A posteriori dietary patterns and risk of inflammatory bowel disease: a meta-analysis of observational studies.

Inflammatory bowel disease (IBD) is a chronic inflammatory disorder which affects the gastrointestinal tract. Many factors, such as genetics, stress, and dietary patterns have been related to the risk of this disease. Adherence to a prudent/healthy dietary pattern, due to its antioxidant and anti-inflammatory properties, help to reduce the risk of many chronic diseases such as IBD. The results from previous studies regarding the association between dietary patterns and risk of IBD, including Crohn's disease (CD) and ulcerative colitis (UC), are inconsistent. This meta-analysis was performed to evaluate the potential relations between dietary patterns and risk of CD and UC. PubMed and Scopus were searched up to October 2017 for eligible studies. Random-effects or fixed-effects models were used to pool the estimated risks for the highest versus the lowest category of extracted dietary patterns. A total of six studies, including four case-control and two cohort studies with 1099 cases and 263112 controls/participants were included in the meta-analysis. A decreased risk of CD was seen for the highest compared with the lowest categories of healthy dietary pattern (OR/RR = 0.39, 95%CI = 0.16-0.62), while no significant association with western dietary pattern was observed (OR/RR = 0.78, 95% CI: 0.51-1.04). Furthermore, no significant relationship was found between healthy (OR/RR = 0.61, 95%CI = 0.04-1.18, random effects) and western/unhealthy (OR/RR = 0.97, 95% CI: 0.67-1.26) dietary patterns and risk of UC. The results of the current meta-analysis showed that a healthy dietary pattern is associated with a lower risk of CD. Further studies are warranted to confirm these findings.

Preoperative computed tomography enterography-based radiomics signature: A potential predictor of postoperative anastomotic recurrence in patients with Crohn's disease.

BACKGROUND: More than half of patients with Crohn's disease (CD) require at least one surgery for symptom management; however, approximately half of the patients may experience postoperative anastomotic recurrence (PAR). OBJECTIVES: This study aims to develop and validate a preoperative computed tomography enterography (CTE)-based radiomics signature to predict early PAR in CD. DESIGN: A total of 186 patients with CD (training cohort, n = 134; test cohort, n = 52) who underwent preoperative CTE and surgery between January 2014 and June 2020 were included in this retrospective multi-centre study. METHODS: 106 radiomic features were initially extracted from intestinal lesions and peri-intestinal mesenteric fat, respectively; significant radiomic features were selected from them and then used to develop intestinal or mesenteric radiomics signatures, using the least absolute shrinkage and selection operator and a Cox regression model. A radiomics-based nomogram incorporating these signatures with clinical-radiological factors was created for comparison with a model based on clinical-radiological features alone. RESULTS: 68 of 134 patients in training cohort and 16 of 52 patients in test cohort suffered from PAR. The intestinal radiomic signature (hazard ratio [HR]: 2.17; 95% confidence interval [CI]: 1.32-3.58; P = 0.002) and mesenteric radiomic signature (HR: 2.19; 95% CI: 1.14-4.19; P = 0.018) were independent risk factors for PAR in the training cohort as per a multivariate analysis. The radiomics-based nomogram (C-index: 0.710; 95% CI: 0.672-0.748) yielded superior predictive performance than the clinical-radiological model (C-index, 0.607; 95% CI: 0.582-0.632) in the test cohort. Decision curve analysis demonstrated that the radiomics-based nomogram outperformed the clinical-radiological model in terms of clinical usefulness. CONCLUSIONS: Preoperative mesenteric and intestinal CTE radiomics signatures are potential non-invasive predictors of PAR in postoperative patients with CD.

Education case: a case-based approach to overlap syndromes in autoimmune liver disease in patient with ulcerative colitis.

Simultaneous occurrence of immune-based gastrointestinal diseases and autoimmune hepatitis, although not common, is of clinical importance. Some clinical and laboratory findings such as severe pruritus and elevated alkaline phosphatase raise suspicion of a biliary disease which overlaps autoimmune hepatitis. A strong clinical suspicion of overlap syndrome in a patient with autoimmune hepatitis prompts more diagnostic evaluations like MRCP, liver biopsy, and secondary laboratory tests. Patients who fall into the category of overlap syndrome proceed with timely monitoring of known complications including colorectal carcinomas, cholangiocarcinomas, and gallbladder cancers. It is strongly recommended that all simultaneous immune-based involvements be searched prior to labeling a patient as having pure autoimmune hepatitis. The current study attempted to express all challenges about a case with overlap syndrome referred to the gastroenterology ward of Taleghani Hospital and to review the latest articles and related guidelines about the diagnosis, treatment, complications, and surveillance of the mentioned patient with autoimmune hepatitis (AIH), primary sclerosing cholangitis (PSC), and inflammatory bowel disease (IBD).

Effect of α-Hemolysin Producing E. coli in Two Different Mouse Strains in a DSS Model of Inflammatory Bowel Disease.

BACKGROUND: Phylogroup B2 Escherichia coli have been associated with ulcerative colitis (UC). In this study, we aimed to compare colonization with the UC-associated E. coli p19A in different mice strains, to investigate the role of alpha hemolysin in a UC mouse model. METHODS: In this study, Sigirr -/- and C57BL/6 mice were chosen, and UC was induced by adding dextran sulfate sodium (DSS) to the drinking water. The mice were pre-treated with ciprofloxacin. p19A expressing luminescence and GFP, alpha-hemolysin knock out p19A-ΔhlyI II, and non-pathogenic lab E. coli DH10B were cultured in LB broth, and orally gavaged into the mice. Colonization with p19A WT was visualized using an in vivo imaging system. RESULTS: p19A WT colonized the colon, ileum, Peyer's patches, liver, and spleen of infected C57BL/6 and Sigirr -/- mice. A total of 99% of the p19A WT infected C57BL/6 mice and 29% of the p19A WT infected Sigirr -/- mice survived to the 4th post infection day. CONCLUSION: UC-associated E. coli p19A WT colonized the intestines of DSS-treated mice and caused extra-intestinal infection. Hemolysin is an important factor in this pathogenesis, since isogenic hemolysin mutants did not cause the same inflammation.

Deficiency in Duox2 activity alleviates ileitis in GPx1- and GPx2-knockout mice without affecting apoptosis incidence in the crypt epithelium.

Mice deficient in glutathione peroxidase (GPx)-1 and -2 (GPx1-/-GPx2-/- double knockout or DKO mice) develop very-early-onset (VEO) ileocolitis, suggesting that lack of defense against reactive oxygen species (ROS) renders susceptibility to intestinal inflammation. Two members of ROS-generating NADPH oxidase family, NOX1 and DUOX2, are highly inducible in the intestinal epithelium. Previously, we reported that Nox1 deficiency ameliorated the pathology in DKO mice (Nox1-TKO). The role of Duox2 in ileocolitis of the DKO mice is evaluated here in Duoxa-TKO mice by breeding DKO mice with Duoxa-/- mice (Duoxa-TKO), which do not have Duox2 activity. Similar to Nox1-TKO mice, Duoxa-TKO mice no longer have growth retardation, shortened intestine, exfoliation of crypt epithelium, crypt abscesses and depletion of goblet cells manifested in DKO mice by 35 days of age. Unlike Nox1-TKO mice, Duoxa-TKO mice still have rampant crypt apoptosis, elevated proliferation, partial loss of Paneth cells and diminished crypt density. Treating DKO mice with NOX inhibitors (di-2-thienyliodonium/DTI and thioridazine/THZ) and an antioxidant (mitoquinone/MitoQ) significantly reduced gut pathology. Furthermore, in the inflamed human colon, DUOX protein expression is highly elevated in the apical, lateral and perinuclear membrane along the whole length of gland. Taken together, we conclude that exfoliation of crypt epithelium, but not crypt apoptosis, is a major contributor to inflammation. Both Nox1 and Duox2 induce exfoliation of crypt epithelium, but only Nox1 induces apoptosis. NOX1 and DUOX2 may be potential therapeutic targets for treating ileocolitis in human patients suffering inflammatory bowel disease (IBD).