Comparison of the effects of liraglutide and sibutramine in obese patients

Background: Obesity is a global noncommunicable pandemic. The low effectiveness of treating obesity is associated with the difficulty of maintaining weight loss due to the reaction of the appetite regulation system. Drugs with central mechanisms of action can help overcome this problem.Aim: The aim of our study was to compare the effects of liraglutide and sibutramine (Reduxin) on the dynamics of weight and cardiometabolic parameters in obese patients without cardiovascular diseases.Materials and methods: We estimated the dynamics of the main metabolic parameters (BMI, glucose, lipid metabolism, blood pressure), the level of hormones involved in the regulation of fat metabolism (leptin, adiponectin, insulin), the ­HOMA-IR index, markers of oxidative stress and inflammation during therapy with liraglutide in comparison with reduxin for 6 months in obese patients.Results: 64 obese patients were included in the study: 25 patients — in the “Liraglutide” group, 39 patients — in the “Sibutramine” group in accordance with the declared inclusion / exclusion criteria. The included patients were young, average body mass index (BMI) (37.92 ± 5.45 kg / m2), average glycemic level was 5.47 ± 0.81 mmol /l, HOMA-IR was 6.01 ± 4.25, blood pressure was at inclusion was within the normal range, but 21.8% of patients received antihypertensive therapy.Both treatment options provided a comparable decrease in body weight (-10.28% vs -9.47%, p = 0.13)., Leptin level (-32.12% vs -41.77%, p = 0.77) and myeloperoxidase (-33.33% vs -19.91%, p = 0.2). The blood pressure level did not change significantly on liraglutide, while on reduxin the level of diastolic blood pressure (dBP) increased significantly (6.87%, p = 0.006). There was a more pronounced decrease in insulin levels compared to the baseline level (-46%, p = 0.005), as well as a decrease in the HOMA-IR index (-50.08, p = 0.005) on liraglutide therapy.An increase in adiponectin levels (+ 45.36% vs 14.01%, p = 0.0045) and a decrease in low density lipoprotein(LDL) cholesterol were significantly more pronounced on reduxin therapy (-15.03% vs -9.4%, p = 0.006).36% of the participants completed their participation in the study ahead of schedule due to the lack of effect in the form of weight loss in the «Liraglutide» group. Side effects in the “Liraglutide” group were observed in 16% of patients. 48% of patients took part in the study within 6 months. In the «Sibutramine» group 33.4% of patients completed the study ahead of schedule for reasons unrelated to the drug intake, the side effects were observed in 20.5% of patients. 46.1% of participants in the «Sibutramine» group received therapy for 6 months.Conclusions: This study confirms the previous findings that both liraglutide and reduxin therapy provide effective weight loss. We found a positive trend in markers of inflammation, atherogenesis and oxidative stress, and leptin levels. Liraglutide therapy was accompanied by a more pronounced effect on the state of carbohydrate metabolism, and reduxin therapy provided a more pronounced dynamics of lipid disorders and adiponexin. Both groups were characterized by a rather low adherence to therapy, but the incidence of side effects requiring stopping therapy was higher in the Sibutramine group

СОВРЕМЕННЫЕ ПРЕДСТАВЛЕНИЯ О КЛЕТОЧНО-МОЛЕКУЛЯРНЫХ МЕХАНИЗМАХ АНГИОГЕНЕЗА

The review contains modern scientific literary data, recently conducted studies, which devoted to studying of molecular, cellular and genetic mechanisms in processes of angiogenesis. The authors describe in detail angiogenesis stages, value of the main proangiogenic and antiangiogenic factors, apoptosis factors, which have different orientation in regulation of blood vessels development. Role of a special population of bone marrow-derived stem cells - endothelial progenitor cells (EPC) in the neovascularization is analyzed. Participation of VEGF-dependent, ANG/Tie-dependent and Notch-signaling pathways, posttranscription regulation of a genome with participation of microRNA in angiogenesis processes are discussed and reviewed.В обзоре представлены современные научные литературные данные, рассмотрены проведенные исследования, посвященные изучению молекулярных, клеточных и генетических механизмов в процессах ангиогенеза. Авторы детально анализируют этапы процесса ангиогенеза, роль ведущих проангиогенных и антиангиогенных факторов, факторов апоптоза, обладающих различной направленностью в регуляции развития кровеносных сосудов. Проводится подробный анализ роли особой популяция стволовых клеток костного мозга - предшественников эндотелиальных клеток - в процессах неоваскуляризации. Обсуждаются и анализируются участие VEGF-, Ang/Tie-зависимых и Notch-сигнальных путей, посттранскрипционной регуляции генома с участием микроРНК в процессах ангиогенеза

ICD-10 code-based definition of heart failure in Saint Petersburg electronic health records: prevalence, health care utilization and outcomes

Aim. To analyze prevalence of heart failure (HF), clinical and demographic characteristics, health care utilization, and outcomes according to the used International Statistical Classification of Diseases and Related Health Problems 10th Revision (ICD-10) codes in regional integrated electronic health record database in Saint Petersburg.Material and methods. The retrospective analysis of the Saint Petersburg regional integrated electronic health record database for 2019 was performed. At least one of the following ICD-10 codes has been considered as HF case: I50.x (standard coding) and/or I11.0, I13.0, I13.2, I25.5, I42.0, I42.9, I09.9, I43.0, I43.1, I43.2, I43.8, I42.5, I42.6, I42.7, I42.8 (extended coding).Results. A total of 64070 adult patients with HF had medical encounters in 2019, 34,5% of whom were identified using standard coding, 65,5% — using extended coding. The combination of codes was observed in 9,9% of cases. HF prevalence/mortality was 1,4%/6,8% in general, as well as 0,49%/15,7% and 0,93%/2,1% with standard and extended coding, respectively. HF patients had high healthcare utilization with the mean number of 14 encounters per patient per year. Actually, 24% of patients had more than 20 both inpatient and outpatient encounters and 54% of patients — at least 1 all-cause hospitalization during the year. Encounters of patients with HF accounted for 4,3% of all visits, 6,5% of all hospitalizations, 4,1% of all outpatient visits and 9,7% of all emergency contacts during the year. Patients identified by the standard coding compared with the extended coding had older age and higher incidence of comorbidities, as well as greater hospitalization and death rates, but lower number of outpatient visits.Conclusion. The prevalence of HF among the adult population of Saint. Petersburg in 2019 was 1,4%. HF was characterized by a high health care utilization and mortality rate reaching 15,7 % per year. The use of different approaches to coding presumably could help to identify different groups of patients with HF, which requires the adaptation of healthcare models and an active monitoring system to reduce the risk of adverse events

РОЛЬ ГАЛЕКТИНА-3 И ЭПИКАРДИАЛЬНОГО ЖИРА В РАЗВИТИИ ФИБРИЛЛЯЦИИ ПРЕДСЕРДИЙ ПРИ МЕТАБОЛИЧЕСКОМ СИНДРОМЕ

Objective. To evaluate the epicardial fat thickness (EFT) in patients with metabolic syndrome (MS), including paroxysmal and persistent atrial fibrillation (AF). To relate EFT to the fibroid heart marker, i.e. galectin 3. Materials and methods. We examined 100 patients with MS (50 with AF), and 50 healthy persons made the control group. Serum galectin 3 was measured by ELISA method. The EFT was measured with echocardiography. Results. EFT in patients with MS was twofold higher than in healthy persons. EFT in patients with MS and AF didn't differ significantly from that in patients with MS without AF. Positive correlation between the levels of EFT and galectin 3 in serum was revealed. Serum galectin 3 and EFT were associated with atrial fibrillation in patients with MS (OR:1,27, 95% CI 1,02-1,58 and OR:1,73, 95% CI 1,37-2,19, correspondingly).Conclusion. Definition of EFT at echocardiography can be used in the assessment of risk AF in patients with MS.Цель работы - определить толщину эпикардиального жира (ТЭЖ) у пациентов с метаболическим синдромом (МС), в том числе с пароксизмальной и персистирующей формой фибрилляции предсердий (ФП); установить связь ТЭЖ с маркером фиброза миокарда - галектином-3. Обследованы 100 пациентов с МС (IDF, 2005), из них 50 больных с ФП. Группу контроля составили 50 практически здоровых людей. Уровень галектина-3 в сыворотке крови оценивался методом ИФА. ТЭЖ определена с помощью ЭхоКГ. Значение ТЭЖ у пациентов с МС было в 2 раза больше, чем у здоровых. У больных с ФП и МС значение данного показателя значимо не отличалось от пациентов с МС без ФП. Установлена корреляция ТЭЖ с уровнем галектина-3. Га-лектин-3 и ТЭЖ были ассоциированы с ФП у пациентов с МС (ОШ: 1,27, 95 % ДИ, 1,02- 1,58 и ОШ: 1,73, 95 % ДИ, 1,37-2,19 соответственно). Определение ТЭЖ при ЭхоКГ может быть использовано в оценке риска развития ФП у пациентов с МС

ВАРИАНТЫ С-572G ГЕНА ИНТЕРЛЕЙКИНА-6 И С-1112Т ГЕНА ИНТЕРЛЕЙКИНА-13 И ОСОБЕННОСТИ КЛИНИЧЕСКОГО ТЕЧЕНИЯ ДИФФУЗНОГО ТОКСИЧЕСКОГО ЗОБА

Relevance. Diffuse toxic goiter (DTG) is an autoimmune thyroid disease, which is based on the excessive secretion of autoantibodies to thyroid-stimulating hormone receptor (TRAb). Over the last decades, high relapse rate of thyrotoxicosis is observed after withdrawal of conservative therapy. At the same time, there are no reliable criteria to predict the efficiency of drug therapy. It is widely discussedin literature that singlenucleotide polymorphism (SNP) at cytokine-encoding genesnot only confers susceptibility to the DTG, but also has impact on the features ofclinical course of the disease .The aim of this study was to determine whether the SNPs in -572C/G (rs1800796) of IL6 or -1112C/Т (rs1800925) of IL13 genes can influence thedevelopment and clinical course of the diffuse toxic goiter (DTG).Materials and methods. We examined 270 patients with diffuse toxic goiter and 200 healthy persons (reference subjects)with the help of molecular genetic analysis of polymorphic variants of the gene encoding the Pro-inflammatory cytokines. Identification of C-572G of IL6 gene and C-1112T of IL13gene was performed using the PCR method followed by the restriction analysis.Results. We determined that the carriage of -572G allele of the rs1800796 in IL6 gene isassociated with the growth of recurrence risk of thyrotoxicosis and the absence of remission of DTGin 1.3 times (р=0.031, OR=1.3, 95 %, CI 0.98–1.76) and the carriage of CC genotype of the rs1800925 in IL13 – in 2.3 times (р=0.026, OR=2.3, 95 %, CI 1.09–4.82) respectively. The obtained results allowed to revealnew genetic markers of an adverse course in patients with diffuse toxic goiter, Saint Petersburg residents.Введение. Диффузный токсический зоб (ДТЗ) – аутоиммунное заболевание, в основе которого лежит образование аутоантител к рецептору тиреотропного гормона. За последние десятилетия отмечается неуклонный рост рецидива тиреотоксикоза после окончания консервативной терапии. При этом достоверных критериев, позволяющих прогнозировать эффективность медикаментозной терапии, не существует. В литературе широко обсуждается, что полиморфизм генов интерлейкинов (ИЛ) влияет как на предрасположенность к ДТЗ, так и на особенности его клинического течения.Целью исследования явилась оценка роли полиморфных вариантов С-572G (rs1800796) гена IL6 и С-1112Т (rs1800925) гена IL13 в развитии и клиническом течении ДТЗ.Материал и методы. Молекулярно-генетический анализ полиморфных вариантов гена, кодирующих провоспалительные цитокины, был выполнен у 270 больных ДТЗ и 200 лиц без аутоиммунной патологии. Идентификация С-572G гена IL6 и С-1112Т гена IL13 проведена методом ПЦР с последующим рестрикционным анализом.Результаты исследования. Установлено, что носительство аллеля -572G гена IL6 ассоциируется с повышением риска рецидива тиреотоксикоза и отсутствием ремиссии ДТЗ в 1,3 раза (р=0,031, OR=1,3, 95 % ДИ 0,98–1,76), а носительство генотипа С-1112С гена IL13 – в 2,3 раза (р=0,026, OR=2,3, 95 % ДИ 1,09–4,82). Полученные результаты позволили выявить новые генетические маркеры неблагоприятного течения у больных ДТЗ, жителей Санкт-Петербурга