Summary Background A limited number of small‐sized studies suggest that bile acid diarrhoea is frequent in patients with chronic watery diarrhoea and previous cholecystectomy. Aim To perform a systematic review and meta‐analysis to assess the prevalence of bile acid diarrhoea in patients with chronic watery diarrhoea and previous cholecystectomy, and their response to colestyramine, including a new consecutive series of patients. Methods MEDLINE and EMBASE were searched up to January 2018. Selected studies included patients with previous cholecystectomy and chronic watery diarrhoea assessed by the 23‐seleno‐25‐homotaurocholic acid (SeHCAT) test. We calculated the pooled rate of bile acid diarrhoea using the inverse double arcsine square root method. Additionally, the medical records of 291 consecutive patients with chronic watery diarrhoea in whom a SeHCAT test was performed were retrospectively reviewed and 74 with previous cholecystectomy were included in the meta‐analysis. Results The search strategy identified eight relevant studies, which, together with the data of the present series, comprise 361 individuals. The pooled bile acid diarrhoea rate was 70% (95% CI 56%‐82%), and was similar when using cut‐offs of 10% or 15%. There was substantial heterogeneity (I2 = 84%). Five studies comprising 166 patients evaluated the effect of colestyramine in patients with bile acid diarrhoea. The pooled colestyramine response rate was 79% (95% CI 63%‐91%) with substantial heterogeneity (I2 = 73%). Conclusions Two‐thirds of patients with chronic watery diarrhoea and previous cholecystectomy have bile acid diarrhoea. Response to colestyramine in these patients is good.

Background The histology of the duodenum of Crohn’s disease (CD) has been scarcely explored. Lymphocytic enteritis (LE) and duodenal atrophy were described in CD but the prevalence is unknown and in some cases it raises the differential diagnosis with celiac disease. It is unknown if there is a cytometric-specific pattern of lymphocyte subpopulations of CD as it occurs in celiac disease (increased TCRγδ+ and decreased CD3− lymphocytes) (Fernández-Bañares F. PLoS One 2014). Objectives: Duodenal evaluation of CD: (1) histopathology, (2) lymphocyte subpopulations and (3) association of histopathological abnormalities with clinical parameters. Methods A total of 134 patients (82 CD, 52 celiac) and 13 controls were prospectively included. Endoscopic, histopathological and clinical parameters were recorded: calprotectin, Harvey–Bradshaw activity index, Montreal classification, treatment regimen, celiac disease work-up, H. pylori and stool parasites. Lymphocyte subpopulations [CD4+, CD8+, DP(CD4+CD8+), DN(CD4-CD8−), TCRγδ and CD3−] were evaluated by flow cytometry. Kruskal–Wallis and U of Mann–Whitney were used as statistical method. Results Twenty-five CD patients (30.5%) showed macroscopic involvement of the upper digestive tract (L4). The histopathological study was normal in 46 (56.1%) and showed abnormalities in 36 [7.3% chronic inflammatory infiltrate (of these one granulomas and three LE); 36% isolated LE]. In 20 cases, LE was considered to be due to CD (62.5%), while in 12 (37.5%) it was due to H. pylori (n = 8), NSAIDs (n = 2) and parasites (n = 2). The gastric and oesophageal mucosa showed abnormalities in 64.2% (chronic gastritis) and 15.4%, respectively. No relationship was found between histopathological abnormalities, activity, treatment and the outcome of CD. CD4+ and CD8+ subpopulations did not differ from controls and CD at diagnosis, but they have an increased ‘helper’ response (CD4+) and a reduced suppressor response (CD8+) in previously diagnosed CD (p < 0.0001). There were no differences in DP(CD4+CD8+), whereas DN(CD4−CD8−) were increased in both early and late CD (p = 0.008 vs. controls). Celiac disease presented much more marked changes than CD with decreased ‘helper’ CD4+, suppressors CD8+ and DP(CD4+CD8+) (p < 0.0001 vs. controls and CD), whereas DN(CD4−CD8−) were much more increased than in CD (p < 0.0001). The characteristic celiac cytometric pattern was not detected in CD. Conclusion LE (not atrophy) is a frequent finding in the duodenum of CD. Despite being indistinguishable from celiac LE, the immune response is completely different and could be used for diagnostic purposes. The increase in ‘atypical’ DN lymphocytes from the early CD suggests that it is an intrinsic immune alteration that deserves further characterisation by using multiparametric cytometry.

Background CD161 is a type C lectin expressed in NKs cells and peripheral T cells (TCRγδ and αβ, NKTs), enriched in intestinal populations. Its expression can be modulated by infections and inflammation. MAIT cells are a subset of innate antimicrobial T-cells abundant in the mucosa but their role in immunological regulation is still unknown. Aim To measure CD161 levels in subtypes of T-lymphocytes of intestinal mucosa: CD4+, CD8+, double positive (DP,CD4+CD8+), double negative (DN,CD4−CD8−), MAIT cells (CD161+TCRVα7.2+) and intraepithelial cells (CD103+) Methods Twenty-six patients with active inflammatory bowel disease (IBD) without immunosuppressive treatment (n = 9 Crohn’s disease -CD- colon, 9 CD ileum, n = 8 ulcerative colitis -UC- and 10 healthy controls (paired biopsies of ileum, right and left colon) were included. Lymphocyte subpopulations were analysed with LSRFortessa cytometer. Non-parametric Kruskal–Wallis test was applied. Results are expressed as % of median (25–75%IQI). Results In healthy mucosa, we did not find differences related to location in any of CD161 subpopulations except for increase of CD3+CD161+CD103+ and decrease of CD3+CD161+CD103− in left colon compared with right colon and ileum. Regarding MAIT cells, a progressive decrease was observed in distal parts of intestine for CD3+MAIT+CD103+ while CD3+MAIT+CD103− subpopulation has a specular behaviour; CD3+CD8+MAIT+ was increased in ileum compared with colon (Table 1). Conclusion There is a regional specialisation for the subset CD103+ of both CD161+CD103+ and MAIT_CD103+ cells in healthy intestine. CD3+CD161+ T cells are reduced in IBD colonic inflammation and could serve as a marker of active IBD but not to sort between CD and UC.