IL-6, TNF-Polymorphisms in children with thrombosis

Interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α) levels and IL-6, TNF-Polymorphisms in children with thrombosis
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DOI:
10.1097/mph.0b013e31815b1a89
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发表时间:
2008-01-01
影响因子:
1.2
通讯作者:
Gurgey, Aytemiz
Gurgey, Aytemiz
中科院分区:
医学4区
文献类型:
--
作者:
Una, Selma;Gumruk, Fatma;Gurgey, Aytemiz

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感染在血栓形成的发病机制中起重要作用,且在儿童患者中尤为突出,儿童感染频率较高。已经表明,由于这些细胞因子对凝血途径的影响,具有高肿瘤坏死因子(TNF)-α和白细胞介素(IL)-6水平的患者可能处于发生血栓性并发症的增加的风险中。编码TNF-α和IL-6的基因的启动子区的功能多态性与这些细胞因子的血浆水平增加相关。本研究的目的是评估急性期反应物,如Greactive蛋白,和细胞因子(TNF-α和IL-6)的血清水平,并调查土耳其儿科血栓形成患者TNF-α-308 G/A和IL-6-174 G/C多态性之间的关联。58名患有血栓形成的儿童(第1组)和89名对照(第2组)被纳入研究。血栓形成前15天内有感染史的患者被归类为la组,血栓形成前没有感染史的患者被归类为1b组。两组间血清TNF-α无显著差异。而IL-6水平在Ia组高于Ib组(P < 0.05)。TNF-α G/A多态性基因型分布和等位基因频率在无感染血栓组和对照组均显著高于有感染史血栓组(P < 0.05)。IL-6-174 C/C基因型在有感染史的血栓形成儿童中显著较高(P < 0.05);两组之间的平均等位基因频率没有差异(表2)。根据我们的结果,有感染史的患者似乎具有更高的活性蛋白和IL-6水平以及IL-6-174 C/C基因型。静脉血栓的发生率高于动脉血栓(P < 0.05)。
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)-alpha 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-alpha 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 Greactive protein, and of cytokines (TNF-a and IL-6) and to investigate the association between the TNF-alpha-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 la and those who had no infection history before thrombosis were classified as group 1b. Serum TNF-alpha did not differ significantly between the groups. However, the IL-6 level was higher in group I a than in group 1b (P < 0.05). The genotype distribution and allele frequencies of TNF-alpha 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 (Table 2). On the basis of our results, patients with a history of infection seem to have higher Greactive 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).