The global rise of inflammatory bowel disease (IBD) reflects environmental shifts, yet how these changes are embedded in the gut microbial ecology remains unclear. We construct a microbiome atlas comprising 245,627 profiles. By classifying countries into three epidemiologic stages, we establish a framework. As the IBD burden increases, the gut microbial alpha diversity declines, and community structures form distinct clusters. This transition is characterized by a gradient of core genera. Integrating six shotgun metagenomic cohorts, we identify the depletion of anabolic pathways in IBD patients. Strain-level analysis reveals that epidemiologic staging shapes genetic architecture within species, identifying an IBD-enriched subclade of Eisenbergiella associated with elevated fecal cholic acid. We develop a microbial inflammatory risk score (MIRS), based on 19 genera, that discriminates IBD from controls (area under the curve [AUC] = 0.92). MIRS correlates with IBD prevalence. Our study provides an atlas linking epidemiology to microbiome ecology and strain evolution, offering a foundation for population-level surveillance and interventions in IBD.

BACKGROUND:Risankizumab is an interleukin (IL)-23 inhibitor that is effective for the treatment of moderate-to-severe Crohn's disease (CD). However, many patients experience loss of response. Switching within the IL-23 inhibitor class to agents with more frequent dosing, such as guselkumab, may represent a salvage strategy, though no supporting data exist. We aimed to describe outcomes following switching between IL-23 antagonists. METHODS:This case series included five CD patients at a Canadian tertiary care center with primary non-response or secondary loss of response to risankizumab who were switched to guselkumab. Data were collected at baseline, during risankizumab therapy, and after switching. RESULTS:Five CD patients with inadequate response to risankizumab were included. One patient (20%) had primary non-response and four (80%) had secondary loss of response. Risankizumab duration ranged from 3 to 38 months (mean 17.4 ± 12.9). Four patients had active disease on baseline endoscopy before switching. Mean follow-up after switching was 3.8 ± 1.9 months. Mean CD-PRO2 improved from 22.7 to 5.2 post-switching. Clinical response (≥50% CD-PRO2 reduction) was achieved in 4/5 patients (80%), and clinical remission (CD-PRO2 < 8) was similarly achieved in 4/5 patients (80%). Among four patients with biochemical data, biochemical response (≥50% reduction in fecal calprotectin [FCal]) and remission (normalization of FCal) each occurred in 75%, with a mean FCal reduction of 618 µg/g. One patient had biochemical worsening despite clinical improvement. No safety concerns were reported. CONCLUSION:In CD patients with loss of response to risankizumab, switching to guselkumab may be effective in selected patients. Larger confirmatory studies are needed.

Primary intestinal lymphangiectasia (PIL) is a rare disorder characterized by malformed and dilated intestinal lymphatic vessels, resulting in impaired drainage and leakage of lymph fluid into the gastrointestinal lumen. This leads to protein-losing enteropathy, causing chronic diarrhea, peripheral edema, weight loss, and hypoalbuminemia due to loss of proteins, lymphocytes, and lipids. Diagnosis relies on endoscopic visualization of pathognomonic white mucosal plaques (representing dilated lymphatics) and histopathological confirmation of lymphatic dilation, after excluding secondary causes like malignancy, surgery, or inflammatory conditions.

Abstract Background Irritable bowel syndrome (IBS) is a prevalent condition in which disrupted communication between the gut and the brain plays a central role in disease manifestation. A dynamic, bidirectional regulatory network links the gut microbiota with the central nervous system (CNS), commonly referred to as the gut–brain axis, and this network exerts broad influence over both gastrointestinal physiology and psychological states. Aims This review specifically concentrates on direct microbiota–CNS communication pathways in the context of IBS. Materials and Methods This narrative review synthesizes existing experimental and clinical evidence related to gut microbiota–brain interactions, with a particular focus on neural and neuroendocrine signaling mechanisms. Results Gut microorganisms affect CNS function via microbial metabolites and neural signalling routes, whereas the CNS modulates gastrointestinal activity through integrated neural and endocrine pathways, involving the autonomic nervous system and the enteric nervous system. Given the complexity of these reciprocal interactions, this review specifically concentrates on direct microbiota–CNS communication pathways, with particular attention to neural circuits and the hypothalamic–pituitary–adrenal axis in the context of IBS. Conclusion Furthermore, we discuss how advances in precision stratification and multi‐omics approaches may facilitate the development of personalized therapeutic strategies, ultimately improving symptom control and restoring balance between gut microbial ecosystems and neural regulation.

Severe oral and gastrointestinal mucositis, though rare with immune checkpoint inhibitors, represents a life-threatening immune-related adverse events (irAE) requiring prompt recognition1,2. Key diagnostic steps include ruling out infections and inflammatory bowel disease. Early high-dose corticosteroids are the cornerstone of therapy, with escalation to biologic agents in refractory cases.

A 53-year-old man presented with abdominal pain and distension, accompanied with vomiting, and weight loss. Then he was treated with gastrointestinal decompression and enema, but the symptom of abdominal pain and distension continued with no relief. He had no drug or food allergies. He had no family history of liver disease, tuberculosis, asthma, and coagulation disorder. On physical examination, the patient had normal vital signs, abdominal distention, and generalized abdominal pain at palpation, with no rebound tenderness. Laboratory findings revealed significantly elevated white blood cells (14.28x109/L), eosinophils (8.23x109/L), C-reactive protein (13.5 mg/L), Serum IgE (487.83 μg/ml), and decreased albumin (34.6 g/L). There was no evidence of a recent infection with malaria, Lyme disease, hepatitis A, B, C or E viruses, Epstein-Barr virus (EBV), cytomegalovirus (CMV) or HIV. Antinuclear antibody was negative. His blood, stool, urine cultures, Clostridium difficile toxin, tumor markers, and T-spot test were negative and chest computed tomography (CT) was normal. Abdominal CT revealed dilatation of all duodenum, jejunum, ileum, and colon with thickened walls. Gastroscope showed hyperemia and edema in the gastric antrum mucosa. Double-balloon enteroscopy and Colonoscopy showed congestion in the small intestinal mucosa and colon mucosa. The histopathology of biopsies from the gastric antrum mucosa and small intestinal mucosa revealed visible eosinophil infiltration (38 and 52 eosinophils per HPF; a normal range at this anatomic site of 20 eosinophils per HPF), repectively. Therefore, the patient was diagnosed with eosinophilic gastroenteritis and intestinal obstruction. Then the patient was treated with an oral intake of prednisone 40 mg daily. Within three weeks, his abdominal distension was in complete relief. And prednisone was administered orally in decreasing amounts over that period. The patient was general in good condition during the follow-up period until now.

BACKGROUND:Inflammatory bowel disease (IBD), including ulcerative colitis (UC) and Crohn's disease (CD), is linked to poor sleep quality, though evidence remains inconsistent. This meta-analysis aimed to evaluate sleep quality in IBD patients and its association with disease activity. METHODS:We systematically searched databases up to February 2025 for studies reporting sleep quality in IBD. Outcomes included pooled prevalence of poor sleep, odds ratios (ORs), and standardized mean differences (SMDs) comparing IBD patients to controls, UC vs CD, and active vs inactive disease. Heterogeneity was assessed using Cochran's Q and I² statistics. RESULTS:Fifty-five studies were included. Poor sleep prevalence was 60% in IBD, 52% in UC, 56% in CD, and 68% in active IBD. IBD patients had higher odds of poor sleep than controls (OR: 1.90, 95% CI: 1.38-2.61; SMD: 0.61, 95% CI: 0.32-0.89). No differences emerged between UC and CD (OR: 0.93; SMD: -0.04). Active IBD patients showed elevated poor sleep risk versus those in remission (OR: 2.09, 95% CI: 1.50-2.90), driven by CD (OR: 2.40, 95% CI: 1.42-4.05). SMDs for active vs inactive disease were 0.49 (IBD overall), 0.40 (UC), and 0.73 (CD). CONCLUSION:Poor sleep is highly prevalent in IBD, particularly during active disease, with significantly higher rates than in healthy controls. Sleep quality did not differ between UC and CD. Addressing poor sleep in IBD management and exploring underlying mechanisms are crucial for improving patient outcomes.

BACKGROUND:Biosimilars of infliximab and adalimumab are increasingly adopted in inflammatory bowel disease (IBD) to reduce healthcare costs, but concerns persist regarding their long-term efficacy, immunogenicity, and safety post-switch. This meta-analysis synthesizes contemporary evidence on outcomes after transitioning from originators to biosimilars. METHODS:We systematically searched PubMed, Embase, MEDLINE, and conference abstracts (inception-June 2025) to identify randomized controlled trials (RCTs) and observational studies comparing biosimilars (CT-P13, SB2, SB5, etc.) with originators in IBD. Primary outcomes included clinical remission, discontinuation rate, adverse events (AEs), C-reactive protein (CRP), and fecal calprotectin (FCAL), and anti-drug antibody (ADA) incidence. Risk of bias was assessed using Cochrane and Newcastle-Ottawa tools. Pooled odds ratios (ORs) and event rates were calculated using random-effects models. RESULTS:Among 37 studies (36 observational, 1 RCTs) encompassing 10812 IBD patients, biosimilars demonstrated comparable clinical remission rates pre- and post-switch in Crohn's disease (CD) (OR = 0.87, 95% CI: 0.74-0.96) and ulcerative colitis (UC) (OR = 1.25, 95% CI: 0.83-1.90). Biomarkers (CRP, fecal calprotectin) remained stable post-transition. Pooled discontinuation rates were 13% (range: 2-36%) after switching. Safety profiles were similar between biosimilars and originators, ADA incidence (OR = 0.96, 95% CI: 0.46-2.02) showed no significant differences. Heterogeneity stemmed from differences in follow-up duration, disease subtype (CD vs. UC), and variable outcome definitions. CONCLUSION:Biosimilars maintain comparable efficacy, safety, and immunogenicity to originators in IBD, supporting their use in single or multiple switching scenarios. Standardized reporting of mucosal healing, drug monitoring, and economic metrics is critical to optimize biosimilar adoption in real-world practice.