Remission Is Maintained after Switch from Dose-Optimised Intravenous Treatment to Subcutaneous Treatment with Vedolizumab in Inflammatory Bowel Disease.

Background and Objectives: The subcutaneous (SC) formulation of vedolizumab has proven to be effective for the maintenance of remission after intravenous induction. Little is known about the efficacy of switching from intravenous maintenance treatment to SC. We aimed to assess the real-world efficacy of switching to SC treatment and to assess the impact of a baseline treatment regimen. Materials and Methods: In this observational cohort study, adult patients with inflammatory bowel disease who were switched to SC vedolizumab maintenance treatment were enrolled. Patients after intravenous induction and patients who switched from intravenous maintenance treatment (every 8 weeks or every 4 weeks) were included. The SC vedolizumab dosing was 108 mg every 2 weeks, regardless of the previous regimen. The clinical, biochemical, and endoscopic disease activity parameters and vedolizumab serum concentrations at the time of the switch and at the follow-up were assessed. Results: In total, 135 patients (38% Crohn's disease, 62% ulcerative colitis) were switched to SC vedolizumab treatment. The median time to the first follow-up (FU) was 14.5 weeks (IQR 12-26), and the median time to the second FU was 40 weeks (IQR 36-52). Nine patients (7%) discontinued SC vedolizumab treatment, with two-thirds of them discontinuing due to active disease. In all dosing regimens, there were no significant changes in the clinical scores and CRP at the baseline and first and second FUs. Clinical and biochemical remission appeared to be maintained irrespective of the previous dosing regimen. Conclusions: The results of this real-world study suggest that the maintenance of clinical and biomarker remission can be achieved in patients who switched from intravenous to SC vedolizumab. The baseline vedolizumab dosing regimen (every 4 weeks versus every 8 weeks) did not have an impact on outcomes.

Biological treatment approach to inflammatory bowel disease is similar in academic and nonacademic centres - prime time for decentralisation of inflammatory bowel disease care?

BACKGROUND: With the increasing number of inflammatory bowel disease (IBD) patients, it is difficult to manage them within specialised IBD teams in academic medical centres: many are therefore treated in nonacademic IBD centres. It is unclear whether the time to introducing biologics is the same in both settings. AIM: We aimed to compare treatment approach with biologics in academic vs. nonacademic centres. METHODS: We analysed Slovenian national IBD registry data (UR-CARE Registry, supported by the European Crohn's and Colitis Organisation), which included 2 academic (2319 patients) and 4 nonacademic IBD (429 patients) centres. RESULTS: The disease phenotype was similar in both settings. In total, 1687 patients received 2782 treatment episodes with biologics. We observed no differences in treatment episodes with TNF-alpha inhibitors (60% vs. 61%), vedolizumab (24% vs. 23%), or ustekinumab (17% vs. 16%) in academic compared to nonacademic centres ( P  = 0.949). However, TNF inhibitors were less often the first biologic in academic centres (TNF inhibitors: 67.5% vs. 74.0%, vedolizumab: 20.3% vs. 17.9%, ustekinumab: 12.1% vs. 8.1%; P = 0.0096). Consequently, more patients received ustekinumab (29.8% vs. 18.3%) and vedolizumab (17.4% vs. 13.5%) and fewer TNF inhibitors (52.7% vs. 68.2%) for Crohn's disease in academic compared to nonacademic centres, with no such differences for ulcerative colitis. The time to initiation of the first biologic from diagnosis was short and similar in both settings (11.3 vs. 10.4 months, P  = 0.2). CONCLUSION: In this nationwide registry analysis, we observed that biological treatment choice was similar in academic and nonacademic settings. These findings support the decentralisation of IBD care.

Gut community alterations associated with Clostridioides difficile colonization in hospitalized gastroenterological patients with or without inflammatory bowel disease.

Clostridioides difficile colonization and development of infection commonly occur in inflammatory bowel disease (IBD) patients and can trigger flare-ups. Both conditions are inherently linked to disrupted gut microbiota. This study included 149 hospitalized gastrointestinal patients, which were divided into IBD (n = 48) and non-IBD patients (n = 101). Patients were tested for C. difficile colonization (qPCR and selective plating), and gut bacterial communities were analyzed with 16S amplicon sequencing. Blood test results were retrospectively collected from the medical records. IBD and non-IBD patients had comparable C. difficile colonization rates (31.7 and 33.3%, respectively). Compared to non-IBD C. difficile-non-colonized patients, IBD and C. difficile-colonized patients shared multiple common bacterial community characteristics including decreased diversity and reduced abundance of strict anaerobic bacteria. Furthermore, certain microbiota alterations were enhanced when IBD was accompanied by C. difficile colonization, indicating a synergistic effect between both medical complications. Conversely, certain microbial patterns were specific to C. difficile colonization, e.g., co-occurrence with Enterococcus, which was most common in IBD patients (81.3%).

Distinct Types of Gut Microbiota Dysbiosis in Hospitalized Gastroenterological Patients Are Disease Non-related and Characterized With the Predominance of Either Enterobacteriaceae or Enterococcus.

Typical disease-associated microbiota changes are widely studied as potential diagnostic or therapeutic targets. Our aim was to analyze a hospitalized cohort including various gastroenterological pathologies in order to fine-map the gut microbiota dysbiosis. Bacterial (V3 V4) and fungal (ITS2) communities were determined in 121 hospitalized gastrointestinal patients from a single ward and compared to 162 healthy controls. Random Forest models implemented in this study indicated that the gut community structure is in most cases not sufficient to differentiate the subjects based on their underlying disease. Instead, hospitalized patients in our study formed three distinct disease non-related clusters (C1, C2, and C3), partially explained by antibiotic use. Majority of the subjects (cluster C1) closely resembled healthy controls, showing only mild signs of community disruption; most significantly decreased in this cluster were Faecalibacterium and Roseburia. The remaining two clusters (C2 and C3) were characterized by severe signs of dysbiosis; cluster C2 was associated with an increase in Enterobacteriaceae and cluster C3 by an increase in Enterococcus. According to the cluster affiliation, subjects also showed different degrees of inflammation, most prominent was the positive correlation between levels of C-reactive protein and the abundance of Enterococcus.