摘要
Background Increased levels of interleukin-6 （IL-6） and C-reactive protein （CRP） have been reported in patients with venous thromboembolisms （VTE）. However, prospective studies did not confirm an association between IL-6, CRP and their polymorphism with the risk of VTE. Methods One hundred and forty patients （including 66 males and 74 females, mean age （55.55±17.11） years） and one hundred and sixty controls （including 74 males and 86 females, mean age （56.58±12.24） years） were involved. An enzyme linked immunosorbent assay （ELISA） method was used for detecting the serum levels of inflammatory factors IL-6 and CRP in both groups. Polymerase chain reaction-restriction fragment length polymorphism （PCR-RFLP） was used for analyzing the distribution of polymorphisms at the -572C/G and -597G/A sites of the promoter of the IL-6 gene and at 1059G/C of the CRP gene. Results Serum levels of IL-6 and CRP were significantly higher in the VTE group than in the control group （P 〈0.05）. The frequencies of-572C/G promoter polymorphisms CC, CG, and GG in the IL-6 gene were found to be 34%, 48%, and 18%, respectively, and the derived allele frequencies for the C and G alleles were 58% and 42%. There was a significant difference in the -572C/G promoter polymorphisms between the VTE group and control group （P 〈0.05）. For the -597G/A polymorphism, individuals all carried the GG and GA type; AA genotypes were not detected. The frequency of the GG, GC, and CC genotypes at the CRP1059G/C promoter was 87.57%, 7.86% and 3.57% in V-rE group, while 86.25%, 10%, and 3.75% in control group, respectively. The frequency of G and C alleles at CRP 1059G/C was 91.43% and 8.57% in VTE group and 91.56% and 8.44% in the control group. The results showed that there was no statistically significant difference of 1059G/C genotype and mutation frequency of the allele between the VTE group and control group （P 〉0.05）. Multiple Logistic regression analysis showed CC homozygotes of the IL-6 -572G/C, body mass index （BMI）, and CRP, IL-6, and high-density lipoprotein cholesterol （HDL-C） were independent risk factors for VTE （P 〈0.05）. Conclusions We found that V-rE was associated with IL-6 and CRP levels, and there was an association of IL-6 and its promoter polymorphism at -572G/C with the risk of VTE. Thus far, a causal relationship between inflammation and VTE remains to be clarified and more prospective data are required.
Background Increased levels of interleukin-6 （IL-6） and C-reactive protein （CRP） have been reported in patients with venous thromboembolisms （VTE）. However, prospective studies did not confirm an association between IL-6, CRP and their polymorphism with the risk of VTE. Methods One hundred and forty patients （including 66 males and 74 females, mean age （55.55±17.11） years） and one hundred and sixty controls （including 74 males and 86 females, mean age （56.58±12.24） years） were involved. An enzyme linked immunosorbent assay （ELISA） method was used for detecting the serum levels of inflammatory factors IL-6 and CRP in both groups. Polymerase chain reaction-restriction fragment length polymorphism （PCR-RFLP） was used for analyzing the distribution of polymorphisms at the -572C/G and -597G/A sites of the promoter of the IL-6 gene and at 1059G/C of the CRP gene. Results Serum levels of IL-6 and CRP were significantly higher in the VTE group than in the control group （P 〈0.05）. The frequencies of-572C/G promoter polymorphisms CC, CG, and GG in the IL-6 gene were found to be 34%, 48%, and 18%, respectively, and the derived allele frequencies for the C and G alleles were 58% and 42%. There was a significant difference in the -572C/G promoter polymorphisms between the VTE group and control group （P 〈0.05）. For the -597G/A polymorphism, individuals all carried the GG and GA type; AA genotypes were not detected. The frequency of the GG, GC, and CC genotypes at the CRP1059G/C promoter was 87.57%, 7.86% and 3.57% in V-rE group, while 86.25%, 10%, and 3.75% in control group, respectively. The frequency of G and C alleles at CRP 1059G/C was 91.43% and 8.57% in VTE group and 91.56% and 8.44% in the control group. The results showed that there was no statistically significant difference of 1059G/C genotype and mutation frequency of the allele between the VTE group and control group （P 〉0.05）. Multiple Logistic regression analysis showed CC homozygotes of the IL-6 -572G/C, body mass index （BMI）, and CRP, IL-6, and high-density lipoprotein cholesterol （HDL-C） were independent risk factors for VTE （P 〈0.05）. Conclusions We found that V-rE was associated with IL-6 and CRP levels, and there was an association of IL-6 and its promoter polymorphism at -572G/C with the risk of VTE. Thus far, a causal relationship between inflammation and VTE remains to be clarified and more prospective data are required.
