Background The relationship between inflammation and venous thromboembolism (VTE) has not been fully elucidated. Methods Based on our previous studies, we detected the plasma levels of serum amyloid A protein… Click to show full abstract
Background The relationship between inflammation and venous thromboembolism (VTE) has not been fully elucidated. Methods Based on our previous studies, we detected the plasma levels of serum amyloid A protein (SAA), interleukin-1 (IL-1), and tumor necrosis factor-a (TNF-a) and their 8 gene polymorphisms by ELISA and a multiplex ligation detection reaction (iMLDR) method in 284 patients with VTE and 268 healthy controls. Results Levels of SAA (P=0.032), IL-1 (P=0.045), and TNF-a (P=0.040) were significantly higher in the VTE group than in the control group. Recessive model analysis of the IL-1 rs1800587 variant showed that the risk of VTE in patients with the GG + GA genotype was significantly higher than that in patients with the AA genotype [odds ratio (OR): 4.444; 95% CI: 1.466-13.470]. Recessive model analysis of the IL-1 rs2234650 polymorphism showed that the risk of VTE in patients with the CC + CT genotype was significantly lower than that in patients with the TT genotype (OR: 0.500; 95% CI: 0.268-0.934). Multivariate logistic regression analysis showed that the TT genotype at IL-1 rs2234650 (OR: 2.086; 95% CI: 1.091-3.985) was an independent risk factor for VTE. The AA genotype of IL-1 rs1800587 (OR: 0.226; 95% CI: 0.074-0.890) was an independent protective factor against VTE. Conclusions In summary, an intrinsic relationship may exist between inflammatory activation and the occurrence of VTE.
               
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