Introduction: The prevalences of malnutrition and sarcopenia in patients with IBD are not precisely known, and nutritional assessment is not standardized. We assessed the prevalence and risk factors of these conditions in outpatients and their impact on clinical outcomes. Methods: This prospective longitudinal study considered patients who had IBD for at least one year, were attending a tertiary IBD center, and were followed for the subsequent year. Results: In a sample of 158 consecutive patients (96 with Crohn’s disease and 62 with ulcerative colitis), the prevalence of malnutrition, according to GLIM criteria, was 13.3%. For identifying patients at risk of malnutrition, the Malnutrition Universal Screening Tool demonstrated better accuracy, (sensitivity 88.9 (65.3–98.6) and specificity 90.2 (83.8–93.4)) than the SaskIBD-NR questionnaire (sensitivity 69.3 (41.1–86.7) and specificity 60.9 (60.9–76.8)). The prevalence of sarcopenia was 34.2%. Considering clinical outcomes, sarcopenia at baseline was significantly associated with hospital admission within a year (p = 45.2% vs. 20.3%, 0.026). Conclusions: Malnutrition and sarcopenia were present in about one-third of IBD patients. Awareness should be raised among physicians caring for IBD patients about the need to evaluate patients’ nutritional statuses to help patients achieve a better quality of life.

Background: Pomegranate (Punica granatum) can be used to prepare a bioactive extract exerting anti-inflammatory activities. Clinical studies demonstrated an improvement in clinical response in inflammatory bowel disease (IBD) patients when pomegranate extract (PG) was taken as a complement to standard medications. However, the molecular mechanisms underlying its beneficial effects are still scarcely investigated. This study investigates the effect of PG on bacterial biofilm formation and the promotion of mucosal wound healing. Methods: The acute colitis model was induced in C57BL/6N mice by 3% dextran sodium sulfate administration in drinking water for 5 days. During the recovery phase of colitis, mice received saline or PG (200 mg/kg body weight) by oral gavage for 11 days. Colitis was scored daily by evaluating body weight loss, bleeding, and stool consistency. In vivo intestinal permeability was evaluated by fluorescein isothiocyanate-conjugated dextran assay, bacterial translocation was assessed by fluorescence in situ hybridization on tissues, whereas epithelial and mucus integrity were monitored by immunostaining for JAM-A and MUC-2 markers. Bacterial biofilm formation was assessed using microfluidic devices for 24 or 48 h. Primary fibroblasts were isolated from healthy and inflamed areas of 8 IBD patients, and Caco-2 cells were stimulated with or without PG (5 μg/mL). Inflammatory mediators were measured at the mRNA and protein level by RT-PCR, WB, or Bio-plex multiplex immunoassay, respectively. Results: In vivo, PG boosted the recovery phase of colitis, promoting a complete restoration of the intestinal barrier with the regeneration of the mucus layer, as also demonstrated by the absence of bacterial spread into the mucosa and the enrichment of crypt-associated fibroblasts. Microfluidic experiments did not highlight a specific effect of PG on Enterobacterales biofilm formation, even though Citrobacter freundii biofilm was slightly impaired in the presence of PG. In vitro, inflamed fibroblasts responded to PG by downregulating the release of metalloproteinases, IL-6, and IL-8 and upregulating the levels of HGF. Caco-2 cells cultured in a medium supplemented with PG increased the expression of SOX-9 and CD44, whereas in the presence of HGF or plated with a fibroblast-conditioned medium, they displayed a decrease in SOX-9 and CD44 expression and an increase in AXIN2, a negative regulator of Wnt signaling. Conclusions: These data provide new insight into the manifold effects of PG on promoting mucosal homeostasis in IBD by affecting pathogen biofilm formation and favoring the regeneration of the intestinal barrier through the regulation of the crosstalk between epithelial and stromal cells.

Accumulating evidence from pre-clinical and clinical studies demonstrate the benefit of dietary fibers for inflammatory bowel disease (IBD). However, the majority of patients avoid or limit their consumption to manage their symptoms during the active and remission phases, although limited research supports these long-term dietary habits. Although recent evidence-based dietary guidelines highlight the importance of promoting an adequate intake of dietary fiber in IBD patients, intervention trials have not yet clearly clarified the quality and quantity of dietary fiber that should be consumed to be equally tolerated by and provide benefit for patients with IBD. This narrative review describes dietary fibers and their characteristics, analyzes the real-word studies on the impact of dietary fiber consumption in IBD in different clinical settings, and concludes with potential future directions in fiber research, focusing on the real-world needs of characterizing the consumption of fiber-rich foods and promoting their adequate intake.

Background and aims: Inflammatory bowel diseases (IBD) are multifactorial chronic inflammatory disorders affecting the gastrointestinal tract. However, a broad spectrum of extraintestinal manifestations (EIMs) is associated with IBD, affecting several organs and systems, such as the skin, musculoskeletal and hepatobiliary systems, and, not least, the eye. Approximately 10% of IBD patients can develop ocular EIMs (O-EIMs) with a higher prevalence in Crohn’s disease (CD). Eye-redness, photophobia, pain, and blurred vision are the common symptoms, with a wide rate of severity and clinical impact on the quality of life. This narrative review aims to summarize the prevalence, pathogenesis, and current evidence-based management of O-EIMs, underlying the importance of a holistic approach and specialties collaboration for a prompt diagnosis and treatment. Methods: PubMed was searched up to December 2023 to identify relevant studies investigating the pathogenesis, epidemiology, and treatment of O-EIMs in IBD patients. Results: The mechanisms underlying O-EIMs are partially unknown, encompassing immune dysregulation, shared antigens between the eye and the gut, genetic predisposition, and systemic inflammation driven by high levels of interleukins and cytokines in IBD patients. The complexity of O-EIMs’ pathogenesis reflects in the management of these conditions, varying from topical and systemic steroids to immunomodulatory molecules and biologic therapy, such as anti-tumor necrosis factor (TNF)-alpha. A multidisciplinary approach is the backbone of the management of O-EIMs.

Background/Objectives: Inflammatory bowel diseases (IBDs), which include Crohn’s disease (CD) and ulcerative colitis (UC), are chronic conditions requiring long-term therapy to maintain remission and improve quality of life. Despite the approval of numerous drugs, IBD continues to present treatment challenges. This review aims to summarize novel therapeutic target agents in phases II and III of development, including sphingosine-1-phosphate receptor modulators (S1P), anti-interleukin-23 (IL-23), and other small molecules and monoclonal antibodies currently under investigation (e.g., anti-TL1A, obefazimod, NX-13, RIPK-inhibitors). Methods: A comprehensive literature search was conducted up to December 2024 to identify relevant articles published in English over the past three–five years, focusing on phase II/III studies for UC and CD. The search included databases such as PubMed, Google Scholar, and the ClinicalTrials.gov portal. Results: Clinical trials underline the potential of novel immunomodulators, including anti-TL1A, obefazimod, NX-13, RIPK inhibitors, and anti-IL-23p19 agents, as promising therapeutic options for IBD. Anti-IL23p19 therapies, such as risankizumab and mirikizumab, alongside guselkumab, exemplify this class’s growing clinical relevance. While some are already in clinical use, others are nearing approval. Conclusions: Ongoing research into long-term safety and the development of personalized treatment strategies remains pivotal to enhance outcomes. Patient stratification and the strategic positioning of these therapies within the expanding treatment landscape are critical for optimizing their clinical impact.

Background and aims: An increased risk of acute pancreatitis (AP) has been reported in patients with inflammatory bowel disease (IBD), but data on its prevalence, etiology, and outcomes are limited. Materials and Methods: A two-step retrospective analysis spanning 10 years (2011–2020) was conducted across 34 European centers. The first step surveyed the prevalence of AP in patients with IBD, while the second gathered data on disease characteristics, etiology, and outcomes. Results: The survey found an expected AP prevalence of 1.13% (780/68,989), though only 0.58% (n = 398) met the inclusion criteria. The mean age was 33.6 ± 14.3; 52% were female, and 56.5% had Crohn’s disease (CD). AP was clinically mild in most cases (86.9%). Among 347 patients with available imaging, no alterations were observed in 81 (23.3%), whereas edematous AP was observed in 218 (62.8%). Drugs (mainly azathioprine) were the leading cause (55.3%), followed by biliary (14.8%) and autoimmune (7.8%) causes. In 13.5% of patients, AP was considered idiopathic. During a median follow-up of 67 months [IQR 34–96] from the index episode, recurrence was observed in 13% of patients, and 1.5% developed chronic pancreatitis. CD patients exhibited distinct risk profiles, including ileal involvement and smoking, whereas ulcerative colitis (UC) patients showed more frequent autoimmune and idiopathic etiologies. Conclusions: The PANDORA study established a 0.58% prevalence of AP in IBD patients, which was lower than expected. AP is usually mild both clinically and radiologically. An ileal location in CD and extensive colitis in UC are usually reported, and azathioprine seems to be the most common cause of AP in this setting, especially a few weeks after its introduction.