ERS Respiratory Channel

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Abstract

Thrombosis is an actual problem in COPD. In the case of thrombosis, both changes in the coagulation system and hyperhomocysteinemia, both a factor in endothelial dysfunction, and high vasoconstriction, which develops due to changes in the production of vascular vascular factors, can lie. Purpose. Determination of the presence and presence of defects in the main genes of thrombophilia, hyperhomocysteinemia and vascular vasoconstrictor endothelin-1 in predicting the risk of thrombosis in patients with COPD.

Materials and methods. In 123 patients diagnosed with stage III-IV COPD (GOLD, 2016), PCR methods were studied for several major congenital thrombophilia genes: Arg506Gln polymorphisms of the Leiden mutation gene, 20210 G/A of the prothrombin gene, the most important hypermocysteinemia genes: Ala222Val polymorphisms of the MTHFR gene, Asp919Gly MTR gene, Ile22Met MTRR gene, Glu429Ala 1298 A>C MTHFR gene and the most potent vasoconstrictor endothelin-1 gene: Lys198Asp polymorphism of the Endothelin-1 gene. To assess the associations groups of COPD patients were divided into 2 groups with (n=83)/without (n=40) thrombosis in history.

Results. It was found that 91.1% of all COPD patients required genetic defects in the main genes. When choosing changes in genes in the group of COPD patients without thrombosis, only 12% require a normal genotype for all genes, while in the group with thrombosis, only 2.5%.

Conclusions: Genetic defects are one of the causes of thrombosis in patients with COPD. Perhaps the role of COPD as a trigger for patients with a genetic predisposition to thrombosis still requires further study to prevent thrombotic events in this category of patients.

Abstract

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