Background: Multiple sclerosis (MS) and inflammatory bowel disease (IBD) are two autoimmune diseases that seriously affect patients' quality of life. Previous studies have established an association between MS and IBD, including Crohn's disease (CD) and ulcerative colitis (UC), but the results were inconsistent. The aim of this study was to quantify the prevalences of and the association between MS and IBD.Methods: The PubMed, Web of Science, and Embase databases were searched through November 2020 for studies reporting data on MS among patients with IBD and vice versa. The main outcomes were the proportion of MS in patients with IBD and vice versa, as well as the association (risk ratio [RR]) of IBD in MS and that of MS in IBD.Results: Based on the analysis of 17 studies, the prevalence of MS in patients with IBD was 0.2% (95% CI 0.1–0.4%), while the prevalence of IBD in patients with MS was 0.6% (95% CI 0.4–0.9%). Patients with MS had a higher prevalence of IBD than controls (RR = 1.53, 95% CI 1.38–1.70, p < 0.00001). There was a similarly high risk of developing CD (RR 1.41, 95% CI 1.14–1.74, p = 0.001) or UC (RR 1.42, 95% CI 1.17–1.71, p = 0.0003) in patients with MS (p for subgroup differences: 0.97). Patients with IBD had a higher prevalence of MS than controls (RR = 1.91, 95% CI 1.06–3.45, p = 0.03).Conclusions: Clinicians should be aware of the increased risk of IBD or MS comorbidity during the diagnostic process. Systematic diagnosis and management at an earlier stage are suggested.

Patients with inflammatory bowel disease (IBD) have a high risk for colorectal cancer (CRC). This cancer type, which is strongly associated with chronic inflammation, is called colitis-associated CRC (CAC). Understanding the molecular pathogenesis of CAC is crucial to identify biomarkers necessary for early diagnosis and more effective treatment directions. The accumulation of immune cells and inflammatory factors, which constitute a complex chronic inflammatory environment in the intestinal mucosa, may cause oxidative stress or DNA damage to the epithelial cells, leading to CAC development and progression. An important feature of CAC is genetic instability, which includes chromosome instability, microsatellite instability, hypermethylation, and changes in noncoding RNAs. Furthermore, the intestinal microbiota and metabolites have a great impact on IBD and CAC. By clarifying immune, genetic, intestinal microecology, and other related pathogenesis, CAC may be more predictable and treatable.

Data from single-center experience or small sample-sized studies have shown that chromoendoscopy (CE) might be superior to white-light endoscopy (WLE) for dysplasia surveillance in ulcerative colitis (UC) patients. We performed a prospective randomized trial with a long-term follow-up to compare the detection rate of dysplasia among WLE with targeted biopsies (WLT), WLE with random biopsies (WLR), and dye-based CE with targeted biopsies (CET) in UC patients. Patients with long-standing UC were enrolled from 11 medical centers from March 2012 to December 2013 and randomized into three arms (WLT, WLR, and CET). Only high-definition endoscopy was used in all three groups. The patients were followed up by annual endoscopy with biopsies through December 2017. With a median follow-up time of 55 months, a total of 122 patients with 447 colonoscopies were finally analysed in the per-protocol set: WLT (n = 43), WLR (n = 40), and CET (n = 39). A total of 34 dysplastic lesions were found in 29 colonoscopies of 21 patients. WLR and CET could identify more colonoscopies that diagnosed dysplasia than WLT (8.1% and 9.7% vs 1.9%; P = 0.014 and 0.004, respectively). WLR obtained more biopsied samples than WLT and CET (16.4 ± 5.1 vs 4.3 ± 1.4 and 4.3 ± 1.4; both P < 0.001). During the second half of the follow-up (37 − 69 months), CET could identify more colonoscopies that diagnosed dysplasia than WLT (13.3% vs 1.6%, P = 0.015) and showed a trend for increasing the detection rate compared with WLR (13.3% vs 4.9%, P = 0.107). For a better outcome of cancer/dysplasia surveillance in patients with long-standing UC, CET appeared to be more effective than WLT and less tedious than WLR. CET was found to be particularly useful when a long-term (>3 years) follow-up was conducted for dysplasia surveillance. The trial was registered on www.chictr.org.cn (ChiCTR1900023689).

Background and Aims: Whether the natural course of ulcerative colitis (UC) in mainland China is similar or different from that in Western countries is unknown, and data on it is limited. We aimed to provide a comprehensive description of the natural course of UC in China and compare it with Western UC patients.Methods: Based on a prospective Chinese nationwide registry of consecutive patients with inflammatory bowel diseases, the medical treatments and natural history of UC were described in detail, including disease extension, surgery, and neoplasia. The Cox regression model was used to identify factors associated with poor outcomes.Results: A total of 1081 UC patients were included with a median follow‐up duration of 5.3 years. The overall cumulative exposure was 99.1% to 5‐aminosalicylic acids, 52.1% to corticosteroids, 25.6% to immunomodulators, and 15.4% to biologics. Disease extent at diagnosis was proctitis in 26.9%, left‐sided colitis in 34.8%, and extensive colitis in 38.3%. Of 667 patients with proctitis and left‐sided colitis, 380 (57.0%) experienced disease extent progression. A total of 58 (5.4%) UC patients underwent colectomy, demonstrating cumulative proportions of surgery at 1, 5, and 10 years after diagnosis of 0.6%, 3.4%, and 8.2%, respectively. In addition, 23 (2.1%) UC patients were diagnosed with neoplasia, demonstrating cumulative proportions of neoplasia at 1, 5, and 10 years after diagnosis of 0.5%, 1.0%, and 3.5%, respectively.Conclusions: Chinese UC patients had similar cumulative proportions of exposure to IBD‐specific treatments but a lower surgical rate than patients in Western countries, indicating a different natural course, and close monitoring needs for UC in China. However, these results must be confirmed in population‐based studies because the hospital‐based cohort in our study might lead to selection bias.