Analiz Riska Zdorovʹû (Mar 2020)
TNF gene polymorphism as a risk factor that can cause arterial hypertension in patients suffering from gastroesophageal reflux disease
Abstract
Comorbidity of arterial hypertension (AH) and gastroesophageal reflux disease (GERD) is widely spread (from 20.6 % to 29 %); despite that fact, risk factors that can cause AH in patients suffering from GERD have still not been examined completely. Experts are discussing a role played by anti-inflammation cytokine of tumor necrosis factor alpha (TNF) both in AH occurrence and GERD pathogenesis as it is its activity that is to a great extent determined by a patient having certain alleles of tumor necrosis factor (TNF) gene. Therefore, it seems vital to study TNF gene G308A polymorphism in patients with combined AH and GERD. Our research goal was to study frequency and variants of TNF gene G308A polymorphism relations with AH risk and AH phenotypic peculiarities in patients suffering from GERD. We examined 58 people who had AH (29 patients with isolated AH, average age being 53 [46; 62], and 29 patients with combined AH and GERD, average age being 56 [51; 59]). Patients from both groups were comparable in terms of sex, age, and examined factors of cardiovascular diseases risks. We applied allele-specific polymerase reaction with test systems produced by “Sintol” LLC (Moscow) to determine G308A (rs1800629) polymorphism of TNF gene. To assess relations between alleles and genotypes and disease risks, we calculated odds ratio (OR) with 95 % confidence interval (CI). We revealed a relation between G308A polymorph marker of TNF gene and systolic blood pressure and disorders in tolerance to dextrose among patients with comorbid AH and GERD. Patients with combined AH and GERD had unfavorable allele A and G/A genotype authentically more frequently (OR 5.14; 95 % CI – 1.06–24.95; р = 0.03, OR 6.08; 95 % CI – 1.18–31.25; р = 0.02 accordingly). We showed that G308A polymorphism was related to AH occurrence in patients suffering from GERD. These data confirm that endothelial dysfunction plays a significant role in AH pathogenesis among such patients.
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