Inflammatory bowel disease (IBD) has increasing socio-medical and economic significance for humans. Although the aetiopathogenesis of IBD is not fully established, it is believed that the imbalance of intestinal microbiota of the gastrointestinal tract and modification of the intestinal immune system are the most important triggering mechanisms of risk, development and progression of IBD, their relapses and activation. Epidemiological, microbiological and immunological studies have identified some pathogenic and commensal intestinal bacteria that can induce disturbances of local immune responses and predispose the risk of IBD. The review deals with the mechanism of participation of commensal intestinal anaerobic gram-negative Akkermansia muciniphila in the destruction and metabolism of the intestinal mucosa and modulation of epigenetic mechanisms, physiological, metabolic, immune and signal functions associated with the development of IBD. The use and limitations of these living bacterial commensals and their low molecular weight components and metabolites in the prevention and treatment of IBD are discussed. Challenges, limitations and potential improvement strategies using some commensal anaerobic bacteria and fecal microbiota transplantation in IBD are also considered.

The incidence of echinococcosis in European countries varies from 0.1 to 10 cases per 100,000 residents and Latvia has relatively high number of cases. The development of cystic echinococcosis is associated with the individual factors of the host organism, as well as immunological reactions and HLA DRB1 is the most polymorphic of the HLA class II genes and therefore it can be used for individual identification. We can conclude that in the case of cystic echinococcosis a more severe course of a disease can be anticipated in the presence of HLA DRB1 alleles *17:01 and *04:01, DQB1 *03:02, DQA1*04:01. As well in the event of cystic echinococcosis HLA DRB1 alleles *01:01 and *15:01, DQA1 *01:01 can be considered as protective. Immunogenetic data could prove significant for therapy planning in accordance with the individual characteristics of a patient, because no data on the optimal duration of therapy and whether the therapy can be terminated without facilitating the relapse of the infection are not currently available.

The aim of this study was to observe the role of the genotype DQ 2.2 in patients with celiac disease (CD): serological and morphological features of celiac disease in patients with the DQ2.2 genotype Materials and methods: We examined 47 patients with СD, diagnosed according to ESPHGAN criteria. All participants were tested for antibodies to tissue transglutaminase-2 (TTG) and deamidated gliadin peptides, morphometric examination of biopsy specimens of duodenal mucosa and genotyping were carried out. Based on the results of genotyping, patients were divided into 2 groups: group 1 comprised 18 patients with the genotype DQ2.2; group of 2-29 patients with other genotypes of CD. Results: an increase of anti-TTG antibodies was observed in all patients in group 1. Moreover, a moderate increase in group 1 was 55.6%, and in the 2nd group, 27.6% (p = 0.07). A significant increase of anti-TTG in group 1-44.4%, in the 2 group - 3.4% (p = 0.001). In addition, the morphological changes of the duodenal mucosa corresponding to the level of Marsh 3b were more often observed in group 1-27.8% than in 2-0% (p = 0.006). Morphometric parameters of duodenal mucosa in group 1 reveal more severe atrophic changes. Conclusion: it is expected that the detection of the genotype DQ2.2 can serve as a predictor of severe serological (a significant increase of anti-TTG antibodies level) and morphological changes in CD.

The aim of the study was to evaluate the diagnostic significance of the rs738409 C> G polymorphism of the PNPLA3 gene as a marker for the formation and progression of liver fibrosis in patients with non-alcoholic fatty disease (NAFLD). Materials and methods. An open case-control study of a group of patients with non-alcoholic fatty liver disease in the amount of 35 people was conducted. Conducted clinical, laboratory examination methods. Additionally, non-invasive serum fibrosis markers were studied: concentrations of insulin, leptin, adiponectin, matrix metalloproteinase-9 (MMP-9) and its inhibitors - tissue inhibitor of matrix metalloproteinase-1 and 2 (TIMP-1, TIMP-2). All patients underwent liver elastometry to assess the stage of fibrosis on the Metavir scale using the FibroScan apparatus (FibroScan). As a potential marker for the progression of liver fibrosis in NAFLD, PNPLA3 148M / I polymorphism (rs738409) was studied by PCR. Results. There are clinical signs that suggest that liver steatosis is more pronounced in carriers of the G allele of the PNPLA3 148M / I gene. For patients with NAFLD C / G PNPLA3 148M / I genotype, a more aggressive course of the disease with the formation of high progressive stages of fibrosis is characteristic. Conclusion. PNPLA3 148M / I polymorphism can be considered as a non-invasive marker reflecting the formation and progression of fibrotic changes in the liver tissue in patients with NAFLD.

The aim was to study the frequency of HFE gene mutations in patients with Wilson disease (WD) as one of the possible modifier genes. Materials and methods: There were examined 90 patients with WD. The frequency and spectrum of mutations in the HFE gene were studied using targeted NGS. Results. Mutations in the HFE gene were found in 30% patients with WD. In two patients was discovered combination of two hereditary diseases - WD and hereditary hemochromatosis, associated with metabolic disorders of copper and iron respectively.

The aim of the work was the study of the polymorphism of a number of genes and their role as predisposing factors in the development of chronic pancreatitis. Materials and methods: A study of genetic polymorphisms in 35 patients with chronic pancreatitis was carried out. Patients were divided into groups. In the experimental group, 8 women and 27 men, whose mean age was 43.2 ± 5.3 years. The control group was made up of hypothetical studies according to generally accepted data for the Caucasoid race. Informed consent to participate in the study was obtained. All patients underwent standard general clinical, biochemical analyzes, as well as human genomic DNA isolated from blood leukocytes was subjected to analysis. Results: It was found that in the experimental group the frequency of gene polymorphism was higher than in the control group. Normal homozygote in the experimental group in the genotype was absent among all genes: MMP1 (-1607delG); 9MMP9 (A-8202G); TIMP-1 (C536T); IL10 (G-1082A); OPG TNFRSF11B- (mutation G1181C); P450 (3A4 CYP3A4 1A / 1B); P-450 (CYP1A1); LPL (Ser447Ter mutation), GSTP1 (mutation Ile105Val). Among heterozygous genes polymorphisms TIMP-1 (C536T), IL10 (G-1082A), LPL (mutation Ser447Ter), P450 (CYP1A1), IL10 (G-1082A) prevailed. The greatest number of pathological homozygotes was detected by MMP1, 9MMP9, P450 (3A4 CYP3A4 1A / 1B), OPG. Conclusions: A study of the genetic polymorphism of the human genome showed that there is a high risk of developing chronic pancreatitis in patients with these polymorphisms (MMP1, 9MMP9, P450 (3A4 CYP3A4 1A / 1B), OPG). Significant differences in the frequency of occurrence of gene mutations in comparison groups were obtained. These polymorphisms are one of the factors predisposing to the development of chronic pancreatitis. The determination of gene polymorphism can be used in surgical practice, including complex diagnosis and predicting the nature of the course of chronic pancreatitis-the development of a cystic form of chronic pancreatitis.

Aim of investigation: comparative analysis of 10 schemes of eradication in patients with duodenal ulcer associated with Helicobacter pylori. Materials and methods: 10 eradication schemes were investigated at the Department of Gastroenterology for 15 years (Central state medical academy of department of presidential affairs, Head of the Department Minushkin O. N.) 297 patients with duodenal ulcer associated with Helicobacter pylori were divided in treatment groups, as follows: 30 patients received triple therapy with omeprazol (O), clarithromycin (C) and metronidazole (M); 98 patients received triple therapy with omeprasol (O), clarithromycin (C) and amoxicillin (A): the dose of clarithromycin and the duration of treatment (5-day, 7-day, 10-day) was selected depending on the degree of Hp contamination (+, ++, +++); 68 patients received sequential therapy with omeprazol (O), clarithromycin (C) and amoxicillin (A); 117 patients received triple therapy with omeprazol (O), clarithromycin (C) and furazolidon (F) and tinidazol (T) - 57 patients or with omeprazol (O), wilprafen (W) and levofloxacin (L) and amoxicillin (A) - 60 patients; and 50 elderly patients received half doses of O+C+A combnation or pantoprazol (P), dazolic (D) and amoxicillin (A). Esophagogastroduodenoscopy (EGS), Giemsa stain in biopsy and rapid urease test (RUT) were used to evaluate the quality of ulcer healing and efficacy of eradication. Student`s t-criterion and Fisher`s method were used in statistical processing (Significant differences in significance level of 95%, p<0,05) Results: O+C+M scheme had the lowest efficacy (60%). 6 of 10 schemes were effective: O+C+A - 80%; sequential scheme - 83% (with (F) - 93%, with (T) - 88%; with (W) 90% or (L) 80%). Discussion: Eradication efficacy increased by 97% with day-degree contamination selection. In elderly patients half doses schemes were effective (O+C+A - 87% and P+D+A 90%).

The aim of the study: to evaluate the composition of gut microbiota in H. pylori-negative and H. pylori-positive patients, as well as to assess the influence of H. pylori eradication therapy on the gut microbiota composition immediately after and one month after completion of therapy. Materials and methods: stool samples from 93 H. pylori-positive and 42 H. pylori-negative (control group) patients were used for analysis. Stool samples immediately after and one month after completion of therapy were collected from 93 and 14 patients, respectively. Gut microbiota composition assessment including the evaluation of alpha diversity (Shannon index) was performed by shotgun sequencing. Results: Firmicutes (56,73±21,81)%, Bacteroidetes (35,97±23,65)%, Actinobacteria (2,42±4,24)%, Proteobacteria (2,37±7,00)%, Verrucomicrobia (0,94±2,54)% were the most represented bacterial phyla in the gut microbiota of H. pylori-positive patients before the eradication therapy. Immediately after eradication therapy the number of Verrucomicrobia and Actinobacteria bacterial phyla decreased, and, conversely, the representation of Proteobacteria phylum increased. In 4 weeks the representation of these phyla did not differ from the initial level. Representation of Firmicutes phylum had a tendency to decrease immediately after the completion of eradication therapy; there was a further decrease in their representation in a month. Bacterial genera: Bacteroides (15,1±17,32)%, Prevotella (14,07±21,60)%, Eubacterium (13,79±10,49)%, Faecalibacterium (6,26±5,85)%, Ruminococcus (5,61±6,00)%, Subdoligranulum (5,34±5,77)%, Butyrivibrio (4,57±13,26)% were predominat in the gut microbiota in H. pylori-positive patients before the treatment. Immediately after therapy the representation of almost all these genera decreased, except Bacteroides which representation increased. The abundance of Escherichia and Klebsiella bacterial genera also increased. One month after the therapy a tendency to return to initial composition was observed for most of bacterial genera. Conclusion: thus, H. pylori eradication therapy affects the gut microbiota composition. Some changes persist for one month after completion of therapy.

The purpose of our work is to study the spontaneous and induced chemiluminescent activity of neutrophilic granulocytes (NG) in patients with rectal cancer in dynamics. Materials and methods. The study included 56 patients with rectal cancer. At the first stage there were 9 people, in the II stage 19 people, on the III 17 and at the IV stage 11 patients. The object of study are neutrophilic granulocytes isolated from venous blood. The control group consisted of 112 healthy blood donors. The intensity of synthesis of active oxygen species of NG was determined by the method of chemiluminescence analysis. Results. The study showed a significant increase in the intensity of spontaneous and induced luminescence and the area under the curve of spontaneous chemiluminescence in the II-IV stages of the disease. When studying zymosan-induced chemiluminescence, the area under the curve is increased in all groups of patients, while in patients at stage IV the total production of ROS is significantly higher than in stages I and II. On the 7^th day after the surgical treatment, the intensity of spontaneous chemiluminescence remains elevated only in patients at the IV stage of the rectal cancer. The intensity of induced chemiluminescence and the area under the curve of spontaneous and induced luminescence are increased at all stages of the disease with respect to control. The activation index was increased in patients at all stages of with rectal cancer both before and after surgery. Сonclusion. As a result of the study, an increase in the intensity of ROS synthesis in patients with rectal cancer was revealed. The total production of reactive oxygen species is higher in the late stage of the disease. An increase in the activation index of neutrophils in all stages of the RPC characterizes the metabolic capabilities of neutrophils to the enhanced synthesis of ROS in functional activation.

Research objective: to study the frequency of gastrointestinal symptoms in patients with inflammatory bowel disease (IBD) depending on the presence of the small intestinal bacterial overgrowth (SIBO). Materials and methods of the study: The study included 152 patients with IBD. All patients would be given a hydrogen breath test (VDT) with lactulose to diagnose SIBO. The analysis of gastrointestinal symptoms in patients depending on the presence of SIBO, as well as the dynamics of symptoms after its correction was carried out. Results: The frequency of SIBO in patients with IBD was 48%. Patients with SIBO were more likely to have symptoms: diarrhea, bloating, flatulence, weakness, whining and irritability. After a 2-week course of correction of SIBO, patients had a decrease in the frequency of these symptoms. Conclusion: The data obtained indicate a high frequency of SIBO in patients with IBD. SIBO is associated with symptoms that may accompany an acute attack of the IBD. The diagnosis of SIBO should be included in routine practice in patients with acute attack of IBD for selection of adequate therapy, which will include correction of microbiota disorders and will not lead to inappropriate change of basic therapy.

Objective: to determine the epidemiological, clinical and laboratory features of viral acute gastroenteritis (AGE) in hospitalized pregnant women and to evaluate of the effectiveness of synbiotics in the treatment of AGE in pregnant women. Materials and methods: The study involved 482 adult patients with AGE hospitalized from February to June 2017, including 103 pregnant women aged from 21 to 37 years. Along with the generally accepted diagnostic methods, feces were studied by PCR using a set of original specific primers to detect rotaviruses of group A and group C, noroviruses of the second gene group (HNoV GII) and astroviruses. Identified virus isolates were genotyped. Results: out of 103 pregnant women with AGE, more than half of cases (53.3%) accounted for viral AGE: norovirus - 51.4% of cases, rotavirus - 1.9%. Astrovirus infection was not registered. Noroviruses of new genotypes GII.P17 / GII.17 and GII.P16 / GII.2, and rotavirus genotype G9P were detected in pregnant women with AGE. In noroviral AGE, the food route of transmission prevailed, the leading factors of transmission were salads and dairy products. The disease proceeded in moderate form and had clinical features characteristic of norovirus infection. In pregnant women with AGE of norovirus etiology and unspecified etiology, using of synbiotic “Normobact” in the combined therapy, the earlier arrest of diarrhea was noted comparing with patients receiving only pathogenetic therapy (p <0.05). Conclusion: the established high frequency of viral AGE in pregnant women shows the need for introducing into clinical practice universal test systems for diagnosing the most common viral pathogens in order to improve therapy. The effectiveness of synbiotic “Normobact” in pregnant women with viral OGE was shown in terms of earlier stopping diarrhea, which makes it possible to recommend it as part of complex therapy.

The mucous membrane of the gastrointestinal tract is an extensive information and communication system that quickly reacts to both external and internal factors of the body, ensuring the maintenance of homeostasis of tissue and blood. The aim of the study was to determine the factors that ensure the appearance of an autoimmune component in damage to the pancreas in rats. Material: manipulations were performed on white Wistar rats weighing 190,0-230,0.Immunization of animals was carried out according to the standard scheme. There were 4 intraperitoneal injections of 2 ml of pancreatic tissue homogenate. Total antibodies (at) to parietal cells (PC) (Parietal Cell antibodies, IgG, IgA, IgM) were determined in plasma by enzyme immunoassay. The animals were divided into one control group and five experimental groups (6 groups of 5 rats in total). Experimental groups: 1st-immunization of intact animals (IM) according to the above scheme. 2nd-acute pancreatitis (AP); 3rd group AP+ IM; 4th-chronic pancreatitis (CP); 5th group-CP+IM. With AP and CP, there is an autoimmune component that interferes with the restoration of damaged pancreatic tissue. Experimental studies have shown that the presence of acute inflammation, accompanied by full blood vessels, hyperemia, edema, hypoxia, necrosis, death of a large number of cells, the release of cellular elements that are endogenous antigens. Inflammation of the pancreas stimulates the immune system of the gastrointestinal tract. In addition, factors contributing to the development of an autoimmune reaction are: alcohol, infection: bacterial, viral and/or parasitic.

Trial objective: study the mechanism of multidirectional effect of Serotonin adipinate on gastric and colon motor activity. Materials and methods: experiments were carried out on Wistar rats (N83) in surgical anesthesia. An electromyogram and hydrostatic pressure in the cavities of organs was registered using an amplifier BioAmp ML132 (Adinstruments, Australia), an analog-to-digital converter Maclab 8e (Adinstruments, Australia), a computer Масintosh Performa 6400/180 and a software program Chart 4.2.3. Trial findings: it was established that intra-arterial injection of Serotonin adipinate at a dose of 0.05 mg/kg and 0.1 mg/kg causes stimulatory and inhibitory gastric reactions; at a dose of 0.15 mg/kg - only stimulatory ones. Colon appeared to have only stimulatory reactions. It was also found that intravenous injection of Serotonin adipinate does not intensify stomach and colon contraction. Conclusion. Organs’ stimulatory reactions occur due to activation of muscle 5HT-receptors, inhibitory ones - due to activation of presynaptic 5HT-receptors, locating on organ’s adrenergic terminals, and ejection of inhibitory transmitter noradrenaline by them. When using Serotonin adipinate in experiment and in clinical practice, it is necessary to take into account that the organs’ effect from serotonin administration into body may be dual: inhibitory at low doses and stimulatory at higher ones.

The article deals with some features of clinical course, diagnostics, treatment of the senile asthenic syndrome in patients with chronic opisthorchosis and hepatobiliary damage. Values of a life style, a role of etiotropny and pathogenic therapy are shown. Separately the role of application of laennec as an important factor of pathogenetic and anti-aging medicine is considered.