Small bowel capsule endoscopy (SBCE) has emerged in the past two decades as the cornerstone for assessing small bowel disorders, and its use is supported by several guidelines. However, there are several limitations, such as the considerable time required for gastroenterologists to review these videos and reach a diagnosis. To address these limitations, researchers have explored the integration of artificial intelligence in the interpretation of these videos. In our review, we explore the evolving and emerging role of artificial intelligence in SBCE and examine the latest advancements and ongoing studies in these areas, aiming at overcoming current limitations.

Clostridioides difficile infection (CDI) is a major complication in inflammatory bowel disease (IBD), due to coexistence of altered microbiota, chronic inflammation, and immune dysregulation. This narrative review summarizes recent evidence on the epidemiology, pathogenesis, risk factors, diagnosis, and management of CDI in IBD. Overall, IBD patients have a four- to five-fold higher risk of CDI than the general population and face more severe courses, higher rates of hospitalization, colectomy, recurrence, and mortality. Pathogenesis involves profound dysbiosis with loss of butyrate-producing Firmicutes and Bacteroidetes, bile acid imbalance that promotes spore germination, and enhanced toxin effects on an already inflamed mucosa. Major risk factors include active colonic disease, broad-spectrum antibiotic exposure, prolonged hospitalization, and corticosteroid or combined immunosuppressive therapy. Diagnosis requires careful integration of stool assays with clinical evaluation, supported by endoscopy or imaging when needed, to distinguish infection from IBD flares. Recommended first-line treatments are fidaxomicin or oral vancomycin, reserving fecal microbiota transplantation for recurrent or high-risk cases. Optimal IBD control is essential to reduce both primary and recurrent infection. CDI and IBD share a mutual pathogenic interplay in which microbial, immune, and therapeutic factors from each condition drive and magnify the other. Early recognition, guideline-based antibiotic therapy, judicious use of immunosuppression, and microbiota-based preventive strategies are crucial to improve patient outcomes and limit recurrence, thus reducing healthcare costs.

Ultra-processed foods (UPFs) provide more than half of daily energy intake in several high-income countries, and their consumption is increasing worldwide. Inflammatory bowel disease (IBD) and irritable bowel syndrome (IBS) are chronic gastrointestinal conditions whose burden has grown alongside industrialized dietary patterns. Here, we summarize the epidemiological, mechanistic and clinical evidence linking UPF consumption to both conditions. Most prospective cohorts and meta-analyses associate higher UPF intake with incident Crohn’s disease, whereas associations with ulcerative colitis are weaker and inconsistent. In IBS, observational studies, including a large prospective cohort, suggest a modest, dose-dependent association with risk, although data are limited and the diagnostic criteria have recently changed with Rome V. Mechanistically, both disorders may converge on the intestinal microenvironment: in experimental models, emulsifiers alter microbial composition and metabolism, the mucus layer, epithelial barrier integrity and mucosal immune activation, and non-nutritive sweeteners alter microbial composition and epithelial barrier function, although human data are limited and causality has not been established. We also discuss IBS-like symptoms in quiescent IBD, dietary management in both conditions, and the main knowledge gaps, including exposure assessment, residual confounding and the need for adequately powered intervention trials.

Non-steroidal anti-inflammatory drugs (NSAIDs) are widely prescribed worldwide for their analgesic, antipyretic, and anti-inflammatory properties. However, their long-term use is associated with substantial gastrointestinal (GI) toxicity. Although upper GI injury has traditionally received greater attention, NSAID-induced enteropathy is now increasingly recognized as a common yet underdiagnosed condition. Advances in small-bowel imaging, particularly capsule endoscopy, have demonstrated that mucosal injury of the small intestine occurs in up to 70–80% of chronic NSAID users and may also develop after short-term exposure in otherwise healthy individuals, often without overt clinical symptoms. When symptoms do occur, NSAID-induced enteropathy is characterized by non-specific clinical manifestations and may lead to severe complications in approximately 1% of cases. The pathogenesis of NSAID-induced enteropathy is multifactorial and more complex than that underlying upper GI damage. It involves prostaglandin depletion, increased intestinal permeability, bile acid-mediated toxicity, enterohepatic recirculation of NSAIDs, and, importantly, interactions with the gut microbiota. Concomitant therapies, particularly proton pump inhibitors, may further aggravate small-bowel injury by promoting intestinal dysbiosis. Growing evidence supports a relevant contributory role for the gut microbiota as both a mediator and a modulator of NSAID-induced toxicity, affecting epithelial barrier function, oxidative stress, immune responses, and bile acid metabolism. This review provides an overview of current knowledge of NSAID-induced enteropathy, with a particular emphasis on the microbiota-driven mechanisms underlying mucosal injury. By integrating emerging microbiota-targeted therapeutic approaches, we propose a management algorithm that may help modify disease progression in a condition that remains frequently overlooked in clinical practice.