LEADING ARTICLE
The human gastrointestinal tract is one of the largest in area — points of contact between the internal environment of the host and environmental factors.
The most important functional element of this interaction is the microbial — tissue complex of the gastrointestinal tract, and its permeability is defined as a key option in the implementation of the mechanisms of adaptation and homeostasis.
The microbiota is represented in various interpretations by the main four domains (archaea, bacteria or eubacteria, eukaryotes and viruses). The combination of these domains into the Biota taxon suggests the need to use the term biota-tissue complex, which more fully reflects the sophisticated interactions of all microbial-tissue complexes of the body.
Metabolic syndrome is associated with current diseases, such as obesity, diabetes, hypertension, which are accompanied by changes in the intestinal microbiota and the functioning of the immune and neuro-humoral systems of the body. Without detracting from the role of heredity and environmental factors, the intestinal microbiota makes a significant contribution to the development of metabolic disorders and obesity by modulating cascading enzymatic reactions of the macroorganism, interacting with receptors directly and/or using its own metabolites and signaling molecules.
The purpose of study was to analyze the literature data obtained in the study of the role of the intestinal microbiota in the development of metabolic syndrome (MS).
Results: A review of current literature on the role of intestinal microbiota in the development of metabolic syndrome is presented. The features of the mucosal microflora of the colon, the role of bacterial films, epithelial lining of the intestinal mucosa in the formation of the intestinal microbial-tissue complex as the leading links of metabolic disorders are discussed. The article presents data on the variability of short-chain fatty acids, bacterial genome in the development of obesity and type 2 diabetes.
CLINICAL GASTROENTEROLOGY
The purpose of the study was to determine the frequency and nature of manifestations of left ventricular diastolic dysfunction in patients with non-alcoholic fatty liver disease with the background of metabolic syndrome (MS).
Characteristics of patients and research methods: To solve this problem, 227 patients with MS (130 men and 97 women) were examined. The study was conducted in two phases. At the first stage, all patients with MS are divided into two groups: patients with NAFLD — 205 people and 22 — without liver damage. At the next stage, a group of NAFLD patients with left ventricular DD (n=136) (66.34%) (the main group) and patients with no DD (n=69) (33.66%) (the comparison group) were identified.
Results of the study: the results of diagnostics, clinical and laboratory manifestations of left ventricular diastolic dysfunction in 136 patients with NAFLD on the background of metabolic syndrome are Presented. Significant factors of development and progression of diastolic dysfunction were identified, which include increased body weight and adipose tissue, insulin resistance, dyslipidemia, hyperuricemia, activity and stage of liver damage. According to the data of structural and functional changes in the myocardium, the role of diastolic dysfunction in the development of chronic heart failure in patients with NAFLD with manifestations of metabolic syndrome has been established.
Conclusion: it was Found that the development of left ventricular diastolic dysfunction in patients with NAFLD is due to the morphofunctional state of the liver.
The goal was to determine the effect of ursodeoxycholic acid (UDCA) in non-alcoholic steatohepatitis (NASH) with impaired glycemic control.
Materials and methods. 67 patients NASH were examined: prediabetes — 38 (56.7%), type 2 diabetes mellitus 29 (43.3%), men — 39 (58.2%), women — 28 (41.8%), age — 45.1 ± 10.2 years. The UDCA dose was 9.4 ± 2.0 mg / kg / day during 59.7 ± 77.6 weeks. Fragments of cytokeratin-18 (FCK-18) (TPS ELISA, Biotech, Sweden), TNF-α (Human TNFα Platinum ELISA, eBioscience, Austria), IL-6 (“Interleukin-6-IFA-Best”, Vector-Best, Russia), insulin (“Insulin TEST System”, Monobind Inc., USA), HOMA-IR were determined.
Results. There was a decrease in the levels of FCK-18 — from 238.1 ± 93.7 to 170.7 ± 79.2 U / l (p <0.05), ALT — 61.3 ± 19.0 to 38.9 ± 19.1 U / l (p <0.05), glucose 5.9 ± 1.3 to 5.5 ± 0.7 mmol / l (p <0.05), insulin 21.9 ± 18.2 to 13.7 ± 9.7 MkU / l, HOMA-IR — 5.8 ± 2.2 to 3.1 ± 0.8 (p <0.05), cholesterol — 6.2 ± 0.9 to 5.3 ± 0.3 mmol / l, LDL — 3.9 ± 0.9 to 3.2 ± 0.6 mmol / l (p <0.05), TNF-α 6.3 ± 1.5 to 5.4 ± 2.1 pg / ml (p <0.05), IL-6–7.1 ± 3.4 to 4, 1 ± 3.2 pg / ml (p <0.05).
Conclusion. UDCA had pleiotropic effects in NASH with impaired glycemic control, reducing cellular apoptosis, necrosis, inflammation, improving insulin sensitivity and lipid homeostasis.
The aim was to investigate features of manometric pattern of type II achalasia.
Materials and methods: High-resolution esophgeal manometry (HRM) was performed in 250 patients with achalasia. In 154 cases patients underwent peroral esophageal myotomy (POEM).
Results: We found that poor results after POEM showed patients with high preoperative esophageal pressurization (>80 mm Hg). The poorest result after POEM we observed in patient with short additional increase of panesophageal pressure (up to 95 mm Hg) withing the contour of panesophageal pressurization.
There is ample evidence that insulin resistance, hyperinsulinemia, and obesity are at the heart of the development of non-alcoholic fatty liver disease (NAFLD). The disease is now considered as the hepatic component of metabolic syndrome (MS).
64 children with NAFLD were assessed for metabolic syndrome stigma. An analysis was also made on the state of the problem according to the literature on the general links of the pathogenesis of these conditions, methods of diagnosis and treatment of NAFLD.
All components of MS are observed with different frequencies in patients with NAFD. This disease, together with type 2 diabetes mellitus, becomes very common diseases in childhood. The incidence of NAFLD in children is constantly growing, it has begun to occur in infants, an outcome in cirrhosis of the liver is possible within childhood, although the prognosis for NAFLD remains definitely uncertain. Weight loss with a low glycemic index diet, regular exercise, and other lifestyle changes are the mainstay of NAFLD treatment, but not yet very effective for various reasons. In these conditions, it is necessary to increase the role of primary prevention of MS and NAFLD.
REVIEW
The aim. The aim of our study was to analyze the available data from literature sources concerning the issues of etiology, pathogenesis, clinic, diagnosis and features of treatment of non-alcoholic fatty liver disease (NAFLD) and non-alcoholic fatty pancreatic disease (NAFPD).
Materials and methods. We conducted a retrospective analysis of foreign literature sources that contain up-to-date information about the state of the problem of NAFLD and NAFPD.
Results. NAFLD and NAFPD develop against the background of metabolic syndrome (MS), systemic insulin resistance, oxidative stress, changes in lipid metabolism. The natural course of NAFPD is associated with high risk of MS progression, occurrence of NAFLD, arterial hypertension, type 2 diabetes mellitus, exocrine pancreatic insufficiency, acute and chronic pancreatitis, pancreas cancer. Correction of the components of MS can reduce the severity of NAFLD and NAFPD; enzyme replacement therapy can improve the function of β-cells in pancreas steatosis.
Conclusion. The alternatives of the pharmacological treatment of NAFLD and NAFPD continue to be actively explored. We emphasize the need of including medications containing pancreatic enzymes in the treatment of NAFLD.
This review presents literature data on the role of the gastric tract in the processes of intoxication and detoxification of endoand exobiotics. The factors that promote the absorption and metabolism of toxic products in the gastrointestinal tract are described. The causes of intoxication and the mechanisms of two-phase detoxification with the participation of phase I enzymes of the biotransformation of xenobiotics in the intestine, in particular cytochrome P-450 isoenzymes, are described in detail. The predominance of the cytochrome P-450 isoenzyme CYP3A4 in the intestine was shown, and among the enzymes of phase II of biotransformation in the intestinal wall, the most important are UDP-glucuronyltransferase and sulfotransferase. The data on the ways of correction of intoxication with the use of a detoxification complex of dietary nutrition are presented. Clinical studies have shown that a specialized program provides antioxidant protection and the work of enzymes of the I and II stages of the metabolism of toxins, a decrease in the absorption and excretion of metabolic products, can significantly reduce the intoxication of the body, which is extremely necessary during the treatment and rehabilitation of diseases of the gastrointestinal tract and other organs and systems. rehabilitation of the body. It was found that the use of products of detox nutritional program LEOVIT DETOX led to a significant decrease in the concentration of urea and creatinine, which indicates an accelerated elimination of toxins and metabolic products formed in the body. A decrease in the concentration in the blood of the main enzymes characterizing the detoxification activity of the liver ALT, AST, GGT was also established.
The aim of the study was to evaluate the detoxification effectiveness of the preventive nutrition Program and individual detoxification products LEOVIT DETOX, designed to affect all stages of Exo — and endobiotic metabolism.
Materials and methods. Detoxification nutrition LEOVIT DETOX includes: specialized food product of dietary preventive nutrition “Complex nutrition program DETOX”, detoxifying jelly and bars — specialized food products of dietary preventive nutrition for detoxification of the body. The DETOX nutrition program is designed for 15 days and contains 30 products. The dynamics of biochemical parameters of liver and kidney function disorders (AST, ALT, GGT, urea, creatinine), blood lipid spectrum (by total cholesterol), fasting blood glucose level, and products of lipid peroxidation in blood serum were measured.
Results. The use of specialized food products of dietary prophylactic nutrition “, a Comprehensive nutrition program DETOX” leads to a significant decrease in the concentration of urea and creatinine, AST, ALT, GGT, cholesterol, glucose, diene conjugate, ketodienes of CARBONYLS and increased total oxidative activity of blood serum were examined.
Conclusion. The use of a specialized food product of dietary preventive nutrition “Complex nutrition program DETOX” provides effective detoxification of the body in diseases of the gastro-intestinal system.
Aim. Conduct a review of studies characterizing the role of herpesvirus infections in the pathogenesis of inflammatory bowel disease (IBD).
Introduction. The study of the role of herpes virus infections in the pathogenesis of inflammatory bowel disease (IBD) is currently of considerable interest to researchers from different countries.
Result. The results of studies on the significance of human herpes viruses (HHV) in inflammatory bowel diseases (IBD) ulcerative colitis (UC) and Crohn’s disease (CD), their effect on the course of these diseases, and refractory treatment of UC and CD in the presence of HHV are presented.
It is shown that most researchers unanimously conclude that the main attention should be paid to Epstein-Barr virus (EBV), cytomegalovirus (CMV) and human herpes simplex virus type 6 (HHV-6), which are found in the mucous membrane of the colon in patients with IBD and affect both the course of the disease and the effectiveness of the treatment. Attention is focused on the fact that it is necessary to differentiate colitis due to HHV and IBD, proceeding against the background of HHV reactivation, since approaches to the treatment of these conditions are different.
Conclusion. Requires targeted research on the role of human herpes viruses in the pathogenesis of IBD.