Why the study?
Does the TNFRSFB1 gene polymorphic variant rs1061622 increase the risk of essential arterial hypertension and alter lipid profiles in people living in Karelia?
Does the TNFRSFB1 gene polymorphic variant rs1061622 increase the risk of essential arterial hypertension and alter lipid profiles in people living in Karelia?
The allele G of the TNFRSF1B gene polymorphic variant rs1061622 is associated with an increased risk of essential arterial hypertension and an atherogenic lipid profile.
Supports TNFRSF1B rs1061622 in EH susceptibility research; hypothesis-generating, requires replication before any clinical consideration.
The association of the TNFRSFB1 gene polymorphic variant rs1061622, which encodes the second type receptor (TNFRII) to TNFα with the development of essential arterial hypertension (EH, stages I–II) was investigated. Statistically significant differences in the frequencies of alleles and genotypes by this polymorphic marker were revealed for the group of healthy people and patients with EH. The risk of developing this disease was almost double in carriers of the allele G (OR = 1.904 (95DI: 1.337–2.709)). The effect of rs1061622 of the TNFRSFB1 gene on the lipid metabolism (total cholesterol, lowdensity lipoprotein cholesterol (LDL–C), high-density lipoprotein cholesterol (HDL–C), triglycerides), as well as the atherogenicity index in the group of healthy donors and EH patients, carriers of certain genotypes for this polymorphic marker of the TNFRSFB1 gene, was studied. An increase in the atherogenic lipid fraction (LDL–C) level in the plasma is associated with the presence of the allele G in the genotype. In healthy donors, either homozygous or heterozygous for the G allele, the content of HDL–C is significantly lower than in TT genotype carriers. The obtained results indicate that the polymorphic variant T>G rs1061622 of the TNFRSF1B gene is probably involved in the predisposition of people living in Karelia to EH (stages I–II). The pathogenetic effect of the TNFRSFB1 gene polymorphism on the formation of this disease is possibly accomplished through modulation of the levels of various lipid fractions.
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Топчиева et al. (2018) studied this question.
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