Thrombophilia as a factor in increasing inflammation in COPD
Abstract
COPD is a disease of high thrombogenic risk. A procoagulant role for inflammation in COPD has been established, but there may be an inverse effect where thrombophilia causes more severe inflammation in COPD by impairing organ perfusion. <b>Purpose:</b> Determine associations between predisposition to thrombophilia and increased inflammation in COPD. <b>Materials and methods:</b> Several major genes of congenital thrombophilia (polymorphisms Arg506Gln of the F5 gene, 20210 G/A of the F2 gene, Ala222Val of the MTHFR gene, Asp919Gly of the MTR gene, Ile22Met of the MTRR gene, Glu429Ala 1298 A>C of the MTHFR gene) were studied by PCR in 92 patients with established COPD diagnosis. According to the results of the study, patients were divided into 3 groups with different genotype variations (homozygote, heterozygote and mutation), with a minimum predisposition to thrombophilia in groups with a homozygous genotype and a maximum in a group with a mutational genotype. The study of inflammation factors IL-1, IL-6 and IL-8 was carried out using ELISA. <b>Results:</b> In the group of patients with normal genotypes, the level of inflammatory factors was lower than in other groups (IL1 - 1.54±0.27 pg/ml; IL6 - 3.9±0.61 pg/ml; IL8 - 3.7±0.49 pg/ml), in comparison with groups with heterozygous (IL1 - 2.9±1.12 pg/ml; IL6 - 4.98±0.84pg/ml; IL8 - 9.7±2.42 pg/ml) and mutational genotype (IL1 - 3.6±1.51 pg/ml; IL6 - 5.1±0.84 pg/ml; IL8 - 15.4±3.43 pg/ml). <b>Conclusions:</b> Data were obtained on the predominance of the level of inflammation in groups of patients with a congenital predisposition to thrombophilia, which indirectly confirms the dependence of the degree of inflammation on thrombophilia.