Objective: The aim of the study was to analyze the correlations between body mass index (BMI) and clinical and laboratory parameters in patients with essential hypertension (EH) depending on angiotensinogen gene (AGT, rs699) polymorphism. Design and method: The case-control study involved 72 patients with stage II EH, 1–3 degrees of blood pressure (BP) elevation, high and very high cardiovascular risk (CVR) (29.16% men, 70.84% women). The mean age of patients was 59.87±7.98 yo. The control group consisted of 48 healthy individuals comparable in age and gender. Polymorphism of the AGT gene (rs699) was studied by polymerase chain reaction (PCR). BMI was defined as the ratio of weight to square of height (kg/m2). All enrolled/screened patients signed the Informed Consent to participate in the research. The parathyroid hormone (PTH) and vitamin 25 (OH) D levels in blood serum were determined by chemiluminescence immunoassay (MAGLUMI). Results: In TT-genotype carriers of the AGT gene (rs699) BMI was directly related to anthropometric parameters of waist circumference (WC), hip circumference (HC) and waist-hip ratio (WHR) (r = 0.70–0.81; p < 0.022), the concentration of vitamin D (r = 0.65; p = 0.043) and inversely with the blood level of ionized Ca2+ (r = -0.71; p = 0.02). Correlation matrix of laboratory, anthropometric indicators in hypertensive TC-genotype carriers showed that BMI is directly related to WC and HC (r = 0.68; p < 0.001 and r = 0.84; p < 0.001), as well as to PTH level (r = 0.43; p = 0.004), with a negative correlation with vitamin D level (r = -0.38 P = 0.011). PTH directly depends on BMI, WC and HC (r = 0.31–0.43; p < 0.042–0.004). A direct link between BMI and WC and HC was found in CC-genotype carriers (r = 0.73; p<0.001 and r = 0.78; p<0.001). Conclusions: Thus, the correlation matrix showed that BMI directly depended on the anthropometric parameters of WC, HC and/or WHR (r = 0.68-0.84; p<0.022-0.001) regardless of the AGT gene genotypes (r = 0,52-0.86; p<0.02-0.001) and inversely correlated with ionized Ca2+ level in the blood (r = -0.71; p = 0.02), but only in TT-genotype carriers of the AGT gene (rs699).
Objective: To evaluate the role of the polymorphism of AGT genes (rs4762) and GNB3 genes (rs5443) in the development of the essential arterial hypertension separately and by combining their polymorphic variants. Design and method: The case-control study involved 100 patients with EAH stage II, 1-3 degrees of blood pressure (BP), high and very high cardiovascular risk. Among the patients there were 21% (21) men, 79% (79) women. The mean age of patients was 59.86±6.22y.o. The control group consisted of 60 almost healthy individuals, relevant in age (49.13±6.28y.o.) and gender distribution (63% - women, 37% - men). To study of polymorphism of AGT (rs4762) and GNB3 (rs5443) genes was performed a qualitative polymerase chain reaction (PCR) in real time. Results: The mutated T-allele of the AGT gene (rs4762) occurs in 15.97% of hypertensive residents of Northern Bukovyna, that is more frequent than in healthy individuals by 9.72% (p = 0.023); homozygous mutations of the AGT gene were not found in the control group at all. Whereas, the relative frequency of polymorphic variants of the GNB3 gene (rs5443, 825C>T) did not differ significantly between groups. The wild C-allele statistically significantly prevails over the mutated T-allele in both groups according to the AGT (rs4762) and GNB3 (rs5443) genes (p<0.001). Binary logistic regression confirmed an increase in the risk of hypertension inheritance according to dominant and additive models in minor T-allele carriers of the AGT gene (rs4762) almost 3 times higher than in C-allele homozygotes (p = 0.04 and p = 0.03). Inheritance of EAH is not associated with polymorphic variants of the GNB3 gene (rs5443). Conclusions: The T-allele of the AGT gene (rs4762) increases the risk of hypertension almost 3 times, whereas, polymorphic variants of the GNB3 gene (rs5443) are not predictors of EAH in the observed.
Objective: The aim of the study was to analyze metabolic and hormonal parameters changes in patients with essential arterial hypertension (EAH) depending on the vitamin D receptor gene (VDR, rs2228570) polymorphism. Design and method: The study involved 100 patients suffering from EAH with target-organ damaging, moderate, high or very high cardiovascular risk. Among them were 79.0% (79) women and 21.0% (21) men, an average age was 59.87±8.02 yo. The control group involved 60 practically healthy persons, matched by age and gender distribution. All enrolled/screened patients signed the Informed Consent to participate in the research. The VDR gene (rs2228570) polymorphism was studied by a real-time polymerase chain reaction (RT-PCR) method. The intact parathyroid hormone (intact PTH) and vitamin 25 (OH) D levels in blood serum were determined by chemiluminescence immunoassay (MAGLUMI). Results: The decreased level of vitamin 25 (OH) D (<30 ng/ml) was found more often in the A-allele carriers of the VDR gene (rs2228570), than in GG-genotype carriers: in the control group - by 36.84% (x2 = 10.32; p = 0.001), in study group - by 42.42% (x2 = 39.27; p<0.001). Hypocalcemia according to the level of ionized blood calcium (Ca2+ <1.12 mmol/l) was registered only in G-allele carriers, both among practically healthy and hypertensive patients. In the control group, GG-genotype carriers had a lower ionized Ca2+ blood level with a compensatory higher concentration of the intact PTH in comparison with A-allele carriers - by 3.42%, 25.19% and 16.03% (p<0.05), respectively. Secondary hyperparathyroidism due to a compensatory increasing of the intact PTH (>65 pg/ml) was found more often in the G-allele carriers of the VDR gene (rs2228570) than in AA-genotype carriers: in control group - by 55.55% (x2 = 11.11; p<0.001), and in the group of patients with EAH - by 62.5% (x2 = 12.5; p<0.001). Conclusions: The GG-genotype of the VDR gene (rs2228570) increases the risk of hypocalcemia by more than 6 times [OR = 6.25; 95% CI: 1.05-37.37; p = 0.046], with the lowest probability in carriers of the A-allele [OR = 0.16; 95% CI: 0.03-0.96].
Objective: The aim of our study was to evaluate the role of AGT (rs4762) and GNB3 (rs5443) gene polymorphisms as risk factors for severe hypertension. Design and method: The case-control study involved 100 patients with EAH stage II, 1-3 degrees of blood pressure (BP), high and very high cardiovascular risk. Among the patients there were 21% (21) men, 79% (79) women. The mean age of patients was 59.86±6.22 y.o. The control group consisted of 60 almost healthy individuals with relevant age (49.13±6.28y.o.) and gender distribution (63% - women, 37% - men). The AGT (rs4762) gene polymorphism was studied by a qualitative polymerase chain reaction (PCR) in real time. Results: Severity of EAH does not depend on polymorphic variants of AGT (rs4762) and GNB3 (rs5443) genes. The distribution showed no statistically significant differences in the aforementioned distribution. Individuals with the first degree of hypertension met more often with the CC genotype of the GNB3 gene (rs5443) by 22.23% than among patients with the T allele (x2 = 3,66; p = 0,055) in patients with EAH. Conclusions: Epidemiological analysis did not confirm the polymorphic variants of the AGT (rs4762) and GNB3 (rs5443) genes as predictors of the severe course of EAH according to the degrees of BP elevation.
Objective: Metabolic changes and obesity play important roles in arterial hypertension pathogenesis and progression. Whereas hepatic steatosis (HS) and AH have multiple common mechanisms of development involving metabolic and immune changes, the aim of study was to investigate the influence of Pro12Ala polymorphism of PPAR-↖2 gene and I/D polymorphism of ACE gene on metabolic profile and cytokines in obese patients with HS and AH. Design and method: Study involved 154 AH patients with HS (87 males, 67 females, age 50.06±7.34). Duration of HS 1-5 years, AH 3-21 years. Metabolic disorders were defined with body mass index (BMI), glycaemia, immunoreactive insulin (IRI), total cholesterol (TC), low and high density cholesterol (LDL-C, HDL-C), triglycerides (TG), C-peptide (CP) levels and HOMA-IR index. TNF- ↑ and leptin plasma levels were assessed by ELISA. Genes’ polymorphism of PPAR-↖2 (Pro12Ala), and ACE (I/D) alone or in combination was studied with PCR. Results: Differences of BMI, plasma glucose, IRI, HOMA-IR, CP and leptin are independent from ACE gene genotypes (p>.05). Pro-allele carriers of PPAR-↖2 gene have higher BMI than AlaAla carriers (32.7±2.1 and 27.9±1.1 kg/m2 vs 25.6±0.8 kg/m2, accordingly (p<.05), leptin level – 14.3±0.41 and 8.6±0.25 ng/ml vs 3.7±0.22 ng/ml, (p<.001), glucose level – to 10.2% and 10.9% accordingly (p<.05); CP level was higher in ProPro-genotype than in Ala-allele carriers to 15.7% (p<.05). Risk group of dyslipidemia are ProPro-genotype carriers of PPAR-↖2 gene with higher level of TC, TG and LDL-C to 16.4%, 17.3% and 27.9% (p<.05) and lower level of HDL-C in women to 25.6% (p = .038). Lipids levels are independent on ACE I/D polymorphism. Baseline TNF-↑ plasma levels did not significantly deviate between genotypes of PPAR-↖2 gene, but D-allele carriers (I/D+DD) of ACE gene had higher baseline TNF-↑ plasma levels (91.61 and 109.11 pg/ml, accordingly p<.01). Conclusions: In HS hypertensive patients metabolic disorders are clearly associated with PPAR-↖2 Pro-allele (carbohydrates) and ProPro-genotype (lipids). Presence of D-allele of ACE gene is associated with reliably higher level of TNF-↑ plasma levels.
Objective: The aim of the study was to analyze lipids` changes in patients with essential arterial hypertension (EAH) depending on the vitamin D receptor gene (VDR, rs2228570) polymorphism. Design and method: The study involved 100 patients suffering from EAH with target-organ damaging, moderate, high, or very high cardiovascular risk. Among them were 79.0% (79) women and 21.0% (21) men, the average age was 59.87±8.02 yo. The control group involved 60 practically healthy persons, matched by age and gender distribution. All enrolled/screened patients signed the Informed Consent to participate in the research. The VDR gene (rs2228570) polymorphism was studied by a real-time polymerase chain reaction (RT-PCR) method. Lipids’ profile in serum was studied by total cholesterol (TC), high- and low-density cholesterol levels(HDL-C, LDL-C), triglycerides (TG) concentration, and atherogenic index (AI). Results: The levels of TC and LDL-C in AA-genotype carriers of the control group exceeded those of GG-genotype carriers by 13.85% (PGG = 0.044) and 22.59% (PGG = 0.045), and the content of HDL-C, on the contrary, was lower - by 16 .56% (PGG = 0.048). The analysis of the lipid profile, taking into account the gender distribution, showed a higher concentration of TC, due to LDL-C, in hypertensive women with AA-genotype than in those with the G-allele: according to the TC- by 7.61-14.07% (RAA<0.03), for LDL-C - by 12.78-17.39% (RAA<0.02), respectively. On the other hand, men with EAH carrying the AA-genotype, on the contrary, had lower levels of TC and LDL-C than those with the G-allele: for TC - by 20.24% (PAA = 0.02), for LDL-C - by 30.20% and 24.45% (PAA<0.04), respectively. In practically healthy carriers of the A-allele of the VDR gene (rs2228570), especially the AA-genotype, the concentrations of TC and LDL-C were within the reference values, but exceeded that in GG-genotype carriers: for TC - by 13.85% (PGG = 0.044), LDL-C - by 22.59% (PGG = 0.045), and the content of HDL-C, on the contrary, was lower - by 16.56% (PGG = 0.048). Conclusions: Thus, the polymorphic site of the VDR gene (rs2228570) is associated with an increased LDL-C in practically healthy individuals, according to the analysis of variance (ANOVA) (F = 4.61; p = 0.014).
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