The article presents data on the features of hypertension (HTN) and the risk factors for its development in patients with psoriasis (PsO) and psoriatic arthritis (PsA). PsO and PsA are often accompanied by cardiovascular diseases which are associated with both chronic systemic Th1-Th17-mediated inflammation and metabolic changes in this group of patients. Currently, data show high rates of HTN in PsO, however, the pathophysiological relationship of these pathologies has not been fully determined. HTN development in PsO and PsA is mediated by many factors. Firstly, metabolism disorders including hyperuricemia, hyperglycemia, dyslipidemia can play a role. Moreover, PsO and PsA often cause stress and depression predisposing to smoking, alcohol consumption, hypodynamia, which are modifiable cardiovascular risk factors. Also, the medications for skin lesions and joint inflammation can lead to high blood pressure. In conclusion, there is no reason to avoid the use of certain antihypertensive drugs in PsO and PsA. Cardiovascular pathology significantly affects the quality of life, social adaptation, and the treatment opportunities of PsO and PsA.

This article is an analysis of current data on arterial hypertension (HTN) as a leading risk factor for premature death. We discuss the reasons of the failure to achieve target levels of blood pressure, and the available approaches to HTN pharmacological treatment by the main classes of antihypertensive drugs in accordance with current clinical guidelines. We show the advantages of fixed combinations (FC) of antihypertensive drugs and the ways to optimize antihypertensive treatment by administration of a triple FC, containing amlodipine, indapamide and perindopril.

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.

Objective. To investigate the molecular mechanism underlying genetic susceptibility to essential hypertension (EH) using polygenic analysis of renin-angiotensin-aldosterone system (RAAS).

Design and methods. Genotyping of renin (REN, rs2368564), angiotensinogen (AGT, rs4762), angiotensin II receptor type 1 (AGTR1, rs5186), chymase 1 (CMA1, rs1800875) and angiotensin-converting enzyme (ACE, rs1799752) polymorphic variants was performed in 346 patients with EH and 377 controls, Russians and Tatars by ethnic origin.

Results. ACE rs1799752polymorphism was significantly associated with EH risk in Tatars (P_Bonf = 0,003) and in the total study group (P_Bonf = 4,09 x 10^–5). Polygenic approach identified 12 genotypes and/or alleles combinations of RAAS genes polymorphisms, significantly associated with EH in the Tatars, and 6 patterns associated with EH in the total study group. The highest risk of disease in Tatar men was associated with REN rs2368564*T + AGTR1 rs5186*C/A + ACE rs1799752*D combination (OR = 16,64, P_Bonf = 0,001), in the total group — with REN rs2368564*T/C + CMA1 rs1800875*G combination (OR = 2,37, P_Bonf = 0,045).

Conclusions. Our findings indicate that EH risk in men of Russian and Tatar ethnicity is significantly associated with ACE rs1799752 polymorphism, and the results of polygenic analysis demonstrate an association of the disease risk with genotype/allele combinations of polymorphic variants in REN (rs2368564), AGTR1 (rs5186), ACE (rs1799752), and CMA1 (rs1800875) genes.

The multifactorial genesis of hypertension (HTN) enforced the investigation of genetically determined component of its etiopathogenesis in various populations.

The aim of present work is to assess the associations between blood pressure (BP) and HTN and polymorphism of a number of genetic markers identified according to GWAS data, in a case-control study based on Siberian population cohort. Design and methods. Design of the work—case-control study in the groups aged 45–69 years old based on a caucasoid population cohort (Novosibirsk). The group of cases included HTN subjects with established diagnosis of HTN under the age of 50 (n = 346)). The control included subjects matched by sex and age to cases, and having at least 2 examinations (6 months apart) with BP levels not exceeding “normal” BP by ESH, 2018 (n = 168). A total of 514 people were included in the analysis. We used standardized epidemiological methods to assess HTN and cardiovascular diseases. Single nucleotide polymorphisms (SNPs) were tested using real-time PCR (ABI 7900HT). The analysis included 16 markers identified in GWAS studies (rs11646213, rs17367504, rs11191548, rs12946454, rs16998073, rs1530440, rs653178, rs1378942, rs1004467, rs381815, rs2681492, rs2681472, rs3184504, rs2384550, rs6495122, rs6773957).

Results. For the polymorphism rs1378942 of cytoplasmic tyrosine kinase gene (CSK), in a multivariable-adjusted logistic regression, the carriers of the AC/CC vs. AA genotypes had odds ratio (OR) of HTN of 1,51 (p = 0,043) independent of age and sex; this excess risk was partly explained by the impact of body mass index (BMI). With respect to the quantitative phenotype, women carrying the AA genotype had diastolic BP (DBP) value 5 mm Hg lower than carriers of AC/CC genotypes (p = 0,026). In a multivariable-adjusted analysis, the polymorphism rs653178 of ataxin 2 gene (ATXN2) was associated with HTN independent of age and BMI (СС vs ТТ/ТС; OR = 0,61; p = 0,022); this relationship was realized due to the contribution of men (p = 0,027). With respect to the quantitative phenotype, in the multivariable analysis, the carriers of СС genotype had DBP value lower than those with ТТ/ТС (p = 0,022) independent of age and BMI, and due to the contribution of men. In a multivariableadjusted analysis, the polymorphism rs6773957 of adiponectin gene (ADIPOQ) was associated with HTN in women regardless of age and BMI (GG v. AA/AG; OR = 0,29; p = 0,001). In unadjusted analysis, we found the association between polymorphism rs2384550 of T box transcription factor gene (TBX3) and the level of systolic BP (SBP) in men (p = 0,043); when comparing homozygous groups, the level of SBP was significantly higher among carriers of the AA genotype versus GG (p = 0,013), but this association was attenuated to insignificant in in a multivariate analysis.

Conclusions. In a case-control study based on Siberian population sample, we found the associations between qualitative and quantitative phenotypes of BP/HTN and polymorphism of 4 SNPs (CSK, ATXN2, ADIPOQ, TBX3 genes). Our data replicated a number of positive results obtained in genomewide studies, and we obtained the evidence of new associations not previously convincingly shown, and of the context dependency of the association between HTN and a number of molecular markers.

Background. The increased prevalence of obesity and associated cardiometabolic diseases attract attention worldwide. Renin-angiotensin system can link obesity and cardiovascular and metabolic diseases.

Objective. To access a comprehensive assessment of cardiometabolic risk factors and gene polymorphisms of the renin-angiotensin system in metabolic phenotypes among young individuals.

Design and methods. The sample consisted of 251 individuals, who were divided into four groups: group 1 — metabolically healthy individuals with normal body mass index (BMI) (n = 62); group 2 — metabolically unhealthy individuals with normal BMI (n = 57); group 3 — metabolically healthy overweight/obese individuals (n = 16); group 4— metabolically unhealthy overweight/ obese individuals (n = 116). All participants answered a questionnaire designed for this study. Anthropometric, clinical and biochemical parameters were assessed. The following polymorphisms were evaluated:, A1166C polymorphism of the angiotensin II type 1 receptor gene (rs5186), M235T polymorphism of the angiotensinogen gene (rs699), T174M polymorphism of the angiotensinogen gene (rs4762), I/D polymorphism of the angiotensinconverting enzyme gene (rs4340).

Results. In young individuals with metabolically unhealthy overweight/ obesity, a higher frequency of coexistent abdominal obesity and hypertension was found in combination with a higher frequency of the allele T of AGT 235M/T. The greater differences in carbohydrate and lipid metabolism in combination with a higher serum levels of leptin and low serum concentrations of adiponectin were also found in young individuals with metabolically unhealthy overweight/obesity.

Objective. Hypertension (HTN) is characterized by a high incidence of comorbidity. An individual approach to the management of such patientsrequires new markers for differential diagnosis. The pathophysiology of most comorbidities is closely related to endothelial dysfunction triggered by an imbalance in redox processes.

The aim of this work is to assess the relationship between plasma level of folic acid (FA) and the state of the redox system of erythrocyte glutathione in patients with HTN and concomitant target organ damage in cardiovascular diseases (HTN + CVD), chronic kidney disease (HTN + CKD) and discirculatory encephalopathy (HTN + DE).

Design and methods. We enrolled 93 patients with HTN admitted to the clinics of the Pavlov University, and 30 donors of the reference group. We assessed plasma concentration of folic acid, the content of reduced glutathione (GSH) and the activity of glutathione reductase (GR) in erythrocytes.

Results. In HTN patients with the deficiency of FA, a lower content of GSH and activity of GR in erythrocytes were found compared to the HTN patients without deficiency and the reference group. In the groups HTN + CVD and HTN + DE, the GSH level and GR activity correlated with the plasma concentration of FA and were lower in the subgroups with FA deficiency. In subgroups with normal FA content, these parameters did not differ from the reference indicators.

Conclusions. The parameters of GSH and GR in patients with HTN + CVD and HTN + DE, but not HTN + CKD, can be considered as potential markers of functional FA deficiency.

Objective. The aim of this study was to assess the association between the level of blood pressure (BP) and the prevalence of coronary heart disease (CHD) in women of working age in an open population of a moderately urbanized Siberian city (on the model of Tyumen).

Design and methods. We included 1000 women of an open urban population aged 25–64 years, 250 people in each of four decades of life (among persons 25–34, 35–44, 45–54, 55–-64 years old), selected by the method of a random representative sample from the electoral lists of the administrative district of Tyumen, the response was 70,3% (703 participants). In all subjects we measured BP; assessed the presence of coronary artery disease — according to standardized epidemiological methods: based on the extended criteria, “definite” CHD (strict criteria) and “possible” CHD (non-strict criteria) were distinguished. Statistical analysis was performed using STATISTICA 12.0 software, the differences were considered significant at p-level ≤ 0,005.

Results. Almost every third woman (25–64 years old) had increased BP (34,7 %), the frequency of increased BP grows with age, reaching 63,3 % in the older group. Low awareness of high BP and low adherence to treatment were found. There was a correlation between the prevalence of CHD and BP level and age. In the presence of increased systolic BP, the chance of developing CHD in women aged 25–64 years in the open population increases by 1,9–2,7 times (p < 0,05), in the presence of increased diastolic BP, the chance of developing CHD according to extended criteria increases by 2,1 times (odds ratio = 2,08, 95 % confidence interval (1,15; 3,74)).

Conclusions. Our results can be used for improving the strategy of primary cardiovascular prevention in preventive programs of the Western Siberia region.

Objective. To assess the association of single nucleotide polymorphisms of genes potentially involved in the comorbidity of bronchial asthma (BA) and essential hypertension (HTN) in patients with different time onset of the diseases.

Design and methods. Genotyping of 92 SNPs was performed using MALDI-TOF mass spectrometry in patients with BA and HTN (n = 97) and healthy individuals (n = 153). The group of patients with comorbid pathology was divided into two subgroups depending on the time of onset of symptoms of BA relative to HTN, and the prevalence of all studied SNPs was compared in each subgroup relative to the control.

Results. The variant rs11590807 regulating expression for UTP25, TRAF3IP3, C1orf74, HSD11B1-AS 1, IRF6 genes in the heart, blood vessels, and lung is associated with BA and HTN, regardless of the time onset of each of these diseases. Associations of other variants are specific with respect for each subgroup of comorbid diseases. The rs1010461 variant, which regulates the expression of RNASE4 and ANG genes, is linked with HTN as the first phenotype of the comorbidity. The rs769214, rs11032700, rs11032699, rs484214, and rs480575 variants, which regulate the expression of CAT gene, are associated with BA as the first phenotype of disease comorbidity.

Conclusions. We found specific associations of the studied polymorphic variants in the development of comorbid phenotypes of BA and HTN, which differ in the time of manifestation of each of the diseases relative to each other.

Glomerulonephritis associated with antineutrophil cytoplasmic antibodies (ANCA) is one of the causes of renal parenchymal disease, which can lead to secondary hypertension (HTN). Clinical course of HTN in this case is usually mild, however, high blood pressure can become the only reason to refer to a primary care physician. We report a case of a 45-year old woman with renal parenchymal disease due to ANCA-glomerulonephritis and secondary HTN. HTN was the only clinical manifestation of the disease led to the hospital admission. With this clinical case we emphasize that primary care physicians should always attempt to identify secondary causes of HTN.