With the recent conditional approval of resmetirom by the US Food and Drug Administration, the treatment of metabolic dysfunction-associated steatotic liver disease (MASLD) has potentially entered a new era, requiring a comprehensive understanding of the strengths and weaknesses of non-invasive tests (NITs) for diagnosing and monitoring MASLD-related fibrosis. This article focuses on F2/F3 liver fibrosis and summarises the current application status of NITs, including serum biomarkers, imaging methods and their combined use in the management of MASLD. The article highlights the application of NITs in several areas, including diagnosis and baseline stratification, monitoring progression of fibrosis, prediction of liver-related clinical events, as well as assessment of disease regression, remission and long-term liver-related outcomes. Furthermore, we compare the advantages and limitations of NITs and propose practical strategies for integrating them into clinical practice. Additionally, we highlight the main challenges currently faced in the application of these NITs and potential future research avenues. We suggest that future studies prioritise the validation of NITs across diverse ethnic populations. We believe it essential to explore the role of NITs in dynamic monitoring and integration of multiomics technologies, artificial intelligence and personalised risk models to improve diagnostic accuracy and treatment planning.

Helicobacter pylori resistance to antibiotics commonly used in eradication regimens is increasing dramatically in many locations; new strategies are needed to manage this infectious disease.

The elimination of HBV covalently closed circular DNA (cccDNA) remains a critical hurdle for chronic hepatitis B (CHB) management.

Atherosclerosis reflects a chronic inflammatory process of arteries. The origin of chronic vascular inflammation has been associated over a long time primarily with lipid disorders, but evidence from the past years has suggested that lipid-independent pathways are also involved. Recent research has demonstrated that the gastrointestinal microbiota has an impact on the development of atherosclerosis. Many clinical studies have revealed that there exist altered gut microbiota and increased intestinal abundance of bacteria from the oral cavity in atherosclerosis-related disorders such as cardiovascular disease or stroke, while several studies have demonstrated insights into underlying mechanisms. Various microbial-derived metabolites, such as the pathogen-associated molecular pattern endotoxin, trimethylamine N-oxide or imidazole propionate, contribute to atherosclerosis, while other bacterial metabolites, such as some tryptophan derivatives, might be protective. Furthermore, gut microbiota and lipid pathways are highly interactive, and the gut microbiota affects lipid absorption and storage, and the gut microbiota also contributes to vascular ageing. Interference with the gut microbiota by prebiotics, probiotics and antibiotics has demonstrated beneficial effects on atherosclerosis mainly in preclinical models. Overall, the gut microbiota has appeared as an important rheostat for vascular inflammation in atherosclerosis, which is controlled by host-microbe interactions that may be therapeutically exploited in the future.

The development of IBD is known to involve early immunological alterations, but our understanding of the changes in antibody epitope repertoires moving from the prediagnostic phase towards disease onset remains incomplete.

IgG4 antibodies exhibit unique structural and functional properties, which distinguish them from other IgG subclasses. Among clinicians, IgG4 has been primarily associated with IgG4-related diseases (IgG4-RDs), such as autoimmune pancreatitis, where its role has been a focus of intense discussion. However, growing evidence reveals that IgG4 is involved in a broader spectrum of immune-regulatory processes, extending beyond IgG4-RDs and positioning it as a key modulator of immune tolerance. In this context, several specific features allow IgG4 to play dual roles, serving as a protective factor in immune regulatory settings, such as allergic responses and antibody therapies that require tolerance induction towards target cells, while its role in IgG4-RDs remains uncertain, potentially contributing to disease or mitigating tissue damage. This review examines the pathophysiological roles of IgG4 in the regulation of immune responses, highlighting its involvement in both homoeostasis and disease. Furthermore, it explores the therapeutic potential of harnessing IgG4's unique features, not only for IgG4-associated diseases, but also for other indications, where promoting beneficial IgG4 responses could offer therapeutic advantages.

Both lifestyle factors and genetic predisposition contribute to the development of diverticulitis.

Coeliac disease is characterised by immune-mediated damage to the small intestine in response to dietary gluten in genetically predisposed individuals. Increased intestinal permeability is a central component to its pathophysiology. This review explores the evidence for increased permeability in coeliac disease and the underlying mechanisms, including the roles of zonulin, inflammatory cytokines, microbial alterations and immune responses to gliadin peptides. We also review comprehensively the therapies targeting barrier integrity and normalising intestinal permeability, including particular diets and supplements, and experimental and improved medications including larazotide acetate and IMU-856. Finally, we highlight the need for reliable biomarkers for evaluating increased permeability in coeliac disease and advocate for further research on therapies which normalise barrier function, particularly as a strategy to maintain remission.

Chronic inflammation and elevated reactive oxygen species are key contributors to hepatocellular carcinoma (HCC) progression.