Abstract

Objective. To assess the role of polymorphism of PTPN22 (C1858T) gebe in the development of hypertension (TNH) in patients with the rheumatoid arthritis (RA).Design and methods. We examined 202 patients with RA, we identified the following groups: patients with RA without HTN was identified (n = 53; 26%); patients with RA in association with HTN (n = 95; 47%), as well as patients with HTN without RA (n = 54; 27%). Healthy volunteers (n = 205) were also divided into 3 groups comparable by age, sex and size with the main groups. We applied clinical, laboratory, instrumental and molecular genetic methodsDNA isolation was performed by the standard phenol-chloroform method. Genotyping by the PTPN22 gene was carried out by the PCR-PDRF analysis method (polymerase chain reaction — polymorphism of the length of restriction fragments). PCR was performed with a set of primers to the corresponding areas of the genome. PCR products were analyzed by electrophoresis in a 4% polyacrylamide gel followed by staining with ethidium bromide.Results. The TT homozygous genotype and the T allele of the С1858Т gene polymorphism PTPN22 were predominant in the RA group and RA + HTN group compared to controls. The risk of RA without HTN is 1,7 fold higher in the TT carriers of the PTPN22 gene genotype, compared to CC and CT genotype carriers. Allele T was significantly more common in the group of patients with RA without HTN than in control group 1 [OR = 1,521 (95% confidence interval 1,0–2,324); р < 0,05]. A similar distribution of genotypes and alleles is seen in the group of RA patients in association with HTN compared to control group 2. No significant difference was found in the group of patients with HTN without RA compared to control group 3.Conclusions. Our study indicates that the homozygous TT genotype and the C1858T polymorphism T allele of the PTPN22 gene are predictors of RA development alone and in association with HTN.

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