To prospectively compare oral contrast-enhanced T2-weighted half-Fourier rapid acquisition with relaxation enhancement (RARE) magnetic resonance (MR) imaging with T1-weighted gadolinium-enhanced fast low-angle shot (FLASH) MR and standard examinations in the evaluation of Crohn disease. Institutional review board approval and informed consent were obtained. Fifty-nine patients with Crohn disease underwent MR imaging after oral administration of a superparamagnetic contrast agent; RARE plain and fat-suppressed sequences and FLASH sequences were performed before and after intravenous injection of gadolinium chelate. References were endoscopic, small-bowel barium, computed tomographic, ultrasonographic, and clinical-biochemical scoring of disease activity. Two radiologists analyzed MR images for presence and extent of Crohn disease lesions, presence of strictures or other complications, and degree of local inflammation. MR findings were correlated with endoscopic, radiologic, and clinical data (kappa statistic and Spearman rank correlation test). T2-weighted MR was 95% accurate, 98% sensitive, and 78% specific for detection of ileal lesions. Agreement between T1- and T2-weighted images ranged from 0.77 for ileal lesions to 1.00 for colic lesions. T2-weighted MR enabled detection of 26 of 29 severe strictures, 17 of 24 enteroenteric fistulas, and all adhesions and abscesses; T1-weighted MR enabled detection of 20 of 29 severe strictures, 16 of 24 enteroenteric fistulas, and all adhesions and abscesses. Complications leading to surgery were found in 12 (20%) patients; these were assessed correctly with either T1- or T2-weighted images. T2-weighted signal intensities of the wall and mesentery correlated with biologic activity (P < .001, r of 0.774 and 0.712, respectively). Interobserver agreement was 0.642-1.00 for T2-weighted and 0.711-1.00 for T1-weighted images. T2-weighted MR can depict Crohn disease lesions and help assess mural and transmural inflammation with the same accuracy as gadolinium-enhanced T1-weighted MR. Combination of gadolinium-enhanced T1- and T2-weighted sequences is useful in the assessment of Crohn disease.

The development of colorectal cancer, responsible for 9% of cancer-related deaths, is favored by a combination of genetic and environmental factors. The modification of diet and lifestyle may modify the risk of colorectal cancer (CRC) and prevent neoplasia in up to 50% of cases. The Western diet, characterized by a high intake of fat, red meat and processed meat has emerged as an important contributor. Conversely, a high intake of dietary fiber partially counteracts the unfavorable effects of meat through multiple mechanisms, including reduced intestinal transit time and dilution of carcinogenic compounds. Providing antioxidants (e.g., vitamins C and E) and leading to increased intraluminal production of protective fermentation products, like butyrate, represent other beneficial and useful effects of a fiber-rich diet. Protective effects on the risk of developing colorectal cancer have been also advocated for some specific micronutrients like vitamin D, selenium, and calcium. Diet-induced modifications of the gut microbiota modulate colonic epithelial cell homeostasis and carcinogenesis. This can have, under different conditions, opposite effects on the risk of CRC, through the production of mutagenic and carcinogenic agents or, conversely, of protective compounds. The aim of this review is to summarize the most recent evidence on the role of diet as a potential risk factor for the development of colorectal malignancies, as well as providing possible prevention dietary strategies.

(1) Background: Vitamin D is an immunoregulatory factor influencing intestinal homeostasis. Recent evidence supports a central role of this micronutrient in the course of Inflammatory Bowel Diseases (IBD). This narrative review aims to provide a general overview of the possible biological mechanisms of action of vitamin D and its therapeutic implications in IBD. (2) Methods: A systematic electronic search of the English literature up to October 2021 was performed using Medline and the Cochrane Library. Only papers written in English that analyzed the role of vitamin D in IBD were included. (3) Results: In vitro and animal studies reported that vitamin D signaling improves epithelial barrier integrity regulating the expression of several junctional proteins, defensins, and mucins, modulates the inflammatory response, and affects gut microbiome composition. Recent studies also suggest that vitamin D deficiency is highly prevalent among IBD patients and that low serum levels correlate with disease activity and, less clearly, with disease course. (4) Conclusions: An increasing body of evidence suggests some role of vitamin D in the pathophysiology of IBD, nonetheless the underlying mechanisms have been so far only partially elucidated. A strong correlation with disease activity has been reported but its implication in the treatment is still undefined. Thus, studies focused on this issue, the definition of vitamin D levels responsible for clinical effects, and the potential role of vitamin D as a therapeutic agent are strongly encouraged.

Objective: To evaluate the efficacy and tolerability of anti-tumour necrosis factor α (TNFα) monoclonal antibody (infliximab) in the treatment of spondyloarthropathy (SpA) associated with active and inactive Crohn’s disease (CD). Methods: Twenty four patients with SpA associated with active or inactive CD (16 active, 8 quiescent) were treated with anti-TNFα monoclonal antibody (infliximab) with repeated infusions for a period of 12–18 months. The treatment aimed at ameliorating the general musculoskeletal and spinal pain, controlling peripheral arthritis and enthesitis, decreasing the BASDAI score, modifying acute phase reactants, and reducing CD activity. Results: Infliximab improved both gastrointestinal (p<0.01) and overall articular symptoms (BASDAI, p<0.01; general musculoskeletal and spinal pain, p<0.01; peripheral arthritis, p<0.01) in patients with active CD. Additionally, infliximab effectively controlled not only axial involvement and peripheral arthritis but also enthesitis (p<0.01) and prevented inflammatory bowel disease reactivation in patients with inactive CD and low inflammatory markers. Amelioration of gut and musculoskeletal involvement persisted for up to 12 months. Conclusion: Infliximab may act on the inflammation of entheses and of periarticular structures, which usually does not cause a change in the haematological markers that are the main indicators of pain and joint ankylosis in SpA. Infliximab induces and maintains remission of CD while at the same time treating active and severe SpA, suggesting that it should be the preferred drug for the treatment of active and severe SpA associated with active or quiescent CD.