Pub Date : 2024-04-04DOI: 10.22141/2224-0721.20.1.2024.1367
N. Pashkovska, V. Pashkovskyy
The review analyzed literature data on the epidemiology, risk factors, and mechanisms of acute cerebrovascular accident (ACVA) in patients with diabetes mellitus. The role of insulin resistance and the effectiveness of therapeutic approaches to its correction in cerebral stroke are considered. Diabetes mellitus is recognized as an independent modifiable risk factor for ACVA. In people with diabetes of different age, the risk of stroke is increased by 2–6 times, and the indicators are especially high in patients of young working age. The presence of diabetes mellitus is associated with more severe symptoms, increased risk of complications, longer hospitalization, and higher mortality. Research results show that insulin resistance is one of the main triggers for the development of ischemic stroke due to embolism caused by oxidative stress, endothelial dysfunction and platelet hyperactivation, as well as due to atherosclerotic changes caused by inflammation, proliferation of smooth muscle cells of the vascular wall, dyslipidemia and hypertension on the background of hyperglycemia and hyperinsulinemia. It has been proven that insulin resistance not only provokes ACVA, but also negatively affects their prognosis. Metformin is a key drug for improving insulin sensitivity and is recognized as one of the most important first-line therapeutic agents to achieve and maintain treatment goals in patients with type 2 diabetes. The results of experimental and clinical studies proved that this agent has a whole range of neuroprotective properties, which generally prevent the development of cerebral ischemia and reduce the negative consequences in case of its occurrence. Animals with experimental acute cerebral ischemia who have been treated with metformin had a better overall neurological score, significantly smaller infarct size, better coordination scores, and higher numbers of neurons and microglia. The neuroprotective effect of metformin in stroke is realized through the AMPK (5’AMP-activated protein kinase) signaling pathway with reduction of oxidative stress, neuroinflammation, stimulation of angiogenesis and neurogenesis, autophagy, and inhibition of apoptosis. According to data from cohort and randomized clinical trials, the use of metformin is associated with a significantly lower risk of developing ACVA. Long-term use of this drug in type 2 diabetes contributes to a milder course of stroke, is associated with better functional recovery, and a decrease in disability and mortality rates.
{"title":"Insulin resistance and stroke: mechanisms and therapeutic approaches","authors":"N. Pashkovska, V. Pashkovskyy","doi":"10.22141/2224-0721.20.1.2024.1367","DOIUrl":"https://doi.org/10.22141/2224-0721.20.1.2024.1367","url":null,"abstract":"The review analyzed literature data on the epidemiology, risk factors, and mechanisms of acute cerebrovascular accident (ACVA) in patients with diabetes mellitus. The role of insulin resistance and the effectiveness of therapeutic approaches to its correction in cerebral stroke are considered. Diabetes mellitus is recognized as an independent modifiable risk factor for ACVA. In people with diabetes of different age, the risk of stroke is increased by 2–6 times, and the indicators are especially high in patients of young working age. The presence of diabetes mellitus is associated with more severe symptoms, increased risk of complications, longer hospitalization, and higher mortality. Research results show that insulin resistance is one of the main triggers for the development of ischemic stroke due to embolism caused by oxidative stress, endothelial dysfunction and platelet hyperactivation, as well as due to atherosclerotic changes caused by inflammation, proliferation of smooth muscle cells of the vascular wall, dyslipidemia and hypertension on the background of hyperglycemia and hyperinsulinemia. It has been proven that insulin resistance not only provokes ACVA, but also negatively affects their prognosis. Metformin is a key drug for improving insulin sensitivity and is recognized as one of the most important first-line therapeutic agents to achieve and maintain treatment goals in patients with type 2 diabetes. The results of experimental and clinical studies proved that this agent has a whole range of neuroprotective properties, which generally prevent the development of cerebral ischemia and reduce the negative consequences in case of its occurrence. Animals with experimental acute cerebral ischemia who have been treated with metformin had a better overall neurological score, significantly smaller infarct size, better coordination scores, and higher numbers of neurons and microglia. The neuroprotective effect of metformin in stroke is realized through the AMPK (5’AMP-activated protein kinase) signaling pathway with reduction of oxidative stress, neuroinflammation, stimulation of angiogenesis and neurogenesis, autophagy, and inhibition of apoptosis. According to data from cohort and randomized clinical trials, the use of metformin is associated with a significantly lower risk of developing ACVA. Long-term use of this drug in type 2 diabetes contributes to a milder course of stroke, is associated with better functional recovery, and a decrease in disability and mortality rates.","PeriodicalId":13962,"journal":{"name":"INTERNATIONAL JOURNAL OF ENDOCRINOLOGY (Ukraine)","volume":"13 9","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140744863","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-03-03DOI: 10.22141/2224-0721.20.1.2024.1359
V.A. Serhiyenko, V. B. Sehin, V.I. Pankiv, A.A. Serhiyenko
Post-traumatic stress disorder (PTSD) and metabolic syndrome (MetS) frequently coexist and share neurobiological and clinical features. In particular, the results of meta-analyses indicate a higher prevalence of MetS in patients with PTSD compared to the general population. PTSD is also a recognized risk factor for MetS. This synchronicity can be partially explained by pathogenetic pathways present in both conditions. These include genetic factors, dysfunction of the hypothalamic-pituitary-adrenal axis, chronic low-grade inflammation, oxidative stress, insulin resistance, and immune dysregulation. Thus, similar mechanisms are involved in the clinical worsening of PTSD and the development of adverse cardiovascular events associated with MetS. Dyssomnias are one of the characteristic clinical features of PTSD. Today, it is believed that posttraumatic circadian rhythm disorders are the core and not a secondary feature of PTSD, which mediate the neurobiological correlates of disorders due to homeostasis imbalance. At the same time, dyssomnias, chronodestruction, and depressive disorders are part of the pathogenesis of insulin resistance, obesity, and MetS. Thus, treatment of dyssomnias is one of the key tasks in the prevention and treatment of comorbid PTSD and MetS. Regulation of sleep processes and circadian rhythms through exogenous intervention, especially with melatonergic drugs, is likely to be a key part of preventing and treating dyssomnias in people who have both PTSD and MetS. The purpose of this review is to analyze the specifics of the relationships between PTSD and MetS, PTSD and dyssomnias, MetS and sleep disorders. We conducted the search in Scopus, Science Direct (from Elsevier), and PubMed, including Medline databases. The key words used were “post-traumatic stress disorder,” “dyssomnias,” “chronodestruction,” and “metabolic syndrome”. The identification of research findings that were not found during online searches involved manual searching of the bibliography of publications.
{"title":"Post-traumatic stress disorder, dyssomnias, and metabolic syndrome","authors":"V.A. Serhiyenko, V. B. Sehin, V.I. Pankiv, A.A. Serhiyenko","doi":"10.22141/2224-0721.20.1.2024.1359","DOIUrl":"https://doi.org/10.22141/2224-0721.20.1.2024.1359","url":null,"abstract":"Post-traumatic stress disorder (PTSD) and metabolic syndrome (MetS) frequently coexist and share neurobiological and clinical features. In particular, the results of meta-analyses indicate a higher prevalence of MetS in patients with PTSD compared to the general population. PTSD is also a recognized risk factor for MetS. This synchronicity can be partially explained by pathogenetic pathways present in both conditions. These include genetic factors, dysfunction of the hypothalamic-pituitary-adrenal axis, chronic low-grade inflammation, oxidative stress, insulin resistance, and immune dysregulation. Thus, similar mechanisms are involved in the clinical worsening of PTSD and the development of adverse cardiovascular events associated with MetS. Dyssomnias are one of the characteristic clinical features of PTSD. Today, it is believed that posttraumatic circadian rhythm disorders are the core and not a secondary feature of PTSD, which mediate the neurobiological correlates of disorders due to homeostasis imbalance. At the same time, dyssomnias, chronodestruction, and depressive disorders are part of the pathogenesis of insulin resistance, obesity, and MetS. Thus, treatment of dyssomnias is one of the key tasks in the prevention and treatment of comorbid PTSD and MetS. Regulation of sleep processes and circadian rhythms through exogenous intervention, especially with melatonergic drugs, is likely to be a key part of preventing and treating dyssomnias in people who have both PTSD and MetS. The purpose of this review is to analyze the specifics of the relationships between PTSD and MetS, PTSD and dyssomnias, MetS and sleep disorders. We conducted the search in Scopus, Science Direct (from Elsevier), and PubMed, including Medline databases. The key words used were “post-traumatic stress disorder,” “dyssomnias,” “chronodestruction,” and “metabolic syndrome”. The identification of research findings that were not found during online searches involved manual searching of the bibliography of publications.","PeriodicalId":13962,"journal":{"name":"INTERNATIONAL JOURNAL OF ENDOCRINOLOGY (Ukraine)","volume":"18 4","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140080809","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-03-03DOI: 10.22141/2224-0721.20.1.2024.1355
O. Prybyla, O. Zinych, N.M. Kushnareva, A. Kovalchuk, K. Shyshkan-Shyshova
Background. The problem of studying the causes and mechanisms of metabolic disorders in metabolic syndrome and type 2 diabetes mellitus (T2DM) is one of the most important questions in modern medicine. It is due to the growing prevalence of dysmetabolic conditions and their serious consequences for the population health in the modern world. The initial hypothesis was that the differences in hormonal and metabolic conditions in patients with T2DM can be explained by the peculiarities of the anabolic-catabolic balance in different metabolic phenotypes. The aim of the work was to study the features of anthropometric and compositional parameters, indicators of carbohydrate, lipid and purine metabolism, anabolic-catabolic balance as predictors of cardiovascular diseases in patients with T2DM, depending on the phenotype. Materials and methods. One hundred and sixty-five patients with T2DM were included in the study, 71 women and 94 men aged from 32 to 82 years (59.0 ± 8.3 years). They had a level of glycated hemoglobin higher than 6.7 % (8.3 ± 1.8 %) against the background of taking oral hypoglycemic agents. Results. During the examination, it was found that the metabolism of patients without general obesity has a predominantly catabolic orientation, which, compared to those with general obesity, is manifested in a lower absolute accumulation of total and visceral fat, a reduced level of uricemia (due to a lower reabsorption of urate in the renal tubules, a lower activity of the anabolic pathway of reutilization), which is accompanied by a lower level of anabolic hormones, insulin and dehydroepiandrosterone sulfate (DHEA-S), and a higher level of the catabolic stress hormone cortisol. General obesity in patients with body mass index ≥ 30 kg/m2 is caused by the predominant influence of anabolic hormones (insulin, DHEA-S), which contribute to the de novo synthesis of fatty acids and purine bases, the reutilization of purines and the reabsorption of uric acid. This leads to the accumulation of fat in the subcutaneous and visceral adipose tissue and an increase in the level of uricemia under the conditions of a lower content of the catabolic hormone cortisol. Conclusions. The application of a set of anthropometric, composition biochemical and hormonal indicators allows for a differential diagnosis of alimentary hypokinetic (anabolic) and stress (catabolic) phenotypes in patients with T2DM. An additional characteristic of the metabolic status in T2DM may be the assessment of uric acid production and excretion in patients with varying degrees of obesity. The listed signs indicate an anabolic type of metabolism in obesity.
{"title":"Cardiometabolic characteristics of type 2 diabetes patients depending on obesity phenotypes","authors":"O. Prybyla, O. Zinych, N.M. Kushnareva, A. Kovalchuk, K. Shyshkan-Shyshova","doi":"10.22141/2224-0721.20.1.2024.1355","DOIUrl":"https://doi.org/10.22141/2224-0721.20.1.2024.1355","url":null,"abstract":"Background. The problem of studying the causes and mechanisms of metabolic disorders in metabolic syndrome and type 2 diabetes mellitus (T2DM) is one of the most important questions in modern medicine. It is due to the growing prevalence of dysmetabolic conditions and their serious consequences for the population health in the modern world. The initial hypothesis was that the differences in hormonal and metabolic conditions in patients with T2DM can be explained by the peculiarities of the anabolic-catabolic balance in different metabolic phenotypes. The aim of the work was to study the features of anthropometric and compositional parameters, indicators of carbohydrate, lipid and purine metabolism, anabolic-catabolic balance as predictors of cardiovascular diseases in patients with T2DM, depending on the phenotype. Materials and methods. One hundred and sixty-five patients with T2DM were included in the study, 71 women and 94 men aged from 32 to 82 years (59.0 ± 8.3 years). They had a level of glycated hemoglobin higher than 6.7 % (8.3 ± 1.8 %) against the background of taking oral hypoglycemic agents. Results. During the examination, it was found that the metabolism of patients without general obesity has a predominantly catabolic orientation, which, compared to those with general obesity, is manifested in a lower absolute accumulation of total and visceral fat, a reduced level of uricemia (due to a lower reabsorption of urate in the renal tubules, a lower activity of the anabolic pathway of reutilization), which is accompanied by a lower level of anabolic hormones, insulin and dehydroepiandrosterone sulfate (DHEA-S), and a higher level of the catabolic stress hormone cortisol. General obesity in patients with body mass index ≥ 30 kg/m2 is caused by the predominant influence of anabolic hormones (insulin, DHEA-S), which contribute to the de novo synthesis of fatty acids and purine bases, the reutilization of purines and the reabsorption of uric acid. This leads to the accumulation of fat in the subcutaneous and visceral adipose tissue and an increase in the level of uricemia under the conditions of a lower content of the catabolic hormone cortisol. Conclusions. The application of a set of anthropometric, composition biochemical and hormonal indicators allows for a differential diagnosis of alimentary hypokinetic (anabolic) and stress (catabolic) phenotypes in patients with T2DM. An additional characteristic of the metabolic status in T2DM may be the assessment of uric acid production and excretion in patients with varying degrees of obesity. The listed signs indicate an anabolic type of metabolism in obesity.","PeriodicalId":13962,"journal":{"name":"INTERNATIONAL JOURNAL OF ENDOCRINOLOGY (Ukraine)","volume":"25 4","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140080950","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-03-03DOI: 10.22141/2224-0721.20.1.2024.1352
M. Shved, I. Yastremska, V.Yu. Kuchmiy, R.M. Ovsiychuk
Background. Patients with type 2 diabetes mellitus (T2DM) have a 2-fold higher risk of developing coronary heart disease and mortality than those without carbohydrate metabolism disturbances. The reason for such negative trends is the occurrence of metabolic stress due to hyperglycemia and insulin resistance, which causes disturbance in energy metabolism and ischemic damage to cardiomyocytes. The purpose of the study is to improve the effectiveness of rehabilitation treatment and assess the dynamics of quality of life in patients with ST-elevation myocardial infarction (STEMI) and T2DM who are at high risk of developing cardiac complications during the inpatient treatment by including the sodium-glucose transport protein 2 (SGLT2) inhibitor dapagliflozin in the comprehensive therapy. Materials and methods. The study group consisted of 38 patients with STEMI and T2DM who received dapagliflozin in addition to percutaneous coronary intervention (PCI). The control group included 37 patients with STEMI and T2DM who received only standard protocol treatment after PCI. In addition to general clinical examinations and assessment of quality of life using the EuroQol Group EQ-5D-5L questionnaire (1990), echocardiography was performed to determine general and local myocardial contractility by the Simpson method; plasma levels of glucose, insulin were evaluated, and insulin resistance was determined by the HOMA-IR. Results. Patients with STEMI and T2DM after PCI most often developed reperfusion syndrome with left ventricular failure and rhythm disturbances. Under the influence of standard medical treatment, a significant clinical and functional improvement was observed, but postinfarction remodeling progressed with impaired systolic and diastolic function and the development of heart failure syndrome, as well as treatment-resistant atrial and ventricular fibrillation paroxysms, supraventricular and ventricular extrasystoles, and bundle branch block. In patients of the study group with STEMI and T2DM on the comprehensive treatment with the SGLT2 inhibitor dapagliflozin, a significant decrease in the frequency of rhythm and conduction disturbances was noted on the second day of observation, as well as a decrease in postinfarction left ventricular remodeling, which ultimately manifested in a statistically significant improvement of myocardial contractility (ejection fraction increased by 6.7 %) and a decrease in diastolic dysfunction. There was also a significant decrease in the frequency and severity of reperfusion arrhythmias, which was achieved due to the cardiometabolic effect of the SGLT2 inhibitor dapagliflozin. Conclusions. The inclusion of the SGLT2 inhibitor dapagliflozin in the comprehensive treatment led to a significant improvement in central cardiac hemodynamic parameters and a decrease in the frequency and severity of reperfusion arrhythmias and acute left ventricular failure, which contributed to the improvement in quality of life.
{"title":"ST-elevation myocardial infarction in patients with type 2 diabetes mellitus. Influence of the SGLT2 inhibitor dapagliflozin","authors":"M. Shved, I. Yastremska, V.Yu. Kuchmiy, R.M. Ovsiychuk","doi":"10.22141/2224-0721.20.1.2024.1352","DOIUrl":"https://doi.org/10.22141/2224-0721.20.1.2024.1352","url":null,"abstract":"Background. Patients with type 2 diabetes mellitus (T2DM) have a 2-fold higher risk of developing coronary heart disease and mortality than those without carbohydrate metabolism disturbances. The reason for such negative trends is the occurrence of metabolic stress due to hyperglycemia and insulin resistance, which causes disturbance in energy metabolism and ischemic damage to cardiomyocytes. The purpose of the study is to improve the effectiveness of rehabilitation treatment and assess the dynamics of quality of life in patients with ST-elevation myocardial infarction (STEMI) and T2DM who are at high risk of developing cardiac complications during the inpatient treatment by including the sodium-glucose transport protein 2 (SGLT2) inhibitor dapagliflozin in the comprehensive therapy. Materials and methods. The study group consisted of 38 patients with STEMI and T2DM who received dapagliflozin in addition to percutaneous coronary intervention (PCI). The control group included 37 patients with STEMI and T2DM who received only standard protocol treatment after PCI. In addition to general clinical examinations and assessment of quality of life using the EuroQol Group EQ-5D-5L questionnaire (1990), echocardiography was performed to determine general and local myocardial contractility by the Simpson method; plasma levels of glucose, insulin were evaluated, and insulin resistance was determined by the HOMA-IR. Results. Patients with STEMI and T2DM after PCI most often developed reperfusion syndrome with left ventricular failure and rhythm disturbances. Under the influence of standard medical treatment, a significant clinical and functional improvement was observed, but postinfarction remodeling progressed with impaired systolic and diastolic function and the development of heart failure syndrome, as well as treatment-resistant atrial and ventricular fibrillation paroxysms, supraventricular and ventricular extrasystoles, and bundle branch block. In patients of the study group with STEMI and T2DM on the comprehensive treatment with the SGLT2 inhibitor dapagliflozin, a significant decrease in the frequency of rhythm and conduction disturbances was noted on the second day of observation, as well as a decrease in postinfarction left ventricular remodeling, which ultimately manifested in a statistically significant improvement of myocardial contractility (ejection fraction increased by 6.7 %) and a decrease in diastolic dysfunction. There was also a significant decrease in the frequency and severity of reperfusion arrhythmias, which was achieved due to the cardiometabolic effect of the SGLT2 inhibitor dapagliflozin. Conclusions. The inclusion of the SGLT2 inhibitor dapagliflozin in the comprehensive treatment led to a significant improvement in central cardiac hemodynamic parameters and a decrease in the frequency and severity of reperfusion arrhythmias and acute left ventricular failure, which contributed to the improvement in quality of life.","PeriodicalId":13962,"journal":{"name":"INTERNATIONAL JOURNAL OF ENDOCRINOLOGY (Ukraine)","volume":"13 10","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140081223","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-03-03DOI: 10.22141/2224-0721.20.1.2024.1357
M. Ryznychuk, O. Bolshova
Background. The vitamin D receptor (VDR) gene is a key regulator of biological processes, including tissue and cell growth and differentiation, bone metabolism, and modulation of immune responses. Several studies have shown that 1,25(OH)2D increases circulating insulin-like growth factor-1 (IGF-1) levels in vivo and in bone cell cultures. It also increases the expression of IGF-1 receptors in growth plate chondrocytes and several IGF-binding proteins in osteoblasts and bone marrow stromal cell cultures. A vitamin D receptor gene polymorphism is associated with adult height and may affect the growth indicators in children with idiopathic short stature. The purpose was to study the growth indicators and vitamin D levels in children with idiopathic short stature depending on the variants of the Taql polymorphism genotype of the VDR gene. Materials and methods. Determination of the Taql polymorphism of the VDR gene (rs731236) was performed using polymerase chain reaction followed by an analysis of the length of the restriction fragments when detected by agarose gel electrophoresis in 35 children with idiopathic short stature. Results. Most children (68.57 %) were heterozygotes, 17.14 % were homozygotes for T/T alleles, and 14.29 % were homozygotes for C/C alleles. The highest growth retardation has been observed in homozygous T/T carriers. Children carrying homozygotes for C/C alleles had the least growth retardation. Growth hormone levels after clonidine stimulation test and IGF-1 levels in blood were within normal limits in all patients. Vitamin D deficiency was found in T/T homozygotes and vitamin D insufficiency in C/T heterozygotes and C/C homozygotes. Conclusions. Among children with idiopathic short stature, the prevalence of the T/C genotype was 68.57 %. The greatest growth retardation occurred in patients with homozygous T/T alleles (SDS = –2.61 ± 0.31). A decrease in serum vitamin D levels was detected in all children. Vitamin D deficiency (43.83 ± 6.47 nmol/l) was found in children homozygous for the T/T allele, and vitamin D insufficiency — in T/C heterozygotes (58.97 ± 11.78 nmol/l) and C/C homozygotes (56.93 ± 19.54 nmol/l).
{"title":"Growth indices and vitamin D content in children with idiopathic short stature depending on the variants of the Taql polymorphism genotype of the VDR gene","authors":"M. Ryznychuk, O. Bolshova","doi":"10.22141/2224-0721.20.1.2024.1357","DOIUrl":"https://doi.org/10.22141/2224-0721.20.1.2024.1357","url":null,"abstract":"Background. The vitamin D receptor (VDR) gene is a key regulator of biological processes, including tissue and cell growth and differentiation, bone metabolism, and modulation of immune responses. Several studies have shown that 1,25(OH)2D increases circulating insulin-like growth factor-1 (IGF-1) levels in vivo and in bone cell cultures. It also increases the expression of IGF-1 receptors in growth plate chondrocytes and several IGF-binding proteins in osteoblasts and bone marrow stromal cell cultures. A vitamin D receptor gene polymorphism is associated with adult height and may affect the growth indicators in children with idiopathic short stature. The purpose was to study the growth indicators and vitamin D levels in children with idiopathic short stature depending on the variants of the Taql polymorphism genotype of the VDR gene. Materials and methods. Determination of the Taql polymorphism of the VDR gene (rs731236) was performed using polymerase chain reaction followed by an analysis of the length of the restriction fragments when detected by agarose gel electrophoresis in 35 children with idiopathic short stature. Results. Most children (68.57 %) were heterozygotes, 17.14 % were homozygotes for T/T alleles, and 14.29 % were homozygotes for C/C alleles. The highest growth retardation has been observed in homozygous T/T carriers. Children carrying homozygotes for C/C alleles had the least growth retardation. Growth hormone levels after clonidine stimulation test and IGF-1 levels in blood were within normal limits in all patients. Vitamin D deficiency was found in T/T homozygotes and vitamin D insufficiency in C/T heterozygotes and C/C homozygotes. Conclusions. Among children with idiopathic short stature, the prevalence of the T/C genotype was 68.57 %. The greatest growth retardation occurred in patients with homozygous T/T alleles (SDS = –2.61 ± 0.31). A decrease in serum vitamin D levels was detected in all children. Vitamin D deficiency (43.83 ± 6.47 nmol/l) was found in children homozygous for the T/T allele, and vitamin D insufficiency — in T/C heterozygotes (58.97 ± 11.78 nmol/l) and C/C homozygotes (56.93 ± 19.54 nmol/l).","PeriodicalId":13962,"journal":{"name":"INTERNATIONAL JOURNAL OF ENDOCRINOLOGY (Ukraine)","volume":"11 10","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140081019","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-03-03DOI: 10.22141/2224-0721.20.1.2024.1354
O. Kuryata, O. Mytrokhina, Yu.S. Kushnir, O. Stadnyk
Background. Post-COVID syndrome is associated with a wide range of chronic symptoms or conditions. Coronavirus disease 2019 (COVID-19) causes metabolic disorders such as hyperglycemia, insulin resistance. Insulin-like growth factor 1 (IGF-1) is associated with an impaired glucose tolerance and a higher risk of developing type 2 diabetes. Currently, the study of molecules regulating carbohydrate metabolism as potential biomarkers of post-COVID syndrome and targets for therapeutic influence is relevant. The purpose of the study was to assess the level of IGF-1 and its relationship with regulation of carbohydrate metabolism, as well as the dynamics of the evaluated indicators under the influence of drug treatment in patients with hypertension and stable coronary heart disease who suffered from COVID-19. Materials and methods. Fifty-five patients who had a mild and moderate COVID-19 were included in the study; their average age was 55.87 [40; 75] years. The results of routine laboratory tests were registered and analyzed. The content of insulin and IGF-1 was assessed by enzyme immunoassay. The HOMA-IR was calculated. Results. In patients with a moderate COVID-19 compared to those with a mild one, a significant decrease in the level of IGF-1 (р = 0.008) was found against the background of increased reference values of glucose, insulin, and HOMA-IR (р < 0.01). The influence of the degree of hypertension on the IGF-1 level was revealed (р = 0.004). An inverse relationship between IGF-1 and glucose level was noted (r = –0.28, p = 0.034). The use of meldonium contributed to a significant decrease in glucose and insulin content (p < 0.001), and an increase in IGF-1. Against the background of taking meldonium, the dynamics of the shift towards a decrease in the HOMA-IR was more significant. Conclusions. An inverse relationship was found between IGF-1 and blood glucose, regardless of the level of insulin and HOMA-IR, in patients with hypertension and stable ischemic heart disease in the post-COVID period. Meldonium has been shown to improve carbohydrate metabolism by normalizing insulin levels and reducing the phenomena of insulin resistance as a potential drug target. Meldonium improved the clinical course of ischemic heart disease and demonstrated good tolerability and safety.
{"title":"Post-COVID syndrome: status of carbohydrate metabolism in patients with hypertension and stable ischemic heart disease","authors":"O. Kuryata, O. Mytrokhina, Yu.S. Kushnir, O. Stadnyk","doi":"10.22141/2224-0721.20.1.2024.1354","DOIUrl":"https://doi.org/10.22141/2224-0721.20.1.2024.1354","url":null,"abstract":"Background. Post-COVID syndrome is associated with a wide range of chronic symptoms or conditions. Coronavirus disease 2019 (COVID-19) causes metabolic disorders such as hyperglycemia, insulin resistance. Insulin-like growth factor 1 (IGF-1) is associated with an impaired glucose tolerance and a higher risk of developing type 2 diabetes. Currently, the study of molecules regulating carbohydrate metabolism as potential biomarkers of post-COVID syndrome and targets for therapeutic influence is relevant. The purpose of the study was to assess the level of IGF-1 and its relationship with regulation of carbohydrate metabolism, as well as the dynamics of the evaluated indicators under the influence of drug treatment in patients with hypertension and stable coronary heart disease who suffered from COVID-19. Materials and methods. Fifty-five patients who had a mild and moderate COVID-19 were included in the study; their average age was 55.87 [40; 75] years. The results of routine laboratory tests were registered and analyzed. The content of insulin and IGF-1 was assessed by enzyme immunoassay. The HOMA-IR was calculated. Results. In patients with a moderate COVID-19 compared to those with a mild one, a significant decrease in the level of IGF-1 (р = 0.008) was found against the background of increased reference values of glucose, insulin, and HOMA-IR (р < 0.01). The influence of the degree of hypertension on the IGF-1 level was revealed (р = 0.004). An inverse relationship between IGF-1 and glucose level was noted (r = –0.28, p = 0.034). The use of meldonium contributed to a significant decrease in glucose and insulin content (p < 0.001), and an increase in IGF-1. Against the background of taking meldonium, the dynamics of the shift towards a decrease in the HOMA-IR was more significant. Conclusions. An inverse relationship was found between IGF-1 and blood glucose, regardless of the level of insulin and HOMA-IR, in patients with hypertension and stable ischemic heart disease in the post-COVID period. Meldonium has been shown to improve carbohydrate metabolism by normalizing insulin levels and reducing the phenomena of insulin resistance as a potential drug target. Meldonium improved the clinical course of ischemic heart disease and demonstrated good tolerability and safety.","PeriodicalId":13962,"journal":{"name":"INTERNATIONAL JOURNAL OF ENDOCRINOLOGY (Ukraine)","volume":"24 7","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140081070","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-03-03DOI: 10.22141/2224-0721.20.1.2024.1361
V. Zhdan, Y. Kitura, M. Babanina, H. Volchenko, M. Tkachenko, O.A. Kyrіan, I. Ivanitsky, V. Lebid
Metabolic syndrome (MS) is a group of interrelated metabolic disorders such as high blood pressure, central obesity, insulin resistance (IR), dyslipidemia. The main mechanisms that indicate a metabolic disorder and contribute to its development are IR and a large amount of circulating free fatty acids. In turn, tissue IR is often combined with other abnormalities including disorders of uric acid metabolism, changes in the hemostasis system, endothelial dysfunction, increased levels of C-reactive protein. At the same time, metabolic disorders are a risk factor for hyperuricemia. MS occurs in 25–60 to 90 % of all gout patients. About 50 % of patients with hyperuricemia have symptoms of MS. Hyperuricemia as a component of MS is a predictor of cardiovascular mortality, development of diabetes mellitus, hypertension and nephrolithiasis. Hyperuricemia is closely related to diabetes, obesity, coronary heart disease, hypertension. On the example of a clinical case, the main components of MS are considered, as well as the issue of the relationship between hyperuricemia, gout and the components of MS. The main idea behind the creation of the MS concept is to select a population of patients at a high cardiovascular risk in whom preventive measures such as lifestyle modification and the use of adequate drugs can significantly affect the main health indicators. The goal of managing patients with MS is to minimize cardiovascular risk and mortality as much as possible. Accordingly, the therapeutic strategy should include optimal ways to modify the lifestyle; lowering blood pressure to the target level and treating comorbid conditions; reducing low-density lipoprotein cholesterol according to the risk profile: > 50 %, and < 70 mg/dL (1.4 mmol/L) in patients at a very high cardiovascular risk; > 50 %, and < 100 mg/dL (1.8 mmol/l) in high-risk patients; reducing fasting serum glucose < 126 mg/dl (7 mmol/l) or glycated hemoglobin < 7 % (53 mmol/mol); maintaining uric acid level < 6.5 mg/dL (0.387 mmol/L), in patients with gout — below 6 mg/dL (0.357 mmol/L). Thus, according to the results of the research, a causal relationship was found between insulin resistance and serum uric acid levels in patients with metabolic syndrome. The strategy for managing patients with metabolic syndrome should include screening and correction of hypertension, carbohydrate purine metabolism, dyslipidemia, and prevention of cardiovascular events.
{"title":"Metabolic syndrome and hyperuricemia: features of patient management (clinical case)","authors":"V. Zhdan, Y. Kitura, M. Babanina, H. Volchenko, M. Tkachenko, O.A. Kyrіan, I. Ivanitsky, V. Lebid","doi":"10.22141/2224-0721.20.1.2024.1361","DOIUrl":"https://doi.org/10.22141/2224-0721.20.1.2024.1361","url":null,"abstract":"Metabolic syndrome (MS) is a group of interrelated metabolic disorders such as high blood pressure, central obesity, insulin resistance (IR), dyslipidemia. The main mechanisms that indicate a metabolic disorder and contribute to its development are IR and a large amount of circulating free fatty acids. In turn, tissue IR is often combined with other abnormalities including disorders of uric acid metabolism, changes in the hemostasis system, endothelial dysfunction, increased levels of C-reactive protein. At the same time, metabolic disorders are a risk factor for hyperuricemia. MS occurs in 25–60 to 90 % of all gout patients. About 50 % of patients with hyperuricemia have symptoms of MS. Hyperuricemia as a component of MS is a predictor of cardiovascular mortality, development of diabetes mellitus, hypertension and nephrolithiasis. Hyperuricemia is closely related to diabetes, obesity, coronary heart disease, hypertension. On the example of a clinical case, the main components of MS are considered, as well as the issue of the relationship between hyperuricemia, gout and the components of MS. The main idea behind the creation of the MS concept is to select a population of patients at a high cardiovascular risk in whom preventive measures such as lifestyle modification and the use of adequate drugs can significantly affect the main health indicators. The goal of managing patients with MS is to minimize cardiovascular risk and mortality as much as possible. Accordingly, the therapeutic strategy should include optimal ways to modify the lifestyle; lowering blood pressure to the target level and treating comorbid conditions; reducing low-density lipoprotein cholesterol according to the risk profile: > 50 %, and < 70 mg/dL (1.4 mmol/L) in patients at a very high cardiovascular risk; > 50 %, and < 100 mg/dL (1.8 mmol/l) in high-risk patients; reducing fasting serum glucose < 126 mg/dl (7 mmol/l) or glycated hemoglobin < 7 % (53 mmol/mol); maintaining uric acid level < 6.5 mg/dL (0.387 mmol/L), in patients with gout — below 6 mg/dL (0.357 mmol/L). Thus, according to the results of the research, a causal relationship was found between insulin resistance and serum uric acid levels in patients with metabolic syndrome. The strategy for managing patients with metabolic syndrome should include screening and correction of hypertension, carbohydrate purine metabolism, dyslipidemia, and prevention of cardiovascular events.","PeriodicalId":13962,"journal":{"name":"INTERNATIONAL JOURNAL OF ENDOCRINOLOGY (Ukraine)","volume":"1 2","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140081274","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-03-03DOI: 10.22141/2224-0721.20.1.2024.1351
S.M. Cherenko, A.Yu. Glagolieva, D.E. Makhmudov
Background. The European Thyroid Association consensus for the management of differentiated thyroid cancer (2006) suggested to avoid radioactive iodine (RAI) after thyroidectomy in patients with unifocal microcarcinoma (≤ 1 cm) with no extension beyond the thyroid capsule and without lymph node metastases. As the new data was collected and the risk stratification was revised, in 2022 the same recommendation was expanded to the patients with microcarcinoma and central neck lymph node involvement. The American Thyroid Association guidelines (2015) advocated no RAI ablation after hemi- or total thyroidectomy for thyroid cancer less than 1 cm with 5 and less micrometastases up to 2 mm in central neck lymph nodes as this strategy has no negative impact on the disease prognosis. In low-risk patients, no sufficient evidence of the obligatory postsurgical radioiodine ablation has been yet demonstrated. The aim of our study was to reveal whether RAI after thyroidectomy can be abandoned or postponed until the disease progression is confirmed in low-risk patients. Materials and methods. Two groups of patients (30 per group, 60 in total) with papillary microcarcinoma Т1N1a (5 and less level VI micrometastases up to 2 mm) were observed during a 5-year follow-up. In the first group, patients received 100 mCi (3.75 GBq) I131 shortly after total thyroidectomy while in the second group, postponed RAI was applied when progression signs were observed (elevated serum thyroglobulin level and US/CT suspected findings) after thyroid surgery. Results. After 5 years, no significant difference between groups was observed regarding post-RAI local recurrences (one in the first group and two in the second group) and/or distant metastases (t-test, p = 0.58). All cases of neck recurrences were treated with subsequent surgical excision, with no new data of progression within the specified follow-up. Conclusions. RAI adjuvant therapy for papillary thyroid carcinoma Т1N1a may not be necessary for patients with small number of level VI micrometastases. Local and distant metastases revealed during the careful follow-up by thyroglobulin level elevation and when using visualization techniques can be effectively treated with postponed RAI therapy and/or surgery.
背景。欧洲甲状腺协会关于分化型甲状腺癌治疗的共识（2006年）建议，对于单灶微小癌（≤1厘米）且未扩展至甲状腺囊外、无淋巴结转移的患者，甲状腺切除术后应避免使用放射性碘（RAI）。随着新数据的收集和风险分层的修订，2022年，同样的建议扩大到微小癌和颈部中央淋巴结受累的患者。美国甲状腺协会指南（2015年）主张，对于甲状腺癌小于1厘米、颈部中央淋巴结有5个或更少2毫米以下微转移灶的患者，在半甲状腺或全甲状腺切除术后不进行RAI消融，因为这种策略对疾病预后没有负面影响。对于低危患者，目前还没有充分证据表明手术后必须进行放射性碘消融。我们的研究旨在揭示甲状腺切除术后是否可以放弃 RAI 或推迟 RAI，直至低危患者的疾病进展得到确认。材料和方法。我们对两组Т1N1a乳头状微癌患者（每组30人，共60人）进行了为期5年的随访观察。第一组患者在甲状腺全切除术后不久就接受了100 mCi（3.75 GBq）的I131治疗，而第二组患者则在甲状腺手术后观察到进展迹象（血清甲状腺球蛋白水平升高和US/CT疑似发现）时推迟接受RAI治疗。结果显示5 年后，RAI 术后局部复发（第一组 1 例，第二组 2 例）和/或远处转移（t 检验，P = 0.58）在组间无明显差异。所有颈部复发病例均接受了后续手术切除治疗，在规定的随访期内没有新的进展数据。结论对于有少量Ⅵ度微转移的甲状腺乳头状癌Т1N1a患者，RAI辅助治疗可能并非必要。通过甲状腺球蛋白水平升高和使用可视化技术进行仔细随访时发现的局部和远处转移灶，可以通过推迟 RAI 治疗和/或手术进行有效治疗。
{"title":"Radioiodine ablation after thyroidectomy could be safely abandoned or postponed in selected stage I papillary thyroid carcinoma patients of low-risk group: an observational prospective study","authors":"S.M. Cherenko, A.Yu. Glagolieva, D.E. Makhmudov","doi":"10.22141/2224-0721.20.1.2024.1351","DOIUrl":"https://doi.org/10.22141/2224-0721.20.1.2024.1351","url":null,"abstract":"Background. The European Thyroid Association consensus for the management of differentiated thyroid cancer (2006) suggested to avoid radioactive iodine (RAI) after thyroidectomy in patients with unifocal microcarcinoma (≤ 1 cm) with no extension beyond the thyroid capsule and without lymph node metastases. As the new data was collected and the risk stratification was revised, in 2022 the same recommendation was expanded to the patients with microcarcinoma and central neck lymph node involvement. The American Thyroid Association guidelines (2015) advocated no RAI ablation after hemi- or total thyroidectomy for thyroid cancer less than 1 cm with 5 and less micrometastases up to 2 mm in central neck lymph nodes as this strategy has no negative impact on the disease prognosis. In low-risk patients, no sufficient evidence of the obligatory postsurgical radioiodine ablation has been yet demonstrated. The aim of our study was to reveal whether RAI after thyroidectomy can be abandoned or postponed until the disease progression is confirmed in low-risk patients. Materials and methods. Two groups of patients (30 per group, 60 in total) with papillary microcarcinoma Т1N1a (5 and less level VI micrometastases up to 2 mm) were observed during a 5-year follow-up. In the first group, patients received 100 mCi (3.75 GBq) I131 shortly after total thyroidectomy while in the second group, postponed RAI was applied when progression signs were observed (elevated serum thyroglobulin level and US/CT suspected findings) after thyroid surgery. Results. After 5 years, no significant difference between groups was observed regarding post-RAI local recurrences (one in the first group and two in the second group) and/or distant metastases (t-test, p = 0.58). All cases of neck recurrences were treated with subsequent surgical excision, with no new data of progression within the specified follow-up. Conclusions. RAI adjuvant therapy for papillary thyroid carcinoma Т1N1a may not be necessary for patients with small number of level VI micrometastases. Local and distant metastases revealed during the careful follow-up by thyroglobulin level elevation and when using visualization techniques can be effectively treated with postponed RAI therapy and/or surgery.","PeriodicalId":13962,"journal":{"name":"INTERNATIONAL JOURNAL OF ENDOCRINOLOGY (Ukraine)","volume":"28 10","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140081042","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-03-03DOI: 10.22141/2224-0721.20.1.2024.1358
I. Chernyavska, N. Kravchun, I. Dunaieva, I.A. Tykha, S.P. Oliynikova, O.S. Rassolova
Background. Obesity remains a global social and medical problem today. The results of recent research demonstrate the presence of overweight in 30–70 % and obesity in 10–30 % of adults, while the prevalence of obesity is increasing at an alarming rate in both economically developed and developing countries of the world. In Ukraine, according to the World Health Organization, 41.2 % of men and 58.5 % of women are overweight or obese. Obesity is a risk factor for the development of a number of diseases — type 2 diabetes, hypertension, coronary heart disease, non-alcoholic fatty liver disease, gastroesophageal reflux disease, obstructive sleep apnea syndrome, etc. The presence of hyperleptinemia and weight loss resistance are common characteristics of obesity. The purpose of the study was to reveal the relationship between leptin levels and cardiometabolic risk in obese patients. Materials and methods. Fifty-three patients (43 women, 10 men) were examined. Body mass index was calculated as the ratio of body weight (kg) to height (m2). The classification criteria of the World Health Organization were used to diagnose overweight, obesity, and its degree. The level of leptin was assessed by an enzyme immunoassay on the ImmunnoChem-2000 device. The relationship between indicators was evaluated using the Spearman’s rank correlation coefficient. Results. Hyperleptinemia in obese patients is an indicator of low-grade inflammation. A significant increase in the serum leptin is noted in obese patients. Correlation analysis of waist circumference with leptin level in women and men demonstrated its importance both before and after treatment. A significant cardiometabolic risk was detected in the examined patients from the Ukrainian population. Against the background of a comprehensive treatment for six months, a decrease in body weight, waist circumference (p < 0.05) and in leptin level (p < 0.05) was noted in both women and men. Conclusions. The relationship was found between leptin level and cardiometabolic risk in obese patients.
{"title":"Relationship between hyperleptinemia and cardiometabolic risk in persons with obesity","authors":"I. Chernyavska, N. Kravchun, I. Dunaieva, I.A. Tykha, S.P. Oliynikova, O.S. Rassolova","doi":"10.22141/2224-0721.20.1.2024.1358","DOIUrl":"https://doi.org/10.22141/2224-0721.20.1.2024.1358","url":null,"abstract":"Background. Obesity remains a global social and medical problem today. The results of recent research demonstrate the presence of overweight in 30–70 % and obesity in 10–30 % of adults, while the prevalence of obesity is increasing at an alarming rate in both economically developed and developing countries of the world. In Ukraine, according to the World Health Organization, 41.2 % of men and 58.5 % of women are overweight or obese. Obesity is a risk factor for the development of a number of diseases — type 2 diabetes, hypertension, coronary heart disease, non-alcoholic fatty liver disease, gastroesophageal reflux disease, obstructive sleep apnea syndrome, etc. The presence of hyperleptinemia and weight loss resistance are common characteristics of obesity. The purpose of the study was to reveal the relationship between leptin levels and cardiometabolic risk in obese patients. Materials and methods. Fifty-three patients (43 women, 10 men) were examined. Body mass index was calculated as the ratio of body weight (kg) to height (m2). The classification criteria of the World Health Organization were used to diagnose overweight, obesity, and its degree. The level of leptin was assessed by an enzyme immunoassay on the ImmunnoChem-2000 device. The relationship between indicators was evaluated using the Spearman’s rank correlation coefficient. Results. Hyperleptinemia in obese patients is an indicator of low-grade inflammation. A significant increase in the serum leptin is noted in obese patients. Correlation analysis of waist circumference with leptin level in women and men demonstrated its importance both before and after treatment. A significant cardiometabolic risk was detected in the examined patients from the Ukrainian population. Against the background of a comprehensive treatment for six months, a decrease in body weight, waist circumference (p < 0.05) and in leptin level (p < 0.05) was noted in both women and men. Conclusions. The relationship was found between leptin level and cardiometabolic risk in obese patients.","PeriodicalId":13962,"journal":{"name":"INTERNATIONAL JOURNAL OF ENDOCRINOLOGY (Ukraine)","volume":"17 3","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140081105","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-03-03DOI: 10.22141/2224-0721.20.1.2024.1360
L.V. Vyunytska, T. Yuzvenko, T. I. Dashuk, V.V. Nikonov, V.L. Vasyuk, N.V. Korotchuk
The literature review deals with the influence of chronic stress on the functioning of the endocrine system. The most significant pathological conditions induced by chronic stress are decompensation of carbohydrate metabolism, disorders of the thyroid gland, reproductive system, depressive disorders, electrolyte disorders. The significance of these pathologies is determined by a pronounced decrease in the quality of life, the occurrence of severe complications, and an increase in mortality. The development of hyperglycemia during the acute period of the disease is an established connection between the stress system and glucose homeostasis, which is confirmed by the development of stress hyperglycemia and increased morbidity. Glucocorticoids have a contrainsular effect, and the significance of their impact on carbohydrate metabolism is due to the pleiotropic action: induction of insulin resistance, stimulation of gluconeogenesis, increase in the blood content of glucagon due to dysregulation of its synthesis and secretion. The effects of stress on the thyroid gland are determined by its duration, characterized by the activation of the pituitary-thyroid system in the acute period and its suppression during long-term and chronic stress. The contribution of the stress component and glucocorticoid deficiency to the development of autoimmune thyroid diseases due to the suppression of cellular and strengthening of humoral immunity is discussed. Under conditions of psychological stress, the development of hypothyroidism was noted in emigrants with anxiety-depressive syndrome and insomnia, as evidenced by a decrease in the concentration of thyroid hormones. A decreased thyroid status in these patients is associated with the severity of chronic stress. Research data show that chronic stress can significantly change a person’s thyroid status, leading to the development of triiodothyronine deficiency syndrome and an increase in the production of inactive reverse triiodothyronine, inducing the development of hypothyroidism. It is possible that the pronounced growth of subclinical forms of hypothyroidism, noted in many countries of the world, is a consequence of chronic stress. The hypothalamic-pituitary-adrenal axis is involved in the formation of stress-induced reactions almost immediately after exposure to the stressor. Stress-induced changes in the endocrine system arise and develop in close connection, forming a vicious circle of pathological changes and emergencies.
{"title":"Stress-induced urgent conditions in endocrinology","authors":"L.V. Vyunytska, T. Yuzvenko, T. I. Dashuk, V.V. Nikonov, V.L. Vasyuk, N.V. Korotchuk","doi":"10.22141/2224-0721.20.1.2024.1360","DOIUrl":"https://doi.org/10.22141/2224-0721.20.1.2024.1360","url":null,"abstract":"The literature review deals with the influence of chronic stress on the functioning of the endocrine system. The most significant pathological conditions induced by chronic stress are decompensation of carbohydrate metabolism, disorders of the thyroid gland, reproductive system, depressive disorders, electrolyte disorders. The significance of these pathologies is determined by a pronounced decrease in the quality of life, the occurrence of severe complications, and an increase in mortality. The development of hyperglycemia during the acute period of the disease is an established connection between the stress system and glucose homeostasis, which is confirmed by the development of stress hyperglycemia and increased morbidity. Glucocorticoids have a contrainsular effect, and the significance of their impact on carbohydrate metabolism is due to the pleiotropic action: induction of insulin resistance, stimulation of gluconeogenesis, increase in the blood content of glucagon due to dysregulation of its synthesis and secretion. The effects of stress on the thyroid gland are determined by its duration, characterized by the activation of the pituitary-thyroid system in the acute period and its suppression during long-term and chronic stress. The contribution of the stress component and glucocorticoid deficiency to the development of autoimmune thyroid diseases due to the suppression of cellular and strengthening of humoral immunity is discussed. Under conditions of psychological stress, the development of hypothyroidism was noted in emigrants with anxiety-depressive syndrome and insomnia, as evidenced by a decrease in the concentration of thyroid hormones. A decreased thyroid status in these patients is associated with the severity of chronic stress. Research data show that chronic stress can significantly change a person’s thyroid status, leading to the development of triiodothyronine deficiency syndrome and an increase in the production of inactive reverse triiodothyronine, inducing the development of hypothyroidism. It is possible that the pronounced growth of subclinical forms of hypothyroidism, noted in many countries of the world, is a consequence of chronic stress. The hypothalamic-pituitary-adrenal axis is involved in the formation of stress-induced reactions almost immediately after exposure to the stressor. Stress-induced changes in the endocrine system arise and develop in close connection, forming a vicious circle of pathological changes and emergencies.","PeriodicalId":13962,"journal":{"name":"INTERNATIONAL JOURNAL OF ENDOCRINOLOGY (Ukraine)","volume":"16 4","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140081164","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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