Metabolic syndrome (MS) is a common phenomenon among the population and is a risk factor for cardiovascular diseases and mortality. The main component of MS is visceral obesity, leading to insulin resistance; additional criteria for MS include arterial hypertension, carbohydrate and lipid metabolism disorders. Calcium metabolism disorders, in particular hypercalcemia, are a fairly common problem and occur in almost 3% of the population of Russia. Its main cause is primary hyperparathyroidism (PHPT), which is based on hyperproduction of parathyroid hormone (PTH) by the parathyroid glands. “Non-classical” symptoms of PHPT include, among other things, metabolic disorders. PHPT can be associated with MS and its components, accompanied by a higher prevalence of obesity, carbohydrate metabolism disorders, dyslipidemia and arterial hypertension. The cardiovascular manifestations of PHPT are dominated by left ventricular hypertrophy, calcification of the heart valves, diastolic dysfunction, and arterial hypertension. Mortality from cardiovascular diseases in PHPT is higher than in healthy individuals, even with a “mild” form, which is why careful monitoring of such patients, timely diagnosis, and treatment of cardiovascular complications are necessary. Atherogenic dyslipidemia in PHPT increases the risk of cardiovascular pathology, but with a clinically expressed form of the disease. Surgical treatment can reduce cardiovascular risks and improve the prognosis of patients, although the lipid profile improves only in patients with a “mild” form of PHPT. Impaired purine and carbohydrate metabolism are also more common in PHPT than in healthy individuals. Parathyroidectomy improves glucose and uric acid levels in patients with PHPT.

Metabolic syndrome is recognized by WHO experts as a “pandemic of the 21st century”. It is widespread and is a pressing medical and social problem. Obesity is a major component of metabolic syndrome. An increase in visceral fat mass, insulin resistance and hyperinsulinemia lead to the development of disorders of carbohydrate, lipid, purine metabolism and arterial hypertension. Vitamin D deficiency has been recognized by many authors as a potential risk factor for the development of obesity, cardiovascular diseases, carbohydrate metabolism disorders, dyslipidemia and arterial hypertension. Vitamin D receptors are expressed in various tissues, including cardiomyocytes, vascular smooth muscle cells and endothelial cells. Vitamin D affects inflammation, cell proliferation and differentiation. However, a number of studies do not confirm a cause-and-effect relationship between vitamin D deficiency and components of the metabolic syndrome. The article presents data on the effect of vitamin D on the development and progression of the main components of metabolic syndrome. The relationship between adipose tissue and vitamin D is shown. The effectiveness of vitamin D administration on weight loss, insulin resistance, dyslipidemia, carbohydrate metabolism and blood pressure is considered.

Magnesium is the second most common intracellular cation and the fourth most common cation in the human body. It is a factor influencing the rate of many enzymes involved in carbohydrate and energy metabolism, provides muscle contraction and relaxation, is necessary for normal neurological function, regulates bone mineralization, its uniform growth, flexibility, strength and increases the reparative potential of bones. Its deficiency is common in many countries and is often underestimated, since the symptoms of hypomagnesemia can be nonspecific. Such symptoms include depression, fatigue, muscle spasms and arrhythmia. Long-term low magnesium levels are associated with an increased risk of chronic non-communicable diseases: osteoporosis, sarcopenia, metabolic disorders, cardiovascular pathology. The main cause of magnesium deficiency is nutritional deficiencies. There is a relationship between low dietary magnesium intake and the risk of developing metabolic syndrome. Magnesium deficiency is common among obese patients, both adults and children. Also, the lack of this microelement is associated with the development of type 2 diabetes and arterial hypertension. Correction of magnesium deficiency through nutrition or medication has a positive metabolic effect.

From the modern point of view, hyperuricemia should be considered as a trigger of inflammatory activity leading to specific joint and renal lesions, as well as to diseases associated with atherosclerosis. HU is also recognized as one of the components of metabolic syndrome, which is characterized by involvement of liver parenchyma with the development of fatty disease, insulin resistance, which promotes glycemia, dyslipidemia, inflammatory activity of the vascular wall associated with endothelial dysfunction. Recently, a universal mechanism of inflammation has been established involving the NLRP3 inflammasome, which generates a key mediator of gout attacks, IL-1β, responsible for the local inflammatory response in the synovial membrane and periarticular tissues involving macrophages and neutrophils. This cytokine is also involved in the inflammatory process characteristic of atherosclerosis, stimulating the release of other cytokines (IL-6 and IL-18), production of endothelin 1 and adhesion molecules, causing migration of leukocytes into the intima, initiating and destabilizing the atherosclerotic plaque. NLRP3 inflammasome activation is carried out by uric acid and cholesterol crystals exclusively after priming by lipopolysaccharides, peroxidation products and other damage factors associated with aging and comorbid conditions typical of gout and cardiovascular diseases. In addition, NLRP3 inflammasome activity is genetically determined with respect to these conditions. This paper provides evidence that targeting factors associated with comorbidity can not only reduce the frequency of gout attacks, but also reduce cardiovascular outcomes. Blocking inflammasome activity is considered as a new universal therapeutic target for rheumatology and cardiology, especially in high cardiovascular risk conditions, which include metabolic syndrome associated with hyperuricemia.

Although most patients with hyperuricemia are never destined to experience an attack of gout or symptoms of urolithiasis, elevated uric acid levels are now a recognized risk factor for cardiovascular morbidity and outcomes. From these perspectives, lowering uric acid in the blood is recognized as desirable. The use of classical urate-lowering drugs is consistent with a paradigm in which each risk factor to be corrected is contrasted with a drug with the desired direction of effect. The extended use in patients with asymptomatic hyperuricemia of classical xanthine oxidase inhibitors, which are highly effective in reducing blood uric acid, is associated with a number of negative consequences, including potentially severe morbidity, the need for dose selection and monitoring, and decreased adherence to agents proven to be effective as cardio- and renoprotective agents. New data on the role of the inflammasome, a complex of intracellular proteins whose activation ensures the formation of interleukins IL-1β, IL-18, allow us to regard hyperuricemia as only one of the triggers of inflammation. This knowledge allows us to emphasize in the problem of renal and cardiovascular diseases associated with hyperuricemia the ability of known cardiac drugs (statins and sodium-glucose transporter type 2 inhibitors - INGLT-2) to reduce the activity of NLRP3 inflammasome, achieving optimal therapeutic efficacy. This strategy seems to be the only correct one in patients with asymptomatic hyperuricemia, also applicable in gout, reducing the need for classical urates-lowering therapy, preventing the inevitable polypharmacy.

Anabolic androgenic steroids (AAS) are pharmacological agents, testosterone derivatives, with a similar structure and mechanisms of action. Replacement therapy with testosterone is the leading method of treating persistent male hypogonadism of various etiologies; however, due to the anabolic effect of AAS on skeletal muscle tissue, this class of drugs is currently widely used by athletes without proper control and supervision by specialists. Such use of AAS is accompanied by serious side effects, which are not always reversible even after discontinuation of testosterone derivatives. The review presents statistical data on the prevalence of AAS use, describes the mechanisms of anabolic action on skeletal muscles, as well as side effects. Possible negative effects of taking large doses of AAS include suppression of the hypothalamic-pituitary-gonadal axis, increased cardiovascular risks, hepatotoxicity, structural and functional disorders of the nervous system. The aim of this review is to raise awareness of the effects of AAS on the body, which will help prevent and minimize the risks associated with the uncontrolled use of this class of drugs.

The prevalence of diabetes mellitus (DM) increases with age. Currently, frailty syndrome (FSS, frailty) in patients with type 2 DM is considered an additional complication to traditional micro- and macrovascular complications. FSS causes changes in body composition and metabolism, forming certain phenotypes that affect the course of type 2 DM, the choice of target glycemic values and hypoglycemic therapy. This article is devoted to the analysis of metabolic changes and phenotypes associated with FSS, their impact on the course of type 2 DM, the choice of hypoglycemic therapy and target glycemic values.

One of the urgent tasks of modern medicine associated with the progressive aging of the population is the formation of a strategy for managing elderly patients with type 2 diabetes mellitus (T2DM), including an interdisciplinary approach taking into account a comprehensive geriatric assessment, optimization of glycemic control, personalized pharmacological therapy and diet therapy. The pathogenesis of T2DM, frailty (FA) and cognitive dysfunction are closely interrelated in the context of aging. Insulin resistance, atherosclerosis, chronic inflammation, oxidative stress and mitochondrial dysfunction are integrally involved in the mechanism of development of pathogenetic links of FA, cognitive impairment and T2DM. Dietary recommendations aimed at adequate intake of macro-/micronutrients help prevent or slow down the development of age-associated diseases, help improve the quality and increase life expectancy in elderly people with T2DM. This literature review analyzes current data on the importance of proper nutrition for glycemic control, prevention of SA, sarcopenia and dementia in elderly patients with type 2 diabetes.

The purpose of this study is to evaluate the effectiveness of complex therapy, including correction of eating behavior, a reduction diet, taking didrogesterone from the 14th to the 25th day of the cycle, 100 mg 2 times a day, as well as taking a complex drug containing myo- and D- chiroinositol in a ratio of 5:1, manganese and folic acid (myoinositol 1000 mg, D-chiroinositol 200 mg, manganese 5 mg, folic acid 200 mcg) 1 sachet 2 times a day in the management of patients with polycystic ovary syndrome (PCOS) and obesity. The object of our study was 28 women of reproductive age with PCOS. All patients underwent a comprehensive clinical and laboratory examination in accordance with the clinical recommendations of Polycystic Ovary syndrome. The content of total cholesterol and high and low density lipoproteins, triglycerides, as well as fasting and post-carbohydrate glucose levels were assessed. The patients showed clinical signs of hyperandrogenism, and there was a visceral type of obesity (CW/CH 0.85±0.01 cm). Impaired glucose tolerance was detected. We prescribed therapy for the patients, taking into account the revealed changes in hormonal balance and insulin resistance. At the first stage of complex therapy, patients were prescribed dietary behavior correction, a reduction diet, didrogesterone from the 14th to the 25th day of the cycle, 100 mg 2 times a day, as well as taking a complex remedy containing myo- and D-chiroinositol in a ratio of 5:1, manganese and folic acid (myoinositol 1000 mg, D-chiroinositol 200 mg, manganese 5 mg, folic acid 200 mcg, dietary supplement, produced by PIZETAPHARMA, S.p.A., Italy), for 3 months, 1 sachet 2 times a day. No adverse reactions were detected during this treatment. As a result of treatment, 18 out of 28 patients had a decrease in BMI to 26.6, and 11 to 25.5, respectively. Comprehensive treatment was continued for the patients. After 3 months, BMI values were re-determined. In 18 (60%) patients, they were 25.5 and in 11-24.5. Normalization of glucose tolerance was noted in all the examined patients after 6 months. 5 patients became pregnant without the use of additional ovulation-stimulating drugs. All the treated patients noted an improvement in their general well-being and quality of life.

Lipid metabolism disorders play a critical role in the initiation, development and progression of a number of socially significant diseases, including obesity, atherosclerosis, ischemic diseases, diabetes mellitus, liver dysfunction, metabolic syndrome and its consequences. Acute normobaric hypoxia, as an exogenous condition that occurs when the partial pressure of oxygen decreases at normal barometric pressure, is one of the hypoxia models used in animal studies. The aim of the research was to study changes in lipid metabolism and the concentration of phospholipid fractions in the blood serum of rats exposed to acute normobaric hypoxia, as well as to evaluate atherogenic indices and the prospects for using natural antihypoxants for the prevention and correction of hypoxic disorders. The results of the study showed that simulated hypoxia causes significant disturbances in lipid metabolism in rats, including a decrease in serum concentrations of phosphatidylcholine, phosphatidylserine, sphingomyelin and antiatherogenic high-density lipoproteins, as well as an increase in the levels of low-density lipoproteins, triglycerides, total cholesterol and valid lipid metabolism (atherogenic) indices. The noted changes can be considered as a pronounced adaptive-compensatory response of the body, which can lead to disturbances in the barrier and transport function of biological membranes. The experiment found that the use of plant antihypoxants contributes to partial compensation for the negative consequences, which confirms their potential for correcting metabolic shifts induced by hypoxia in the areas of improvement and development of biohacking technologies aimed at increasing the duration and quality of life.

Purpose of the study: to determine the reasons for the increase in the incidence of colon and stomach cancer, as well as the insufficient effectiveness of colon cancer screening and prevention programs. Material and methods of research: clinical and endoscopic, most often annual studies of the colon in 4134 patients over a 15-year period with morphological assessment of the changes detected (more than 11,000 preparations); the method of esophagogastroduodenoscopy with biopsy of gastric tumors (113 studies); special methods of morphological studies, including electron microscopy, detection of hybrid cells; methods of vital chromo- and colonomicroscopy, including for prospective study of the structure of the mucous membrane in the zone of probable development of cancerous tumors during subsequent observations; the method of gastromicroscopy; a laboratory method for studying the concentration of carcinoembryonic antigen (CEA) in homogenates of tissues of the mucous membrane and cancerous tumors. Research results: annual dynamic observations of patients for 15 years showed that development of sporadic cancer in the colon occurred in 3.4% of patients. In most of them (83.8%) cancer tumors appeared during annual intervals between observations without any visible connection with previous adenomas; we stated the absence of practical possibility to predict timing and localization of development of cancer tumors in them. Tumors with high growth rates appeared on the border between the epithelial surface with signs of moderate diffuse hyperplasia (DH) and the epithelial surface of small adenomas (A) with moderate dysplasia of gland epithelium. It was established that in cases of rapid development of cancer adenoma and carcinoma are not consecutive stages of malignancy, but on the contrary - a synchronous process. This type of cancer tumors develops as a result of fusion (hybridization) of cells of hyperplastic epithelium and epithelium of adenomas. A more pronounced increase in the concentration of CEA in tumors compared to the surrounding mucous membrane confirmed the embryonic origin of tumors of this type. Cells with morphological features of hybrids were also found in gastric cancer tumors. Conclusion: A pathoembryonic theory is presented with a complete cycle of morphological changes, including the diversity of the structure of the surface epithelium in the colon and the discovery of hybridization of cells from adjacent differently structured epithelia as a biological mechanism leading to the initiation of cancer with high growth rates (similar changes were found in gastric tumors). It is also shown that tumors with slow growth rates in the colon are formed mainly from previous adenomas as they recur and the degree of dysplasia of the glandular epithelium increases in them in accordance with the generally accepted views on the process of carcinogenesis in the colon. Known promoters of hybridization of epithelial somatic cells include polyethylene glycol, which is widely used in medicine, as well as in the food industry; there is reason to believe that a significant part of such substances (fusogens) have not been identified to date. A number of signs suggest that hybrid cells also play a significant role in the metastatic process.

The aim: of the study of the features of the course of hypertension, depending on the presence in patients of the most common concomitant diseases of the gastrointestinal tract in remission (gastric ulcer, non-alcoholic fatty liver disease, chronic biliary-dependent pancreatitis). Materials and methods: 107 patients with hypertension and concomitant diseases in the remission stage were examined using modern laboratory and instrumental methods. Results: We found that hypertension with concomitant peptic ulcer disease proceeds most favorably with the lowest lipid spectrum indices, minimal changes in carotid vessels. When hypertension is combined with non-alcoholic fatty liver disease, the studied indices were higher. Hypertension in combination with chronic biliary-dependent pancreatitis proceeded most severely with maximum atherosclerotic manifestations.

The aim of the study is to substantiate the effectiveness of therapy in a patient with obesity and pathology of the reproductive system by using orlistat in combination with auxiliary substances. The subject of our study is a patient, H., 22 years old, the patient was diagnosed with ovarian dysfunction. E28.2. Glandular hyperplasia of the endometrium. N85. Grade 1 obesity (BMI 32.74). E 66. Glaucoma. H 40. The patient was prescribed didrogesterone from the 14th to the 25th day of the cycle, 100 mg 2 times a day, lifestyle modification, eating behavior, a reduction diet, a drug containing orlistat at a dosage of 120 mg in combination with excipients: acacia gum - 210 mg, lauryl sulfate -12 mg, mannitol 580 mg, crospovidone - 50 mg and magnesium stearate - 8 mg 3 times a day with meals.taking the ADEK vitamin complex 600 mg 1 capsule 1 time a day with meals. After 3 months, the weight decreased by 11 kg and amounted to 87 kg (BMI 29.07, which corresponds to overweight) after 6 months, by another 13 kg to 74 (BMI 24.73, which corresponds to normal body weight). The waist circumference has decreased from 82 cm to 71 cm. The progesterone level was 46.3 nmol/L, which corresponds to the average reference values. Ultrasound of the pelvic organs revealed no pathology, and the patient did not complain. There were no side effects. Thus, a significant decrease in the patient’s body weight against the background of the proposed method of therapy can be explained by the good tolerability of the treatment. The proposed treatment option for an obese patient made it possible to correct disorders of the reproductive system and, thus, prevent the occurrence of endometrial hyperplastic processes, dysmetabolic disorders and, subsequently, reduce the risk of reproductive losses during pregnancy planning.

The aim of the study is to substantiate a rational approach to choosing a method of contraception from the standpoint of metabolic neutrality in an obese woman based on a clinical case study. The object of our research is the medical history of patient Z., 43 years old. The patient applied to select a method of contraception for her. When applying, an examination was conducted, which included the collection of complaints, anamnesis, blood pressure measurement, general examination, with examination and palpation of the mammary glands, determination of body mass index (BMI), gynecological and ultrasound examination of the pelvic organs, mammography, general and biochemical blood tests, taking swabs for oncocytology, the degree of purity of the vagina, gonorrhea. Diagnosis: Uterine leiomyoma (intramural, intramural - subserous). Heavy menstruation with a regular cycle. Chronic posthemorrhagic iron deficiency anemia of mild degree. Grade 1 obesity (BMI 31.8). The patient was recommended to administer levonogrestrel - releasing intrauterine system (levonorgestrel in the form of an intrauterine therapeutic system) (LNH - IUD) as well as taking iron supplements. During an examination conducted three months after the installation of the LNH-IUD, the woman did not complain, menstruation became moderate, lasting up to three days. Ultrasound of the pelvic organs showed a decrease in the size of myomatous nodes, and the endometrium was free of pathology. 10 months after the introduction of the LNH - IUD, menstruation is scanty and spotty, amenorrhea occurs for 13 months. Subsequently, no growth of myomatous nodes was detected. The weight dropped to 72 kg. The BMI was 24.24 (normal). At the end of the five-year period of use of the LNH-IUD in this patient, it was removed and a new one was introduced to ensure a contraceptive effect and the prospect of further use as a component of MGT. Thus, the use of intrauterine contraception using the LNH-IUD is the most rational method for obese women, as it is a highly effective and safest method.

The prevalence of hypothyroidism in the population is quite high. According to the World Health Organization, thyroid dysfunction ranks second among endocrine diseases, followed by diabetes mellitus. Hypothyroidism has many manifestations, so a doctor of any specialty in his practice has a chance to meet a patient with hypothyroidism both with an established diagnosis and with the need for differential diagnostics of various pathological conditions with impaired thyroid function. This article presents a clinical observation of a patient with long-term uncompensated postoperative hypothyroidism, which caused complications in various organs and systems. The clinical observation demonstrated the effectiveness of replacement therapy in the treatment of hypothyroidism and its complications. It is necessary to remember about the timely diagnosis of “masks” of hypothyroidism, such as gynecological disorders, pathology of the cardiovascular and hepatobiliary systems, lipid metabolism disorders with the progression of atherosclerosis, changes in the skin and its appendages, leading to a sharp decrease in the quality of life of patients. An interdisciplinary approach to the management of such patients ensures timely correction of complications, improving the quality and duration of life of patients.

Crohn’s disease (CD) remains one of the most mysterious and serious problems of modern gastroenterology and proctology. Despite the fact that almost 100 years have passed since the first description of this pathology, known scientific achievements have not been able to fully reveal the etiological and pathogenetic mechanisms of the disease. The diversity of clinical manifestations of the disease, caused by multilevel damage to the gastrointestinal tract, as well as the addition of systemic (extraintestinal) manifestations, significantly complicate the recognition of the disease, often leading to diagnostic errors and a fairly long period of diagnosis verification. The most difficult and late to recognize is CD with localization of the process in the upper gastrointestinal tract. Also complex is the low-symptom version of CD, manifested for a long time by one or two slightly expressed clinical signs, not always related to the intestine, or associated mainly with extraintestinal manifestations. This article presents an interesting case from clinical practice of observing a patient with a stricturing form of CD with damage to the upper gastrointestinal tract with extraintestinal manifestations.

Non-alcoholic fatty liver disease (NAFLD) can be called the silent pandemic of the 21st century. The prevalence of this disease is progressively increasing worldwide, affecting an increasing number of people of working age, mainly in developed countries, negatively affecting the health of the population. Considering the fact that the pathogenesis of NAFLD is primarily associated with metabolic disorders and changes in glucose-insulin homeostasis, steatohepatosis is an independent risk factor for the development of type 2 diabetes mellitus and its complications, cardiovascular diseases and cardiovascular mortality due to progressive atherosclerosis. Treatment of NAFLD includes two main goals: prevention of disease progression, which consists in regression of steatosis, prevention of steatohepatitis and subsequent fibrosis, as well as active intervention in the development of metabolic disorders leading to the formation of cardiometabolic risks. The clinical case we presented demonstrates the need for an interdisciplinary approach to managing patients with metabolic syndrome to minimize the risks of development and progression of comorbid pathology.

Psoriasis is a chronic multifactorial inflammatory disease that can manifest itself in various clinical forms. In addition to smooth skin, this disease can affect folds, joints (psoriatic arthritis) and nails. Purpose of the study. Due to the variety of clinical forms, severity of psoriasis and concomitant diseases that we can observe in patients, universal treatment regimens have not yet been developed. Therefore, the purpose of the study is to use an interdisciplinary complex approach to the treatment of psoriasis in patients with concomitant carbohydrate metabolism disorders. Materials and methods. This article considers 2 clinical cases of inverse psoriasis occurring against the background of concomitant diseases (diabetes mellitus type 2, hepatitis C) using individual treatment regimens. Results and their discussion. Basic treatment of psoriasis includes the use of both systemic and topical drugs. In the treatment of inverse psoriasis in a patient with type 2 diabetes mellitus, together with systemic treatment with immunosuppressive drugs, we used therapy aimed at normalizing glycemia. Topical combined topical glucocorticosteroids in the form of a cream, as well as aniline dyes, were used externally. In the treatment of inverse psoriasis in a patient with type 2 diabetes mellitus in combination with hepatitis C, together with systemic treatment with hepatoprotectors, monoclonal antibody preparations are used, as well as hypoglycemic drugs. Topical combined topical glucocorticosteroids in the form of an ointment, aniline dyes, and aqueous solutions of antiseptics were used externally. In the presented clinical cases, patients are under the supervision of doctors of related specialties for a comprehensive approach to the treatment of patients with comorbid conditions. Conclusions. To determine the most appropriate tactics for the treatment of inverse psoriasis in patients with concomitant pathology, an interdisciplinary approach to patient management is required.

Currently, the problem of obesity and metabolic syndrome, which are part of the group of chronic non-infectious diseases, has acquired serious medical and social significance and a global scale due to the steady worldwide increase in prevalence, which forces scientists to look for the reasons for such negative epidemiological trends. In recent years, the concept of early programming, which is based on the postulate that the origins of most chronic diseases in adults are formed in childhood, has become one of the most interesting issues discussed in the medical community. This review presents current scientific evidence supporting the concept of the early origins of chronic diseases, with a focus on obesity and metabolic syndrome. The authors consider the key factors that determine the characteristics of metabolic processes that underlie the formation of human health or predispose to the development of metabolic diseases, especially in the early periods of development, focusing on risk factors for obesity and possible areas of preventive interventions.

Metabolic syndrome is traditionally associated with cardiovascular diseases, obesity and type 2 diabetes and plays a critical role in their development, while its causal relationship with the formation of cognitive deficit and the progression of neurodegenerative disorders is increasingly being considered. Long-term metabolic dysregulation can cause disruption of the phenotype and functional role of astrocytes, which is manifested by impaired brain hydrodynamics, substrate supply and interneuronal connections, decreased glymphatic clearance, accumulation of neurotoxic proteins and subsequent deterioration of cognitive performance. Dysfunction of astrocytes and direct influence on the metabolic supply of neurons, homeostasis of brain metabolites and processes of synaptic plasticity and functional activity of nerve cells can be an important mechanism that opens up a unique opportunity to modify many diseases, including various aspects of metabolic syndrome and neurodegenerative processes.

Nonalcoholic fatty liver disease (NAFLD) is the most common liver pathology, affecting about 38% of the global population. It represents a spectrum of conditions, starting from the fat accumulation in hepatocytes (steatosis) and progressing to liver inflammation (steatohepatitis) with varying degrees of fibrosis, as well as a risk of developing cirrhosis and hepatocellular carcinoma. With the accumulation of scientific data and improvements in diagnostic methods, an understanding has emerged that metabolic dysfunction is central to the pathogenesis and consequences of NAFLD. In 2020 a proposal was made to revise the nomenclature and classification of NAFLD to metabolic dysfunction-associated steatotic liver disease (MASLD), emphasizing the underlying metabolic dysfunction of this condition. This review discusses the differences in the definitions and classification of NAFLD and MASLD, the clinical burden and consequences of MASLD as a multisystem disease, with a focus on the pathogenetic interrelationships between MASLD and metabolic syndrome.

The aim of the work: to study the possibilities of using the levels of fatty acids in the membranes of erythrocytes and blood serum to distinguish between initial and severe fibrosis in patients with fatty liver disease of alcoholic and mixed genesis (alcoholic + metabolic). Materials and methods. 110 patients with fatty liver disease of alcoholic and mixed genesis were examined, the average age was 47.9 ± 9.8 years. Depending on the degree of fibrosis, patients were divided into two groups - group 1 with mild fibrosis (F0-1) (n=76), group 2 - with severe fibrosis (F2-4) (n=34) (FibroScan® 502 (Echosens, France). The content of fatty acids (FA) in the membranes of erythrocytes and blood serum was determined using gas chromatography/mass spectrometry (Agilent 7000B (USA). Results. Fatty acids of the membranes of erythrocytes and blood serum were identified, the levels of which made it possible to distinguish between patients with initial and severe fibrosis with fatty liver disease of alcoholic and mixed (alcoholic + metabolic) genesis. Severe fibrosis (F2-4) was associated with increased levels of total saturated (p=0.00018), stearic C18:0 (p=0.001), palmitic C16:0 (p=0.004), lauric C12:0 (p=0.07), the SFA/MUFA ratio (p=0.0018) in erythrocyte membranes and serum SFA/MUFA levels (p=0.008), dihomo-γ-linolenic C20:3n-6 (p=0.04). On the contrary, in severe liver fibrosis, compared with the initial stages, lower levels of serum pentadecanoic acid C15:0 (p=0.04), erythrocyte α-linolenic C18:3n-3 (p=5.45e-10), total MUFA content (p=6.83e-08 for erythrocyte membranes and p=5.55e-06 for blood serum), individual MUFA (for erythrocyte elaidic t-C18:1 - p=2.42e-06, for its serum level - p=0.0002; for serum 7-palmitoleic 7-C16:1 - p=0.0003; for serum palmitoleic 9-C16:1 - p=0.013; for its level in erythrocyte membranes - p=0.042); lower concentrations of two omega-6 PUFAs both in erythrocyte membranes (for hexadecadienoic C16:2n-6 - p=2.69e-07, for eicosadienoic C20:2n-6 - p=8.52e-07) and in blood serum (for C16:2n-6 - p=1.33e-05, for C20:2n-6 - p=0.002). A panel including erythrocyte levels of two fatty acids and total monounsaturated fatty acids - C20:2n-6, MUFA, C16:2n-6 - was optimal for differentiating groups of patients with fibrosis grade F2-4 from F0-1, which provided an AUC of 0.862 (95% CI 0.781-0.94), sensitivity of 88.8%, specificity of 86.4%. Conclusions. Fatty acids of erythrocyte membranes and blood serum should be considered as promising diagnostic markers and potential targets for therapeutic interventions to prevent the progression of liver fibrosis in patients with fatty liver disease of alcoholic and mixed genesis.

Relevance: the effect of overweight on the progression of chronic kidney disease (CKD) in old age has a number of paradoxical features, which arouses the keen interest of the world scientific community. The problem has a high applied significance due to its close relationship with the dangerous manifestations of metabolic syndrome and its proven association with cardiovascular mortality. Objective: to determine the factors of metabolic syndrome that influence the dynamics of CKD progression in elderly patients with DM2. Material and methods: In a population sample of elderly patients with type 2 diabetes (66 participants), a single-stage observational study of clinical and metabolic status indicators was conducted. 69 indicators available in outpatient settings were studied, patterns of interrelationships were determined, the significance of differences in average values between BMI and the original calculated diagnostic parameter Glomerular filtration rate reduction Index (RI_GFR) was determined, which makes it possible to give an objective quantitative characteristic of the rate of progression of CKD. Results: a significant correlation was established between BMI and GFR in dichotomized groups; the closeness of the relationship between the rate of GFR decrease and the main components of the metabolic syndrome (obesity, dysglycemia and elevated blood pressure) was confirmed and evaluated; a paradoxical quadratic approximating relationship between BMI and GFR in the group of rapid progression of CKD was revealed. Conclusions: overweight and the main components of the metabolic syndrome affect the rate of progression of CKD in elderly patients with DM2; the approximating curve of the quadratic dependence of the GFR level on BMI demonstrated a U-shaped shape and different orientation of the apexes in the groups of slow and rapid progression of CKD (with insufficient significance due to the limitations of the study).

The review article presents generalized data on the relationship of the components of the metabolic syndrome (visceral obesity, hypertension, dyslipidemia, hyperuricemia) with chronic kidney disease, discusses common pathogenetic mechanisms and their mutual aggravating effects. The article discusses the features of drug correction of the components of the metabolic syndrome, taking into account renoprotection and cardioprotection in patients with chronic kidney disease. The review article presents generalized data on the relationship of the components of the metabolic syndrome (visceral obesity, hypertension, dyslipidemia, hyperuricemia) with chronic kidney disease, discusses common pathogenetic mechanisms and their mutual aggravating effects. The article discusses the features of drug correction of the components of the metabolic syndrome, taking into account renoprotection and cardioprotection in patients with chronic kidney disease.

Sarcopenia is a disease characterized by a strong progressive decrease in the mass and functions of skeletal muscles. The causes of sarcopenia are aging, physical inactivity, impaired nutritional effects and concomitant diseases. Chronic kidney disease (CKD) can be a prerequisite for the development of sarcopenia, and also have a negative effect on the systemic level. Albuminuria and proteinuria lead to a negative nitrogen balance as a result, when the loss of protein leads to its synthesis. The accumulation of uremic toxins against the background of CKD contribute to systemic inflammation and catabolism of muscle tissue. Joining in the late stages of the cardiorenal syndrome of CKD, aggravation of systemic disorders and limitation of heart failure are ensured. All of the above mechanisms of pathogenesis lead to impaired synthesis and increased degradation of cellular tissue proteins. Therefore, the treatment of sarcopenia against the background of CKD should be comprehensive, taking into account the degree of renal dysfunction.

The liver is a large organ, the mass of which exceeds 1% of the human body mass. The liver is involved in the metabolism of proteins, fats and carbohydrates, and acts as a glycogen depot. Sarcopenia is a known complication of chronic liver disease, and is almost always observed in patients with cirrhosis, especially in patients with decompensated disease. It is of interest to study the mechanisms of pathogenesis of liver pathology as a cause of sarcopenia. Impaired synthesis of skeletal muscle protein and increased proteolysis by autophagy contribute to sarcopenia. Hyperammonemia is the most studied mediator of the liver-muscle axis. Against the background of hyperammonemia, increased expression of myostatin, impaired mitochondrial function and intermediate products of the tricarboxylic acid cycle are noted. Hormonal imbalance in the body, malnutrition, vitamin deficiency, chronic inflammation, hypermetabolism and insulin resistance are important links in the pathogenesis of chronic liver diseases. Sarcopenia occurs in the majority of patients with liver diseases. There are no effective methods to prevent or eliminate sarcopenia in liver diseases. This review discusses the main mechanisms of sarcopenia pathogenesis in chronic liver diseases. The liver is a large organ, the mass of which exceeds 1% of the human body mass. The liver is involved in the metabolism of proteins, fats and carbohydrates, and acts as a glycogen depot. Sarcopenia is a known complication of chronic liver disease, and is almost always observed in patients with cirrhosis, especially in patients with decompensated disease. It is of interest to study the mechanisms of pathogenesis of liver pathology as a cause of sarcopenia. Impaired synthesis of skeletal muscle protein and increased proteolysis by autophagy contribute to sarcopenia. Hyperammonemia is the most studied mediator of the liver-muscle axis. Against the background of hyperammonemia, increased expression of myostatin, impaired mitochondrial function and intermediate products of the tricarboxylic acid cycle are noted. Hormonal imbalance in the body, malnutrition, vitamin deficiency, chronic inflammation, hypermetabolism and insulin resistance are important links in the pathogenesis of chronic liver diseases. Sarcopenia occurs in the majority of patients with liver diseases. There are no effective methods to prevent or eliminate sarcopenia in liver diseases. This review discusses the main mechanisms of sarcopenia pathogenesis in chronic liver diseases.

Sarcopenic obesity is the coexistence of excess adipose tissue accumulation and low muscle mass and/or function. There is fatty infiltration of skeletal muscles - myosteatosis, as well as excess accumulation of predominantly visceral fat. Obesity can independently lead to loss of muscle mass and function due to the negative impact of adipose tissue-dependent metabolic disorders, such as oxidative stress, inflammation, and insulin resistance, all of which negatively affect muscle mass. In addition, obese individuals have a high prevalence of chronic non-communicable diseases that negatively affect muscle metabolism (both anabolism and catabolism). Aging is accompanied by systemic metabolic disorders, chronic inflammation, mitochondrial dysfunction, and insulin resistance. Age itself is a non-modifiable risk factor for many pathological conditions and diseases, including sarcopenic obesity. It is of interest to study the pathophysiological mechanisms of development of sarcopenic obesity and the development of possible treatment strategies aimed at improving systemic metabolism.

Aim of the study: to evaluate the possibility of using catestatin as a biomarker for the diagnosis of metabolic syndrome. Materials and methods: the study was based on a search for publications mainly over the past 5 years in the PubMed and Google Scholar databases for the keywords “catestatin”, “metabolic syndrome”, “insulin resistance”, “dyslipidemia”. Results: catestatin is a multifunctional peptide that can become a promising tool for the diagnosis of metabolic syndrome. It affects the adrenergic system, reducing sensitivity to catecholamines and causing vasodilation. In addition, catestatin affects the metabolism, reducing the levels of triglycerides and leptin. It also regulates insulin resistance and has an anti-inflammatory effect. Conclusion: catestatin may be a useful tool for the diagnosis and treatment of metabolic syndrome. However, further research is needed to fully understand its role and determine best practices.

Metabolic syndrome (MS) is a common comorbid condition in patients with hypertension (HTN), associated with an increased risk of cardiovascular complications. The role of catestatin (CST), a chromogranin A breakdown product with vasodilatory, cardioprotective, and metabolic properties, has attracted growing interest. The aim of this review is to analyze current data on the relationship between CST and MS components in patients with HTN. A systematic search was conducted in the PubMed, Scopus, and Web of Science databases. A total of 18 original studies (a total sample of 2,547 patients) met the inclusion criteria. It was shown that reduced CST level is associated with the presence of MS (odds ratio 2.47; 95% confidence interval 1.83-3.34), abdominal obesity (r= -0.38; p<0.001), insulin resistance (r= -0.29; p<0.01) and dyslipidemia (r= -0.25; p<0.05) regardless of gender, age and duration of hypertension. CST can be considered as a potential biomarker of MS and a therapeutic target in patients with high cardiometabolic risk.

Population ageing contributes to the growth of metabolic syndrome (MS), cardiovascular pathology, neurodegenerative diseases, and cognitive impairment. The components of MS (visceral obesity, arterial hypertension, dyslipidemia, carbohydrate metabolism disorders) are closely related to nutrition and appear before the development of cognitive impairment. According to a number of authors, the Mediterranean diet has a positive effect on the cardiovascular system and can prevent cognitive dysfunction. In addition, it is known that the consumption of a number of foods has a therapeutic effect on the components of metabolic syndrome and can improve cognitive status. At the same time, there are ambiguous opinions on this matter in the literature. In this regard, this work is devoted to the analysis of available data on the relationship between MS and its components with cognitive impairment, as well as the role of nutrition in the prevention and treatment of these pathologies.

Obviously, obesity is currently a global health problem. Eating disorders, including anorexia nervosa, a neuropsychiatric disorder characterized by a conscious refusal to eat and a significant decrease in body weight, are discussed much less frequently. The high probability of a fatal outcome in anorexia nervosa is due to a wide range of its complications, primarily in the reproductive and endocrine systems. The most common adverse effects of anorexia nervosa are hypogonadotropic hypogonadism and amenorrhea, impaired growth hormone action, hypercorticism, decreased bone mineral density, and the risk of fractures. These complications do not always resolve on their own even after the resumption of rational nutrition and normalization of body weight. Moreover, anorexia nervosa is most common among females in adolescence, that is, during the period of active linear growth, reaching peak bone mass, and puberty. Awareness of the pathophysiology and clinical manifestations of endocrine disorders associated with anorexia nervosa can help in examining patients and choosing a further therapeutic strategy, especially since a unified protocol for the treatment of anorexia nervosa has not yet been developed.

Obesity is a pressing medical and social problem for all countries, including the Russian Federation. Obesity is the main component of metabolic syndrome and aggravates the course of many diseases, including endocrine ones. Obesity is a pressing medical and social problem for all countries, including the Russian Federation. Obesity is the main component of metabolic syndrome and aggravates the course of many diseases, including endocrine ones. It can be both a cause and a consequence of pathological processes. The article presents data on the effect of obesity on thyroid function. The relationship between adipose tissue and thyroid hormones is shown. The connection between obesity and hypothyroidism - overt and subclinical, autoimmune thyroiditis - is discussed. The issues of the relationship between the components of metabolic syndrome and thyroid function are considered. Weight loss was shown to improve thyroid function.

The review article presents data on the history of bariatric surgery and its main directions, the leading mechanisms of weight loss as a result of bariatric surgery, the transformation of bariatric surgery into metabolic surgery and its role in preventing the progression of chronic kidney disease in obese patients, reducing the risks of adverse cardiovascular outcomes in patients with cardiorenometabolic syndrome.

Dietary fiber plays a crucial role in the modification of intestinal microbiota, providing a prebiotic effect, such as stimulation of growth and/or nutrient function of intestinal microorganisms. The most modern form of dietary fiber, which serves as the basis and goal of clinical practice, is partially hydrolyzed dietary fiber. As a result of this review, the effectiveness of the use of partially hydrolyzed dietary fiber in various diseases and conditions is obvious. gastrointestinal tract.

The intestinal microbiota is an important link involved in the digestion process, synthesis and metabolism of amino acids, carbohydrates, fats, vitamins, trace elements and biologically active compounds. Intestinal bacteria produce metabolites, affecting the development, growth and maintenance of the host muscles. Mutual interactions between microbes, metabolites and muscles establish a bidirectional intestine-muscle axis. Violation of the intestinal microflora is one of the causes of malnutrition. In turn, malnutrition is one of the risk factors and one of the causes of sarcopenia. Deterioration in the absorption of food macro- and micronutrients, vitamins can lead to catabolism of muscle tissue and a decrease in skeletal muscle mass. Toxins of pathogenic and opportunistic intestinal microorganisms can contribute to systemic intoxication and systemic chronic inflammation. The intestinal microbiota plays a key role in maintaining the dynamic balance of intestinal epithelial and immune cells, which is crucial for overall organ homeostasis. Prebiotic, probiotic, and synbiotic preparations are recommended for the prevention and treatment of disrupted intestinal microbiome. Fecal microflora transplantation is sometimes used. In general, normalization of the gastrointestinal microflora is an important treatment method in the complex therapy of sarcopenia.

Celiac disease is an autoimmune disease of the small intestine caused by dietary gluten in genetically susceptible individuals. Gluten-free diet (GFD) is not only an effective strategy for treating celiac disease, but also a major factor regulating the composition and functions of intestinal microbiota, long-term adherence to which contributes to the development of microbial dysbiosis. Despite strict exclusion of gluten, patients continue to have symptoms of intestinal dyspepsia. The article discusses the effect of pre-/metabiotic therapy on the clinical course and composition of intestinal microbiota in patients with celiac disease for a therapeutic strategy of biotic therapy in addition to GFD. The aim. Evaluate the effectiveness of metabiotic, containing biologically active metabolites of the probiotic bacterial strain Bacillus subtilis SA49, a complex of 11 microbial and plant enzymes, and soluble short-chain fructooligosaccharides (scFOS) in correcting the symptoms of intestinal dyspepsia in patients with celiac disease on long-term GFD. Materials and methods. 24 patients diagnosed with celiac disease on BGD received metabiotic, containing biologically active metabolites of the probiotic bacterial strain Bacillus subtilis SA49, a complex of 11 microbial and plant enzymes, and scFOS. Results. After the therapy, the patients were evaluated for dyspepsia, and the composition of the colon microbiota and the results of the coprogram were quantified. The results showed a decrease in dyspepsia and amylorhea, normalization of stool consistency, and a change in the microbial balance of the intestine: an increase in the representation of Lactobacillus spp., Faecalibacterium prausnitzii, and Akkermansia muciniphila, a decrease in anaerobic imbalance and the representation of Escherichia coli and Enterobacter spp. Conclusion. Administration of metabiotic containing biologically active metabolites of the probiotic bacterial strain Bacillus subtilis SA49, a complex of 11 microbial and plant enzymes, and scFOS contributed to regression of clinical symptoms, restoration of microbial balance, and normalization of stool consistency in patients with celiac disease.