of PSC was 0.5-1.3 per 100,000 individuals in Western countries, 1,2 whereas no relative information is available in Asian countries. The prevalence of PSC was approximately 0.095-0.13 per 10,000 inhabitants in Asian countries, which is 10-fold lower than the prevalence in Western countries. 3 Although the exact etiology and pathogenesis of PSC are still unknown, several studies have shown an association of PSC with certain genetic, environmental, and immunologic factors. There is no curative treatment for PSC, and a considerable number of patients develop severe clinical sequelae, such as portal hypertension, liver cirrhosis, and end-stage liver disease, eventually requiring liver transplantation (LT). Moreover,

The intestinal mucosa in inflammatory bowel disease (IBD) contains increased frequencies of lymphocytes and a disproportionate increase in plasma cells secreting immunoglobulin (Ig)G relative to other isotypes compared to healthy controls. Despite consistent evidence of B lineage cells in the mucosa in IBD, little is known of B cell recruitment to the gut in IBD. Here we analyzed B cells in blood of patients with Crohn's disease (CD) and ulcerative colitis (UC) with a range of disease activities. We analyzed the frequencies of known B cell subsets in blood and observed a consistent reduction in the proportion of CD27−IgD− B cells expressing all Ig isotypes in the blood in IBD (independent of severity of disease and treatment) compared to healthy controls. Successful treatment of patients with biologic therapies did not change the profile of B cell subsets in blood. By mass cytometry we demonstrated that CD27−IgD− B cells were proportionately enriched in the gut-associated lymphoid tissue (GALT) in IBD. Since production of TNFα is a feature of IBD relevant to therapies, we sought to determine whether B cells in GALT or the CD27−IgD− subset in particular could contribute to pathology by secretion of TNFα or IL-10. We found that donor matched GALT and blood B cells are capable of producing TNFα as well as IL-10, but we saw no evidence that CD27−IgD− B cells from blood expressed more TNFα compared to other subsets. The reduced proportion of CD27−IgD− B cells in blood and the increased proportion in the gut implies that CD27−IgD− B cells are recruited from the blood to the gut in IBD. CD27−IgD− B cells have been implicated in immune responses to intestinal bacteria and recruitment to GALT, and may contribute to the intestinal inflammatory milieu in IBD.

SummaryBackgroundMucosal healing is an important treatment target in patients with ulcerative colitis.AimsTo explore the optimal colonoscopic strategy to determine the risk for clinical relapse in patients with ulcerative colitis.MethodsWe enrolled 325 consecutive patients with ulcerative colitis in clinical and biochemical remission from April 2018 to March 2019. Five colonic segments were endoscopically and histologically assessed systematically. For endoscopic evaluation, we used three different modes of the Ulcerative Colitis Endoscopic Index of Severity (UCEIS): “original,” “worst affected,” and “pancolonic.” The Geboes score was used for histological evaluation. We prospectively followed up the patients and defined clinical relapse as the primary endpoint.ResultsWithin 1 year after colonoscopy, 18.2% of patients experienced a clinical relapse. Receiver operating characteristic curve analysis showed areas under the curve of 0.755, 0.817, and 0.852 for the “original,” “worst affected,” and “pancolonic” groups, respectively; hence, pancolonic UCEIS obtained the highest predictive value. Using the pancolonic UCEIS cutoff value of 3, Kaplan–Meier curve analysis showed that patients with endoscopic activity had a significantly lower relapse‐free rate than those with endoscopic remission (P < 0.01). Multivariate analysis demonstrated endoscopic (pancolonic UCEIS >3) and histological (Geboes >3.0) activities as independent risks for relapse (HR: 3.96 and 3.48, respectively). Combining pancolonic UCEIS ≤3 and Geboes score ≤3.0 to provide 1‐year relapse avoidance was 92.0% sensitive and 97.0% specific.ConclusionEvaluating disease remission by complete colonoscopy is relevant, and the combination of pancolonic endoscopic and histological evaluations may appropriately evaluate mucosal healing.