Original Article
Correlation study of venous thromboembolism with SAA, IL-1, and TNF-a levels and gene polymorphisms in Chinese population
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.
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.
