Development Of Hypertension In Patients Research Articles

Peculiarities of pulmonary arterial hypertension development in patients with chronic tuberculous pleural effusion

Objective. To study the peculiarities of pulmonary arterial hypertension in patients with chronic tuberculous pleural effusion and to evaluate the possibilities of an indirect method of its diagnosis as a screening measure. Materials and Methods. Catheterization of the right heart is considered the "gold standard" for determining pulmonary artery pressure. The known etiopathogenic agents due to pulmonary hypertension cause the development of pulmonary heart, in the presence of which the patient will have an undesirable outcome in the next 3 years. Every year, new patients with pulmonary arterial hypertension are identified. In our opinion, chronic pleurisy affects the development of this complication, which led us to study the problem. Results. Indicators of pulmonary arterial hypertension depended on the stage of chronicity of pleurisy: in the presence of stage II, they were higher. After pleurectomy on the 8th - 10th day, the pressure in the pulmonary artery decreased by 10 - 24 mm Hg. Conclusions. The pressure of pleural effusion on the lung reduces the venous pool and is transmitted to the pulmonary artery, which is accompanied by the release of a number of substances, including serotonin, which cause broncho- and vasospastic reactions. After pleurectomy on the 8th - 10th day, the pressure in the pulmonary artery decreases in most patients, which confirms the effect of the stage of chronic pleurisy on pulmonary hypertension.

Evidence for a relationship between genetic polymorphisms of the L-DOPA transporter LAT2/4F2hc and risk of hypertension in the context of chronic kidney disease

BackgroundChronic kidney disease (CKD) and hypertension are chronic diseases affecting a large portion of the population frequently coexistent and interdependent. The inability to produce/use adequate renal dopamine may contribute to the development of hypertension and renal dysfunction. The heterodimeric amino acid transporter LAT2/4F2hc (SLC7A8/SLC3A2 genes) promotes the uptake of L-DOPA, the natural precursor of dopamine. We examined the plausibility that SLC7A8/SLC3A2 gene polymorphisms may contribute to hypertensive CKD by affecting the L-DOPA uptake.Methods421 subjects (203 men and 218 women, mean age of 78.9 ± 9.6 years) were recruited and divided in four groups according to presence/absence of CKD, defined as reduced estimated glomerular filtration rate (eGFR < 60 ml/min/m2) calculated using the creatinine-based Berlin Initiative Study–1 (BIS1) equation, and to presence/absence of hypertension (systolic blood pressure ≥ 140 and/or diastolic blood pressure ≥ 90 mmHg). Subjects were analysed for selected SNPs spanning the SLC7A8 and SLC3A2 loci by Sequenom MassARRAY iPLEX platform.ResultsThe most significant SNP at the SLC3A2 (4F2hc) locus was rs2282477-T/C, with carriers of the C-allele having a lower chance to develop hypertension among CKD affected individuals [OR = 0.33 (CI 0.14–0.82); p = 0.016]. A similar association with hypertensive CKD was found for the SLC7A8 (LAT2) rs3783436-T/C, whose C-allele resulted associated with decreased risk of hypertension among subjects affected by CKD [OR = 0.56 (95% CI 0.35–0.90; p = 0.017]. The two variants were predicted to be potentially functional.ConclusionsThe association between SLC3A2 and SLC7A8 variants to hypertension development in patients with renal failure could be linked to changes in L-DOPA uptake and consequently dopamine synthesis. Although the associations do not survive correction for Bonferroni multiple testing, and additional research is needed, our study opens new avenues for future basic and translational research in the field of hypertensive CKD.

Heart rate variability and cardiovascular risk factors in patients with rheumatoid arthritis: A longitudinal study.

It is established that the risk of cardiovascular disease (CVD) is increased in patients with Rheumatoid Arthritis (RA). Heart rate variability (HRV) is a method for evaluating the activity in the cardiac autonomic nervous system. Our aim was to assess the longitudinal development of HRV in patients with RA and compare with healthy controls. Furthermore, we wanted to investigate associations between HRV, inflammatory disease activity and cardiovascular complications in patients with RA over time. HRV was assessed with frequency-domain analysis at baseline and after five years in 50 patients with early RA, all being younger than 60years. HRV indices were age-adjusted based on the estimated age-dependency in 100 age and sex matched healthy controls. Additionally, clinical data including serological markers, disease activity, and blood pressure were collected from the patients. Eleven years after inclusion CVD was assessed. At baseline, patients with RA presented with lower HRV compared to controls during deep breathing (6 breaths/min), paced normal breathing (12 breaths/min) and after passive tilt to the upright position. No significant change in HRV was observed at the five-year follow-up. A significant negative correlation was found between HRV parameters and systolic blood pressure (SBP) at baseline. A significant positive correlation was found between heart rate and inflammatory markers at baseline but not after five years. Nine patients had developed CVD after 11years, but no significant association was found with baseline HRV data. This study showed that patients with RA have autonomic imbalance both at an early stage of the disease and after five years, despite anti-rheumatic medication, but no correlation between HRV and inflammation markers were observed. Reduced HRV was also significantly negatively correlated with increased SBP. Hypertension is a common finding in patients with RA. Thus, significant decline of HRV could be a useful early marker for development of hypertension in patients with RA.

Predictors for arterial hypertension in middle aged adults

Abstract Funding Acknowledgements Type of funding sources: None. Background Subclinical atherosclerosis is a marker for development of future atherosclerotic cardiovascular disease. However, it is still unclear whether subclinical atherosclerosis predicts hypertension in patients who have not diagnosed it yet. Aim of the study was to evaluate possible significance of subclinical atherosclerosis for the development of hypertension in patients who have not diagnosed hypertension yet. Methods 418 middle aged adults who had subclinical atherosclerosis and without hypertension enrolled in this study (aged 31-49 years, mean age 39.12±12.0 years, male=53%). All participants were examined general clinical, anthropometric, laboratory and instrumental measures. Subclinical atherosclerosis were diagnosed using ultrasound methods via ankle-brachial index (ABI) using established cutoffs. All patients followed up to 6 years. Mean follow up was 4.5±2.1 years. All statistical analysis were performed using STATA software. Results During the mean follow up period 17% (71) patients were diagnosed hypertension (SPB&amp;lt;140 mmHg and/or DBP&amp;lt;90 mmHg). Among them 12% (50) were males whilst 5 % (21) were females and men tended to have more levels of blood pressure than women did (P&amp;lt;0.05). During the follow up period, subclinical atherosclerosis level has increased more than 20% to those who was diagnosed hypertension. Patients who developed hypertension tended to have more smokers (OR 1.58, 1.14-2.28, CI 95%, P&amp;lt;0.05), BMI&amp;lt;30 kg/m2 (OR 1.57, 1.12-1.98, CI 95%, P&amp;lt;0.05), family history of hypertension (OR 1.45, 1.09-1.87, CI 95%, P&amp;lt;0.05), frequent stress at work (OR 1.35, 1.06-1.82, CI 95%, P&amp;lt;0.05) and financial problems at home (OR 1.23, 1.05-1.72, CI 95%, P&amp;lt;0.05). Conclusion Subclinical atherosclerosis is a predictor for new onset hypertension in men especially for those who were smoker, obese and had family history of hypertension as well as frequent stressed at work.

Clinical and morphological aspects of the development of secondary ophthalmic hypertension in uveal melanoma

Ophthalmic hypertension is mostly associated with medium- or large-sized melanomas. The pathogenesis of persistent IOP elevation in uveal melanoma is not fully understood at present. Purpose. To analyze the clinical and morphological mechanisms of the development of secondary ophthalmic hypertension in patients with uveal melanoma. Material and methods. The case histories of 26 patients with T3N0M0-T4N0M0 uveal melanoma were analyzed retrospectively from 2015 to 2019. The main group included 18 patients with secondary monolateral IOP elevation while the control group was composed of 8 patients with normal IOP. Tumors in both groups were comparable in size. All patients underwent eradication treatment (enucleation/exenteration). Enucleated eys were histologically examined. Results. Pronounced pathological changes of the iridocorneal angle, iris and ciliary body were found morphologically in all specimens with elevated IOP. The following dominating mechanisms ofophthalmic hypertension were detected: iris and anterior chamber angle neovascularization; tumor-associated chronic uveitis; obstruction of trabecular meshwork by cellular elements (pigment-rich macrophages, blood cells, inflammatory cells); fibrosis and deformation of trabecular meshwork and Schlemm's canal; closed angle glaucoma with lens-iris diaphragm shift; tumor invasion into the angle. Conclusions. Investigation of morphological changes in patients with UM and found resemblances with already studied non-tumor forms of glaucoma may help find previously undetectable receptors for the development of targeted anti-tumor drugs.

ASOSIASI GLUKOSA DARAH, STATUS GIZI, MOOD DAN LAMA MENDERITA DIABETES TERHADAP TEKANAN DARAH PADA PASIEN DIABETES MELITUS TIPE 2

The percentage of diabetes incidence increased from 6.9% to 8.5% in Indonesia starting from 2013 to 2018. In 2012 the mortality rate due to diabetes was 1.5 million deaths. Hyperglycemia above the threshold increases 2.2 million deaths and the risk of cardiovascular disease. DM caused 1.5 million deaths in 2012. Blood sugars higher than the upper limit resulted in an additional 2.2 million deaths, increasing the risk of cardiovascular disease. Blood pressure patterns change during the development of hypertension in patients with or without diabetes mellitus. Diabetes mellitus and hypertension often occur together. Knowing the common causes and mechanisms of disease allows for a more effective and proactive approach to its prevention and treatment. The purpose of this study was to identify the relationship of blood glucose, nutritional status, mood and length of suffering in patients with Type II Diabetes Mellitus (DM Type II) to blood pressure. The research instruments used were Blood glucose monitoring system GE100, Spygnomanometer (Automatic Blood Pressure Monitor HEM-7130), weight scales, height measuring devices and FACES Test. The study used a cross-sectional correlational quantitative method with a consecutive sample technique of 51 diabetic patients. Spearman's test is used in this research. The results of the correlation test with the significance value of p are 0.000 and 0.004 . Blood Glucose Levels and Mood/mood have a correlation with blood pressure and have a strong and moderate correlation strength. Further research is needed to holistically identify changes in blood pressure in patients with diabetes.

Prevention of Incident Hypertension in Patients With Obstructive Sleep Apnea Treated With Uvulopalatopharyngoplasty or Continuous Positive Airway Pressure: A Cohort Study.

PurposeTo determine whether treatment with uvulopalatopharyngoplasty (UPPP) or continuous positive airway pressure (CPAP) in patients with obstructive sleep apnea (OSA) prevents hypertension, compared to those not receiving any treatment.MethodsA retrospective cohort study was conducted among 413 patients with OSA (age ≥ 35 years) at the Shuang Ho Hospital between 2009 and 2016. The patients were divided into three groups: UPPP, CPAP, and non-treatment groups. Data about the personal characteristics, history of comorbidities, and polysomnography (PSG) reports were collected at baseline. A Cox model with inverse probability of treatment weighting was used to adjust for confounders and baseline diversity.ResultsAfter multivariate adjustment and weighting for incident hypertension, patients in both the CPAP and UPPP groups showed a significant preventive effect on hypertension than in the non-treatment group. Moreover, patients in the CPAP group had lower event rates than those in the UPPP group.ConclusionUPPP can prevent the development of new-onset hypertension in patients with OSA. CPAP had a better preventive effect than UPPP. UPPP might be a good alternative for reducing the risk of the onset of hypertension when compliance to CPAP is poor.

Associative role of polymorphism of the РТРN22 (C1858T) gene in the development of hypertension in patients with the rheumatoid arthritis

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 &lt; 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.

Circulating proteomic biomarkers related to the development of chronic thromboembolic pulmonary hypertension in patients with acute pulmonary embolism

Abstract Background Chronic thromboembolic pulmonary hypertension (CTEPH), known as a complication of acute pulmonary embolism (PE), can be attributed to both persistent organized thrombi and small-vessel disease. It has been reported that patients with acute PE are more likely to develop CTEPH or have a worse prognosis in follow-up if they have pulmonary hypertension (PH) or right ventricular dysfunction in their acute phase; in acute PE, increased pulmonary arterial pressure can be induced by a combination of mechanical obstruction and pulmonary vasoconstriction. However, it remains unknown whether contributors to the increase pulmonary arterial pressure in acute phase would persistently influence the pulmonary vasculature, which could further lead to the development and progression of CTEPH. Purpose To investigate underlying contributors related to pulmonary hypertension in acute PE that would persistently influence the pulmonary vasculature in the development of CTEPH, and to explore potential biomarkers predictive of CTEPH in acute PE. Methods Plasma from patients with acute PE were collected and classified into Group 1 (with PH) and Group 2 (without PH) according to the presence of PH, which was defined by echocardiographic estimated “high probability” of PH as recommended in the 2015 ESC/ERS Guidelines for the diagnosis and treatment of PH. In addition, plasma from patients with acute PE who had not developed PH both in their acute and follow-up phase but had persistent thrombi (Group 3) were also studied and compared to that of CTEPH patients (Group 4). Differential expression proteins (DEPs) between 4 groups were identified in terms of data-independent acquisition-based quantitative proteomic analysis. Results Twenty-two DEPs were identified between Group1 and Group 2, and 105 DEPs were identified between Group 3 and Group 4. Among two groups of DEPs, 8 proteins were in common: antithrombin-III, osteopontin, properdin, desmoplakin, C1QA (complement C1q subcomponent subunit A), LDHA (L-lactate dehydrogenase A chain), IGKV1D-33 (immunoglobulin kappa variable 1D-33) and PEPD (Xaa-Pro dipeptidase). The level of LDHA, antithrombin-III, osteopontin and properdin were decreased both in acute PE patients with PH and CTEPH patients, while the level of desmoplakin, C1QA and IGKV1D-33 were increased in the above two groups. Regarding PEPD, its level was lower in acute patients with PH but was higher in CTEPH. Based on underlying pathogenic mechanism and the percentage of missing value, osteopontin, properdin, desmoplakin, C1QA, LDHA and PEPD were further validated as potential biomarkers predictive of CTEPH in acute PE. Conclusions Contributors to the increase pulmonary arterial pressure in acute PE can be further involved in the development of CTEPH, and these proteins can be potential biomarkers to help guide the management and follow-up strategy in acute PE. Funding Acknowledgement Type of funding sources: Public grant(s) – National budget only. Main funding source(s): Chinese Academy of Medical Sciences Innovation Fund for Medical Sciences (CIFMS; No. 2017-12M-1-009); National Key Research and Development Program of China (No: 2016YFC1304400) Differential expression proteinsRelative intensity of proteins

Clinical significance of 24-hour blood pressure monitoring in prediction of hypertension development in patients with gout

Aim.The aim of the study was to develop the model for establishing early diagnosis of hypertension in patients with gout. The model was based on data of 24-hour blood pressure monitoring.Material and Methods.A total of 69 patients with gout were enrolled in a single-stage cross-sectional prospective study. Three study groups were assigned as follows: group 1 (main group) comprised hypertensive men with gout (n = 41); group 2 (comparison group) comprised normotensive men with gout (n = 28); group 3 (control) included relatively healthy men (n = 30). Daily blood pressure monitoring was performed on an outpatient basis using a BPLab device (Peter Telegin, Russia).Results. The significant intergroup differences were found in the following parameters: lowest, mean, and highest 24-hour systolic blood pressure (SBP) values in patients of main and comparison groups (р &lt; 0.001) and in patients of main and control groups (р &lt; 0.001); mean and maximum 24-hour diastolic blood pressure (DBP) values in patients of main and comparison groups (р &lt; 0.001) and in patients of main and control groups (р &lt; 0.001); lowest, mean, and highest 24-hour pulse blood pressure (PBP) values in patients of main and comparison groups (р &lt; 0.001) and in patients of main and control groups (р &lt; 0.001); mean, and maximum 24-hour PBP values in patients of comparison and control groups (р &lt; 0.001). Median values of the lowest, mean, and highest 24-hour SBP in hypertensive patients with gout were significantly higher than the corresponding values in normotensive patients with gout and healthy men of group 3 (p &lt; 0.001). Median values of mean and maximum 24-hour DBP in main group were higher than the corresponding values in comparison group and control group (p &lt; 0.001). Median values of the lowest, mean, and highest 24-hour PBP in hypertensive patients with gout exceeded the corresponding values of patients of control group (p &lt; 0.001). Median values of the mean and maximum 24-hour PBP in main group exceeded the corresponding values of patients of comparison group (p &lt; 0.001). Based on the binary logistic regression model, the prognostic algorithm for hypertension development in gout patients was created using the parameters of 24-hour blood pressure monitoring as predictors and the cut-off K value. If the value of K was &gt; 0.54, then the hypertension development was predicted in gout patients. The sensitivity of developed diagnostic model was 0.84, and the specificity was 0.95.Conclusion.Тhe proposed model, based on the assessment of average-daily values of the lowest, mean, and highest SBP, allowed to establish early diagnosis of hypertension in patients with gout with the accuracy of up to 90%.

The contribution of the AGT, GNB3, MTHFR, MTRR, ApoE, and PPARα polymorphisms to the development of masked arterial hypertension in patients with low and moderate cardiovascular risk

Aim: To assess the probability of masked arterial hypertension (MAH) in patients with low and moderate cardiovascular risk depending on polymorphisms in selected genes.Materials and methods: Ninety two (92) patients (mean age, 41.93±8.92 years) with low and moderate cardiovascular risk without any documented cardiovascular disorders were assessed clinically and had 24-hour ECG monitoring performed, as well as genotyping on the following markers: AGT Thr174Met rs4762, GNB3 C825T rs5443, MTHFR C677T rs1801133, MTRR Ile22Met rs1801394, ApoE Cys130Arg rs 429358, and PPARα G/C rs4253778. Depending on the presence of MAH, the patients were divided into two groups: with newly diagnosed arterial hypertension corresponding to the MAH criteria (n=58, 63%) and with normal office-based and ambulatory blood pressure and normal blood pressure according to the results of 24-hour ECG monitoring (n=34, 37%).Results: Two groups were not different by their age, cardiovascular risk factors, concomitant diseases and clinical characteristics. There were more men than women in the MAH group (р=0.028). In MAH patients, the most prevalent was Ile22Met rs1801394 A/G polymorphism of the MTRR gene (the odds ratio (OR) and relative risk (RR) for MAH were 4.23 [95% сonfidence interval (CI) 1.56–11.72] and 2.17 [1.25–4.12], respectively). The Cys130Arg rs 429358 Т/С genotype polymorphism of the АроЕ gene was also significant. The probability of MAH in the patients with АроЕ Т/С genotype was more than 3-fold higher: OR 3.67 [95% CI 1.34–10.28], RR 2.15 [95% CI 1.17–4.36]. The correlation analysis showed a moderate association between MAH and MTRR and АроЕ gene polymorphisms (Q=0.62 and Q=0.57, respectively).Conclusion: In patients with low and moderate cardiovascular risk, the probability of MAH depends not only from their gender, but also from their genetic background. The candidate genes for MAH in such patients are Ile22Met rs1801394 A/G polymorphism of the MTRR gene and Cys130Arg rs 429358 Т/С polymorphism of the АроЕ gene.

Volume management of hypertension in patients with chronic kidney disease

Chronic kidney disease (CKD) and hypertension are two closely interlinked public health problems. Kidney is an important organ for regulating blood pressure. Renal lesions may lead to increased blood pressure, and hypertension further accelerates the progression of renal disease, thereby forming a vicious circle which affects the prognosis of patients. Volume overload is an important mechanism in the development of hypertension in patients with CKD. Therefore, more emphasis should be put on volume management of CKD patients with hypertension.

Mechanisms and factors of arterial hypertension development in patients with various types of morphologically verified glomerulonephritis

The literature review provides scientific data on the main mechanisms of the development and progression of arterial hypertension in patients with glomerulonephritis, including genetically determined ones. The mechanisms of vascular kidney damage during the formation of hypertension with hyperuricemia and obesity have been specified. Morphological data are discussed according to which not only vascular damage to arterial structures, but also hyperplasia of intact glomeruli and changes in tubulointerstitium are involved in the formation of hypertension syndrome.

Features of clinical and laboratory indicators in alcoholic liver disease in combination with arterial hypertension depending on T786C polymorphism of the eNOS gene

The goal of the work. Assess the relationship between eNOS gene genotypes (T786C) and some clinical and laboratory parameters in patients with alcoholic liver disease (ALD) in combination with arterial hypertension (AH).Material and methods. 97 patients diagnosed with AHP were examined: 62 patients with ALD with AH (group A) and 35 patients with ALD (group B). Serum content of C-reactive protein, tumor necrosis factor-α (TNFα), transforming growth factor-β1 (TGFβ1), interleukin-10 (IL-10), 8-isoprostane, D-dimer was determined by enzyme-linked immunosorbent assay. The functional state of the endothelium was assessed by the content in the blood of stable metabolites of nitrogen monoxide (nitrites / nitrates), endothelin-1 (ET-1), intercellular adhesion molecules-1 (ICAM-1). Total blood coagulation potential (plasma recalcification time), prothrombin time (PT), thrombin time (TT), activated partial thromboplastin time (APTT), plasma fibrinogen levels, antithrombin III (ATIII) activity, factor XIII (F XIII) activity was determined by traditional methods. Spontaneous platelet aggregation was also studied. To determine the eNOS mutation (T786C), rs2070744 used a protocol with oligonucleotide primers using the method of allele-specific PCR.Results. When studying the frequency of genotypes by the polymorphic variant of the eNOS gene (T786C), it was found that the frequency of TT genotype among patients with ALD with hypertension was 46.8%, CT - 57.1% and SS - 17.2%. Among patients with ALD, the following distribution of genotypes was found: TT - 25.7%, ST - 57.1% and SS - 17.2%. We found a significant difference between the group of patients with ALD with AH and the isolated group of ALD by TT genotype. It was found that the level of ET-1 and the intercellular adhesion molecule (ICAM-1) were significantly higher in patients with ALD with AH by TT genotype compared with the isolated course of ALD. However, the level of total nitric oxide in the combined course of ALD with hypertension was lower than in patients with ALD without hypertension in the presence of this genotype. At the same time, in the combined course of ALD and hypertension, the level of systemic inflammation and oxidative stress is associated with the TT genotype by a polymorphic variant of the eNOS gene (T786C). When studying the state of hemostasis in the combined course of ALD and hypertension, it was found that APTT for the TT genotype was 17.7% higher than in group B. This indicator also had a difference in the middle group between the TT and CT genotypes (by 13.1%) and TT and CC (by 28.3%). The level of D-dimer between groups A and B also had a significant difference in the TT genotype (higher by 14.7% for the combination of ALD and AH). Spontaneous platelet aggregation was significantly higher by 7.7% in patients with ALD with hypertension by TT genotype. In the latter group of patients, factor XIII was significantly lower by 12.6% compared with the group of patients with ALD. Indicators such as plasma recalcification time, prothrombin index and time, thrombin time did not differ significantly between groups of patients.Conclusion. The development of hypertension in patients with ALD is associated with the presence of a homozygous TT genotype for a polymorphic variant of the eNOS gene (T786C). It was found that in patients with ALD with hypertension by TT genotype higher levels of ET-1 and intercellular adhesion molecules ICAM-1 are observed at a lower level of total nitric oxide compared with patients with ALD. The most probable differences in systemic inflammation (IL-10, CRP, TGFβ1) and oxidative stress marker (8-isoprostane) are characteristic of the TT genotype for the polymorphic variant of the eNOS gene (T786C) in patients with ACP with hypertension compared with the isolated course of ALD. Hemostasis parameters such as APTT, antithrombin III, D-dimer, spontaneous platelet aggregation and factor XIII were associated with the TT genotype in patients with ALD with hypertension by the polymorphic variant of the eNOS gene (T786C).

Urate-lowering therapy exerts protective effects against hypertension development in patients with gout.

Many studies have demonstrated that hyperuricemia is associated with hypertension (HTN) development, but few studies have explored whether urate-lowering therapy (ULT), which reverses hyperuricemia, decreases the risk of incident HTN. In this retrospective cohort study, we compared the risk of incident HTN of gout patients between those undergoing and not undergoing ULT. Risks of new-onset diabetes mellitus (DM) and chronic kidney disease (CKD) were also examined. In total, 2712 gout patients from 2000 to 2012 were enrolled. Overall incidence rates of HTN, DM, and CKD were compared between 1356 patients undergoing ULT recipients and 1356 matched control patients. After adjustment for sex, age, area, comorbidities, and drugs used, the incidence rates of HTN were 4.8 and 3.0 per 100 person years for non-ULT and ULT patients, respectively. ULT patients had a lower adjusted hazard ratio (aHR) of HTN (aHR: 0.64, 95% confidence interval [CI]: 0.54-0.75, p < 0.001) than non-ULT patients. The lower risk of incident HTN after xanthine oxidase inhibitors exhibited a significant dose-response trend. ULT patients also had a lower risk of DM (aHR: 0.55, 95% CI: 0.43-0.70) than non-ULT patients. ULT patients exhibited no significant difference in CKD development (aHR: 1.04, 95% CI: 0.85-1.27) as compared with non-ULT patients. The present study revealed that ULT was associated with lower risks of incident HTN and DM, and the protective effect of xanthine oxidase inhibitors seemed to have a dose-response relationship.

GOUT AND ARTERIAL HYPERTENSION: THERAPY PECULIARITIES

The article highlights the issues on comorbidity between gout and hypertension. Emphasis is placed on the necessity in searching for a well-balanced approach toward the treatment this type of comorbidity. Gout is a major social and economic problem in the modern society that leads to a progressive physical incapability, limitation of professional activity, thus impairing the quality of life. Arterial hypertension occurs in patients with gout in 5 - 50% of cases, and in combination with components of metabolic syndrome its prevalence rises up to 80%. As a result, the development of hypertension in patients with gout leads to a deterioration of the kidney functioning due to the combination of two pathological conditions for which the kidneys are either functioning organs or target organs. Management of arterial hypertension by general practitioner requires the searching for the most optimal approach in using metabolically neutral antihypertensives to avoid provoking medication-induced exacerbation of arthritis. In addition, the treatment of such category of patients should also provide the optimal nephroprotective effect and decrease the uric acid concentration in the serum that will contribute to the additional prevention of gout attacks.&#x0D; The aim of the study is to evaluate the nephroprotective, antihypertensive, hypolipidemic effects of the proposed combined therapy in the patients with comorbidity between gout arthritis and arterial hypertension.&#x0D; The study was conducted at the Regional Medical and Diagnostic Centre of Rheumatological Diseases, M.V. Sklifosovskyi Poltava Regional Clinical Hospital, which is the clinical base of the Department of Family Medicine and Therapy, Ukrainian Medical Stomatological Academy. 60 patients with mean age of 54.2 ± 8.6 years were enrolled to the study. The patients suffering from gout arthritis and comorbid hypertension formed the main group. The control group consisted of 60 patients matched by age, demographic and clinical parameters.&#x0D; Following the 12-month treatment period, we have registered clinical effects of the combination therapy proposed in patients with gout and comorbid hypertension. We observed a decrease in blood lipids values in the study groups: total cholesterol decreased by 16.0% in the main group and by 8.0% in the control group, high-density lipoproteins – by 5.6% in the main group and by 6.4% in the control group, low density lipoproteins – by 3.3% in the main group and by 3.4% in the control group, triglycerides – by 22.2% in the main group and 12.3% in the control group.&#x0D; We observed statistically significant improvement in the glomerular filtration rate in the main group (6.4% of cases vs. 1.3% in the control group). The blood creatinine in the both study groups decreased significantly. The uric acid blood concentration decreased by 32.6% in the main group compared to 24.6% in the control group. During the six month period of the therapy the necessity for non-steroidal anti-inflammatory drugs cut down by 58% in the study group vs. 37% in the control group.&#x0D; Conclusions. After 12 month period of therapy proposed, the patients with gout and comorbid hypertension demonstrated clinically confirmed improvement in both study groups (87.7% of patients in the main group vs. 48.6% in the control group). The efficacy of the proposed treatment was assessed by physicians up to 87%, vs. 88% efficacy assessed by the patients in the main group.

The role of insertion-deletion polymorphism of the ACE gene in development of arterial hypertension in patients with chronic obstructive pulmonary disease

Objective. This study aims to establish the role of insertion-deletion polymorphism of the angiotensin-converting enzyme gene in development of arterial hypertension in patients with chronic obstructive pulmonary disease.&#x0D; Materials and Methods: The study group consisted of 96 patients: Group 1 (25 individuals with COPD), Group 2 (23 individuals with AH), Group 3 (28 individuals with COPD and AH). The control group consisted of the 20 healthy subjects. I/D genotypes of ACE were determined by polymerase chain reaction (PCR) amplification. Plasma ACE activity was determined photometrically by a commercially available kit.&#x0D; Results and Discussion: The distribution of polymorphic variants of the ACE gene among COPD-only patients genotype spreading was close to the data obtained in controls. In hypertensive patients, there were fewer ID heterozygotes and more ІІ homozygotes compared to controls. In the COPD+AH category of patients, II genotype was predominant in 7.1% subjects, DD genotype was predominant in 10.0% subjects and the proportion of ID heterozygotes was 17.1% lower compared to controls. The II genotype had a positive relationship with patient age and a negative relationship with body weights and respiratory rates of COPD+AH patients. The ID genotype was associated with increased respiratory rates; however, its correlation with the duration of the disease was negative.&#x0D; Conclusion: The data obtained in the study allow suggesting that polymorphism of the ACE gene doesn’t relate to development of AH in patients with COPD. The highest activity of ACE was found in patients with combination of COPD and AH; maximum findings of ACE activity were seen in patients with DD genotype.&#x0D; Bangladesh Journal of Medical Science Vol.19(3) 2020 p.543-551

Association between biologic disease modifying anti-rheumatic drugs and incident hypertension in patients with rheumatoid arthritis: Results from prospective nationwide KOBIO Registry.

There has been some debate between biologic disease modifying anti-rheumatic drugs (bDMARDs) treatment and hypertension (HTN) in rheumatoid arthritis (RA). The aim of this study was to determine the effect of bDMARDs on the development of HTN in patients with RA.A total of 996 patients eligible for analysis were recruited from the Korean College of Rheumatology Biologics & Targeted Therapy (KOBIO) registry from 2012 to 2018. The bDMARDs were tumor necrosis factor (TNF) inhibitors, abatacept, and tocilizumab. The cDMARDs included methotrexate, hydroxychloroquine, and leflunomide. The incidence rate and 95% confidence interval of HTN were estimated using the Kaplan-Meier method. Hazard ratio (HR) of risk factors associated with hypertension was assessed by cox proportional hazard model analysis.Among the 996 patients, 62 patients (6.2%) were newly diagnosed with HTN. There were differences in incidence rate of HTN among conventional DMARDs (cDMARDs), TNF inhibitors, tocilizumab, and abatacept during the follow-up period (P = .015). Kaplan-Meier analysis showed that there was a significant difference in incident HTN only between cDMARDs and tocilizumab (P = .001). Systolic blood pressure and positive rheumatoid factor were associated with development of HTN (HR = 1.049, P = .016 and HR = 1.386, P = .010, respectively). Cox proportional hazard model analysis showed no difference in the development of HTN between bDMARDs and cDMARDs in RA.This study showed that bDMARDs treatment might not increase risk of incident HTN in patients with RA, compared to cDMARDs.

Short-chain fatty acids accompanying changes in the gut microbiome contribute to the development of hypertension in patients with preeclampsia.

Preeclampsia (PE) is regarded as a pregnancy-associated hypertension disorder that is related to excessive inflammatory responses. Although the gut microbiota (GM) and short-chain fatty acids (SCFAs) have been related to hypertension, their effects on PE remain unknown. We determined the GM abundance and faecal SCFA levels by 16S ribosomal RNA (rRNA) sequencing and gas chromatography, respectively, using faecal samples from 27 patients with severe PE and 36 healthy, pregnant control subjects. We found that patients with PE had significantly decreased GM diversity and altered GM abundance. At the phylum level, patients with PE exhibited decreased abundance of Firmicutes albeit increased abundance of Proteobacteria; at the genus level, patients with PE had lower abundance of Blautia, Eubacterium_rectale, Eubacterium_hallii, Streptococcus, Bifidobacterium, Collinsella, Alistipes, and Subdoligranulum, albeit higher abundance of Enterobacter and Escherichia_Shigella. The faecal levels of butyric and valeric acids were significantly decreased in patients with PE and significantly correlated with the above-mentioned differential GM abundance. We predicted significantly increased abundance of the lipopolysaccharide (LPS)-synthesis pathway and significantly decreased abundance of the G protein-coupled receptor (GPCR) pathway in patients with PE, based on phylogenetic reconstruction of unobserved states (PICRUSt). Finally, we evaluated the effects of oral butyrate on LPS-induced hypertension in pregnant rats. We found that butyrate significantly reduced the blood pressure (BP) in these rats. In summary, we provide the first evidence linking GM dysbiosis and reduced faecal SCFA to PE and demonstrate that butyrate can directly regulate BP in vivo, suggesting its potential as a therapeutic agent for PE.

Ассоциативная роль полиморфизма гена eNOS (4a/4b) в развитии артериальной гипертензии у больных ревматоидным артритом

Aim: to study a contribution of eNOS (4a/4b) gene polymorphism in the development of arterial hypertension (AH) in patients with rheumatoid arthritis (RA).Patients and Methods: 143 patients with RA were examined, among which a group of patients without AH (n=50) and a group of patients with RA in association with AH (n=93) were selected. Healthy volunteers (n=151) were also divided into 2 groups, comparable in age and gender to the main groups. A range of clinical, laboratory, and instrumental methods were used in this study. We also conducted molecular genetics. Blood samples were taken from all patients in the study. DNA was isolated using the phenol-chloroform DNA extraction method. Genotyping for the eNOS gene was performed by PCR-RFLP (Polymerase Chain Reaction — Restriction Fragment Length Polymorphism) analysis. PCR was performed with a set of primers to the corresponding genome regions. PCR products were analyzed by electrophoresis in a 4% polyacrylamide gel followed by staining with ethidium bromide.Results: during the molecular genetics, there was a statistically significant prevalence of 4a/4a homozygous genotype and 4a alleles of eNOS gene polymorphism in patients with RA in association with AH versus these parameters in patients with RA without AH. The estimated risk concerning odds ratio of RA occurrence in association with AH in carriers of 4a/4a genotype in the eNOS gene was 3.635 times higher versus carriers of 4a/4b and 4b/4b genotypes. 4a allele was significantly more common in the group of patients with RA in association with AH versus the control group (OR=3.458 [95% CI 1.571–4.575]; p&lt;0.05). There were no statistically significant values in the group of patients with RA without AH versus the control group with healthy volunteers.Conclusion: 4а/4a homozygous genotype and 4a allele of the eNOS 4a/4b gene polymorphism are predictors of RA development in association with AH.KEYWORDS: rheumatoid arthritis, cardiovascular pathology, arterial hypertension, molecular genetics, single-nucleotide polymorphism, genetic association.FOR CITATION: Chernova A.A., Nikulina S.Yu., Tolstokorova Yu.A. Association of eNOS (4a/4b) gene polymorphism with the development of arterial hypertension in patients with rheumatoid arthritis. Russian Medical Inquiry. 2020;4(8):471–474. DOI: 10.32364/2587-6821-2020-4-8-471-474.