The human microbiota is a variety of different microorganisms. The composition of microbiota varies from host to host, and it changes during the lifetime. It is known that microbiome may be changed because of a diet, bacteriophages and different processes for example, such as inflammation. Like all other areas of medicine, there is a continuous growth in the area of microbiology. Different microbes can reside in all sites of a human body, even in locations that were previously considered as sterile; for example, liver, pancreas, brain and adipose tissue. Presently one of the etiological factors for liver disease is considered to be pro-inflammatory changes in a host’s organism. There are lot of supporting data about intestinal dysbiosis and increased intestinal permeability and its effect on development of liver disease pointing to the gut–liver axis. The gut–liver axis affects pathogenesis of many liver diseases, such as chronic hepatitis B, chronic hepatitis C, alcoholic liver disease, non-alcoholic liver disease, non-alcoholic steatohepatitis, liver cirrhosis and hepatocellular carcinoma. Gut microbiota has been implicated in the regulation of brain health, emphasizing the gut–brain axis. Also, experiments with mice showed that microorganisms have significant effects on the blood–brain barrier integrity. Microbiota can modulate a variety of mechanisms through the gut–liver axis and gut–brain axis. Normal intestinal flora impacts the health of a host in many positive ways, but there is now significant evidence that intestinal microbiota, especially altered, have the ability to impact the pathologies of many diseases through different inflammatory mechanisms. At this point, many of the pathophysiological reactions in case of microbial disbyosis are still unclear.

Malabsorption is a complex and multifaceted condition characterised by the defective passage of nutrients into the blood and lymphatic streams. Several congenital or acquired disorders may cause either selective or global malabsorption in both children and adults, such as cystic fibrosis, exocrine pancreatic insufficiency (EPI), coeliac disease (CD) and other enteropathies, lactase deficiency, small intestinal bacterial overgrowth (SIBO), autoimmune atrophic gastritis, Crohn's disease, and gastric or small bowel resections. Early recognition of malabsorption is key for tailoring a proper diagnostic work‐up for identifying the cause of malabsorption. A patient's medical and pharmacological history is essential for identifying risk factors. Several examinations such as endoscopy with small intestinal biopsies, non‐invasive functional tests and radiological imaging are useful in diagnosing malabsorption. Because of its high prevalence, CD should always be looked for in cases of malabsorption with no other obvious explanations and in high‐risk individuals. Nutritional support is key in the management of patients with malabsorption; different options are available, including oral supplements, enteral or parenteral nutrition. In patients with short bowel syndrome, teduglutide proved effective in reducing the need for parenteral nutrition, thus improving the quality of life of these patients. Primary care physicians play a central role in the early detection of malabsorption and should be involved in multidisciplinary teams for improving the overall management of these patients. In this European consensus, involving ten scientific societies and several experts, we have dissected all the issues around malabsorption, including the definitions and diagnostic testing (Part 1), high‐risk categories and special populations, nutritional assessment and management, and primary care perspective (Part 2).

Chronic viral hepatitis B and C remain major global health challenges, contributing significantly to liver-related morbidity and mortality. Despite antiviral therapies and vaccines for HBV, progression to cirrhosis and hepatocellular carcinoma remains common. For HCV, the lack of a vaccine and high chronicity rates further complicate outcomes. Recent evidence highlights gut–liver axis dysfunction and microbiota dysbiosis in disease progression, immune dysregulation, and fibrosis. Notably, alterations in microbiota composition, including reduced commensal bacteria such as Bifidobacteria and Lactobacilli and an increase in putatively harmful Enterobacteriaceae and Veillonellaceae, have been observed in HBV/HCV infections and cirrhosis. While antiviral therapies do not directly target the gut microbiota, they can contribute to partial restoration of microbial balance by reducing hepatic inflammation and improving gut–liver axis integrity. Nonetheless, post-treatment patients remain at elevated risk of HCC due to persistent epigenetic and immune-mediated changes. Emerging interventions, including probiotic strains, prebiotics, and symbiotics, demonstrate potential in enhancing gut health, alleviating inflammation, and enhancing the quality of life for liver disease patients. Moreover, the gut microbiota is gaining increasing recognition as a potential non-invasive biomarker for early disease detection and monitoring. Ultimately, modulating the gut microbiota could become an integral component of future strategies for managing chronic liver diseases and preventing their complications.

Background. Differences between populations might be reflected in their different genetic risk maps to complex diseases, for example, inflammatory bowel diseas

Background: Certain Enterobacteriaceae strains have been associated with the development of ulcerative colitis (UC). Extended-spectrum β-lactamase (ESBL)-producing Enterobacteriaceae are the most commonly found multi-drug-resistant (MDR) bacteria colonizing the gut in UC patients and might trigger a more severe disease activity in UC patients. Objective: The aim of this study was to evaluate whether disease activity is higher in UC patients with gut colonization with ESBL-producing Enterobacteriaceae. Materials and methods: A cross-sectional, pilot study was carried out in a tertiary medical center in Latvia. Demographic data were collected; UC disease activity and extent were evaluated according to the full Mayo score, Montreal classification, and adapted Truelove and Witt’s index. Rectal swabs with fecal biomaterial were collected, ESBL-producing Enterobacteriaceae were isolated, and bacterial plasmid genes responsible for ESBL production, blaCTX-M, blaTEM, and blaSHV, were detected. UC disease activity was compared in patients with and without gut colonization with ESBL-producing Enterobacteriaceae. Results: A total of 65 patients with UC were included in the initial analysis. Gut colonization with ESBL-producing Enterobacteriaceae was found in seven (11%) patients – mostly Escherichia coli [5 (71%)] containing the blaCTX-M bacterial plasmid gene. Patients with gut colonization with ESBL-producing Enterobacteriaceae had more severe disease compared with patients without gut colonization according to the full Mayo score (5.86 vs. 3.40; P=0.015), Montreal classification (moderate disease vs. clinical remission; P=0.031), and adapted Truelove and Witt’s index (moderate disease vs. mild disease; P=0.008). Conclusion: Gut colonization with ESBL-producing Enterobacteriaceae may increase UC disease activity. Further research is needed to analyze the possible confounding factors that could contribute toward this outcome.

The aim of this study was to assess the relationship between HLA Class II alleles in two groups of patients in Latvia: patients with cystic and alveolar echinococcosis. The study included 37 patients from the Rīga East Clinical University Hospital with echinococcosis (29 patients with cystic echinococcosis and eight patients with alveolar echinococcosis) and 100 healthy control persons without echinococcosis. HLA Class II allele genotyping was performed using Real-time polymerase chain reaction–sequence specific primer (RT-PCR-SSP). The odds ratios (OR), with 95% confidence intervals (95% CI), were calculated using statistical analysis performed with IBM SPSS Statistics for Windows, Version 22.0, to evaluate the risk of developing the disease in an individual having a particular HLA genotype. 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 *07:01, -DQB1 *03:02, and *03:01, -DQA1*04:01 and haplotypes HLA-DRB1*04:01/-DQB1*03:01/ -DQA1*03:01, HLADRB1*11:01/ -DQB1*03:01 /-DQA1*05:01. However, in the group with alveolar echinococcosis it was associated with the HLA-DRB1 alleles *17:01 and *07:01, -DQB1 *05:01 and haplotypes HLA- DRB1*17:01/-DQB1*02:01-2/-DQA1*01:01, HLA-DRB1*11:01/ -DQB1*03:01/-DQA1*01:03 and HLA-DRB1*11:01/-DQB1*03:01/-DQA1*03:01. HLADRB1*15:01/-DQÂ1*06:02-8/-DQA1*05:01 and HLA-DRB1*13:01/-DQB1*02:01-2/-DQA1*05:01 haplotypes were protective in all patient groups. The limitations of this exploratory study indicate that a broader study needs to be conducted for revealing specific risk and protective HLA Class II haplotypes for patients with cystic and alveolar echinococcosis in Latvia.