The advent of immunotherapy, specifically of immune checkpoint inhibitors (ICIs), for the treatment of solid tumors has deeply transformed therapeutic algorithms in medical oncology. Approximately one-third of patients treated with ICIs may de velop immune-related adverse events, and the gastrointestinal tract is often affected by different grades of mucosal inflammation. Checkpoint inhibitors colitis (CIC) presents with watery or bloody diarrhea and, in the case of severe symptoms, requires ICIs discontinuation. The pathogenesis of CIC is multifactorial and still partially unknown: anti-tumor activity that collaterally effects the colonic tissue and the upregulation of specific systemic inflammatory pathways (i.e., CD8+ cytotoxic and CD4+ T lymphocytes) are mainly involved. Many questions remain regarding treatment timing and options, and biological treatment, especially with anti-TNF alpha, can be offered to these patients with the aim of rapidly resuming oncological therapies. CIC shares similar pathogenesis and aspects with inflammatory bowel disease (IBD) and the use of ICI in IBD patients is under evaluation. This review aims to summarize the pathogenetic mechanism underlying CIC and to discuss the current evidenced-based management options, including the role of biological therapy, emphasizing the relevant clinical impact on CIC and the need for prompt recognition and treatment.

Background/Objectives: Inflammatory bowel disease (IBD) and eosinophilic gastrointestinal diseases (EGIDs) are complex, multifactorial chronic inflammatory disorders affecting the gastrointestinal tract. Their epidemiology, particularly for eosinophilic esophagitis (EoE), is increasing worldwide, with a rise in the co-diagnosis of IBD and EGIDs. Both disorders share common risk factors, such as early exposure to antibiotics or specific dietary habits. Moreover, from a molecular perspective, eosinophilic infiltration is crucial in the diagnosis of eosinophilic disorders, and it also plays a pivotal role in IBD histological diagnosis. Indeed, recent evidence highlights the significant role of eosinophils in the health of the intestinal mucosal barrier and as mediators between innate and acquired immunity, even indicating a potential role in IBD pathogenesis. This narrative review aims to summarize the current evidence regarding the common clinical and molecular aspects of EGIDs and IBD and the current state of knowledge regarding overlap conditions and their pathogenesis. Methods: Pubmed was searched until May 2023 to assess relevant studies describing the epidemiology, pathophysiology, and therapy of EGIDs in IBD. Results: The immune pathways and mechanisms underlying both EGIDs and IBD remain partially known. An improved understanding of the role of eosinophils in overlapping conditions could lead to enhanced diagnostic precision, the development of more effective future therapeutic strategies, and a more accurate prediction of patient response. Consequently, the identification of red flags indicative of an eosinophilic disorder in IBD patients is of paramount importance and must be evaluated on a case-by-case basis.

Endoscopy is the mainstay of inflammatory bowel disease (IBD) evaluation and the pillar of colorectal cancer surveillance. Endoscopic equipment, both hardware and software, are advancing at an incredible pace. Virtual chromoendoscopy is now widely available, allowing the detection of subtle inflammatory changes, thus reducing the gap between endoscopic and histologic assessment. The progress in the field of artificial intelligence (AI) has been remarkable, and numerous applications are now in an advanced stage of development. Computer-aided diagnosis (CAD) systems are likely to reshape most of the evaluations that are now prerogative of human endoscopists. Furthermore, sophisticated tools such as endocytoscopy and probe-based confocal laser endomicroscopy (pCLE) are enhancing our assessment of inflammation and dysplasia. Finally, pCLE combined with molecular labeling could pave the way to a new paradigm of personalized medicine. This review aims to summarize the main changes that occurred in the field of IBD endoscopy and to explore the most promising novelties.

Background The gender gap in the authorship of scientific research may affect career advancement. Our aim was to assess the potential gender gap in gastrointestinal (GI) journals. Methods A systematic review was performed of the GI literature and ongoing research in the period 2020–2022. A total 10 GI journals and ongoing research on clinicaltrials.gov were selected for review. The gender gap in first and senior authorship was evaluated for each article and ongoing research project. Associations between the gender gap and possible predictors were measured and results are presented as odds ratios (ORs) with 95%CI. Results The number of first female authors (FFAs) and senior female authors (SFAs) in published articles were 1408/4207 (33.5%) and 911/4207 (21.7%), respectively. There were 781/2654 (29.4%) female principal investigators (PI)s for the ongoing research. On comparison of non-endoscopic vs. endoscopic topics, the latter were associated with the gender gap (hepatology, OR 2.15 [95%CI 1.83–2.55]; inflammatory bowel disease, OR 2.12 [95%CI 1.60–2.45]; upper and lower GI, OR 1.31 [95%CI 1.18–1.73]); as well as the type of article (original article vs. editorial, OR 1.92 [95%CI 1.58–2.33]). The type of research was also associated with the gender gap (clinical vs. preclinical studies, OR 0.88 [95%CI 0.66–0.91]). Conclusion Our results demonstrated a correlation between the gender gap and the design and topic of the research. Future strategies for improving equity in career development in GI endoscopy should focus on closing the gender gap in equity of authorship.

Due to the greater risks of adverse events (AEs) and the lower rate of submucosal invasive cancer (SMIC), large proximal colonic polyps are frequently treated by piecemeal endoscopic mucosal resection (EMR) in the West. However, this implies the risk of surgery to radicalize non-curative endoscopic resection in case of early colorectal cancer (CRC). We evaluated procedure outcomes in patients undergoing ESD for proximal colonic lesions at risk of SMIC.All consecutive patients with lesions at risk of SMIC proximal to splenic flexure referred for ESD at a tertiary center were prospectively included from 2019 to 2021. En bloc, R0, and curative resection rates were primary outcomes, while length of hospitalization, AEs, need for surgery due to AEs, and recurrence rates were secondary outcomes.A total of 116 patients (mean age: 68.4±10.91 years; men: 69.8%) were included. En bloc, R0, and curative resection rates were 84.5%, 78.4%, and 72.4%, respectively. T1 adenocarcinoma was reported in 25% of lesions (29/116). Eleven patients (9.5%) underwent secondary surgery due to non-curative resections; residual disease was found in one patient. Most frequent AE was intra-procedural perforation (9.9%); no AE required surgery. Median follow-up was 36 months; three of 97 recurrences (3.1%) at 6 months and one of 85 recurrence (1.2%) at 36 months were reported, which were all endoscopically treated.In expert hands, ESD is effective and safe for proximal colonic lesions at risk of SMIC for the favorable balance between risk of AEs and benefit of avoiding unnecessary surgery, even for early CRC.

The advent of immunotherapy and specifically of immune checkpoint inhibitors (ICIs) for the treatment of solid tumors has deeply transformed therapeutic algorithms in medical oncology. Approximately one third of patients treated with ICIs may develop immune-related adverse events, being the gastrointestinal tract often affected with different grades of mucosal inflammation. Checkpoint inhibitors colitis (CIC) presents with watery or bloody diarrhoea and in case of severe activity requires ICIs discontinuation. The pathogenesis of CIC is multifactorial and still partially unknow: anti-tumor activity that collaterally effects the colonic tissue and the upregulation of specific systemic inflammatory pathways (i.e., CD8+ cytotoxic and CD4+ T lymphocytes) are mainly involved. Many open issues remain on treatment timing and options, and biological treatment, above all with anti-TNF alpha, can be offered to these patients aiming to rapidly resume the oncological therapies. This review aims to summarize the pathogenetic mechanisms underlying CIC and to discuss evidenced-based management including the role of biological therapy.