Tu1818 - Vitamin a Modulates Mucosal Inflammation by Augmenting Th1/Th17 Differentiation in Inflammatory Bowel Disease

2018 ◽  
Vol 154 (6) ◽  
pp. S-1028
Author(s):  
Ritika Rampal ◽  
Mohamad Nahidul Wari ◽  
Amit K. Singh ◽  
Ujjwal K. Das ◽  
Sawan Bopanna ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Vitamin A ◽  
Bowel Disease ◽  
Mucosal Inflammation ◽  
Inflammatory Bowel ◽  
Th17 Differentiation

scholarly journals P027 Vitamin A modulates mucosal inflammation by augmenting Th1/Th17 differentiation in inflammatory bowel disease

2018 ◽  
Vol 12 (supplement_1) ◽  
pp. S107-S107
Author(s):  
R Rampal ◽  
M N Wari ◽  
A K Singh ◽  
U K Das ◽  
S Bopanna ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Vitamin A ◽  
Bowel Disease ◽  
Mucosal Inflammation ◽  
Inflammatory Bowel ◽  
Th17 Differentiation

scholarly journals Factors affecting clinical decision-making in inflammatory bowel disease and the role of point-of-care calprotectin

2018 ◽  
Vol 11 ◽  
pp. 1756283X1774473 ◽  
Author(s):  
Yannick Derwa ◽  
Christopher J.M. Williams ◽  
Ruchit Sood ◽  
Saqib Mumtaz ◽  
M. Hassan Bholah ◽  
...  
Keyword(s):  
Decision Making ◽  
Inflammatory Bowel Disease ◽  
Disease Activity ◽  
Medical Therapy ◽  
Bowel Disease ◽  
Clinical Decision Making ◽  
Point Of Care ◽  
Clinical Decision ◽  
Mucosal Inflammation ◽  
Inflammatory Bowel

Objectives: Patient-reported symptoms correlate poorly with mucosal inflammation. Clinical decision-making may, therefore, not be based on objective evidence of disease activity. We conducted a study to determine factors associated with clinical decision-making in a secondary care inflammatory bowel disease (IBD) population, using a cross-sectional design. Methods: Decisions to request investigations or escalate medical therapy were recorded from outpatient clinic encounters in a cohort of 276 patients with ulcerative colitis (UC) or Crohn’s disease (CD). Disease activity was assessed using clinical indices, self-reported flare and faecal calprotectin ≥ 250 µg/g. Demographic, disease-related and psychological factors were assessed using validated questionnaires. Logistic regression was performed to determine the association between clinical decision-making and symptoms, mucosal inflammation and psychological comorbidity. Results: Self-reported flare was associated with requesting investigations in CD [odds ratio (OR) 5.57; 95% confidence interval (CI) 1.84–17.0] and UC (OR 10.8; 95% CI 1.8–64.3), but mucosal inflammation was not (OR 1.62; 95% CI 0.49–5.39; and OR 0.21; 95% CI 0.21–1.05, respectively). Self-reported flare (OR 7.96; 95% CI 1.84–34.4), but not mucosal inflammation (OR 1.67; 95% CI 0.46–6.13) in CD, and clinical disease activity (OR 10.36; 95% CI 2.47–43.5) and mucosal inflammation (OR 4.26; 95% CI 1.28–14.2) in UC were associated with escalation of medical therapy. Almost 60% of patients referred for investigation had no evidence of mucosal inflammation. Conclusions: Apart from escalation of medical therapy in UC, clinical decision-making was not associated with mucosal inflammation in IBD. The use of point-of-care calprotectin testing may aid clinical decision-making, improve resource allocation and reduce costs in IBD.

Inflammatory bowel disease

2018 ◽  
Author(s):  
Satish Keshav ◽  
Alexandra Kent
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Age Of Onset ◽  
Anal Verge ◽  
Age At Onset ◽  
Mucosal Inflammation ◽  
Gi Tract ◽  
Disease Extent ◽  
Inflammatory Bowel ◽  
Different Characteristics

Inflammatory bowel disease (IBD) encompasses ulcerative colitis (UC) and Crohn’s disease (CD). Both conditions cause chronic relapsing inflammation in the gastrointestinal (GI) tract, but have different characteristics. UC causes diffuse mucosal inflammation limited to the colon, extending proximally from the anal verge, with the rectum involved in 95% of patients. UC is described in terms of the disease extent: proctitis (confined to the rectum), proctosigmoiditis (disease confined to the recto-sigmoid colon), distal disease (distal to the splenic flexure), and pan-colitis (the entire large intestine). The extent of disease can change, with proximal extension seen in approximately a third of patients with proctitis, although there is great variation between studies. CD causes inflammation that can affect the entire thickness of the wall of the intestine, and is not confined to the mucosa. CD can affect any part of the GI tract. The terminal ileum is affected in approximately 80% of cases, the colon in approximately 60% of cases, and the rectum and perianal region in approximately 40% of cases. CD is classified by location (ileal, colonic, ileocolonic, upper GI tract), by the presence of stricturing or penetrating disease, and by the age of onset (before or after the age of 40). Penetrating disease refers to the development of fistulae, which can lead to complications such as abscesses or perforations. An earlier age at onset is associated with more complicated disease. The diagnosis of UC or CD is established through a combination of clinical, endoscopic, radiological, and histological criteria rather than by any single modality. Occasionally, it is not possible to establish an unequivocal diagnosis of CD or UC in IBD, and a third category, accounting for nearly 10% of cases, is used, termed IBD unclassified.

scholarly journals Colorectal Cancer in Inflammatory Bowel Disease

2020 ◽  
Vol 33 (05) ◽  
pp. 305-317
Author(s):  
Martina Nebbia ◽  
Nuha A. Yassin ◽  
Antonino Spinelli
Keyword(s):  
Colorectal Cancer ◽  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Severe Disease ◽  
Critical Role ◽  
Mucosal Inflammation ◽  
Surgical Approaches ◽  
Increased Risk ◽  
Significant Difference ◽  
Inflammatory Bowel

AbstractPatients with inflammatory bowel disease (IBD) are at an increased risk for developing colorectal cancer (CRC). However, the incidence has declined over the past 30 years, which is probably attributed to raise awareness, successful CRC surveillance programs and improved control of mucosal inflammation through chemoprevention. The risk factors for IBD-related CRC include more severe disease (as reflected by the extent of disease and the duration of poorly controlled disease), family history of CRC, pseudo polyps, primary sclerosing cholangitis, and male sex. The molecular pathogenesis of inflammatory epithelium might play a critical role in the development of CRC. IBD-related CRC is characterized by fewer rectal tumors, more synchronous and poorly differentiated tumors compared with sporadic cancers. There is no significant difference in sex distribution, stage at presentation, or survival. Surveillance is vital for the detection and subsequently management of dysplasia. Most guidelines recommend initiation of surveillance colonoscopy at 8 to 10 years after IBD diagnosis, followed by subsequent surveillance of 1 to 2 yearly intervals. Traditionally, surveillance colonoscopies with random colonic biopsies were used. However, recent data suggest that high definition and chromoendoscopy are better methods of surveillance by improving sensitivity to previously “invisible” flat dysplastic lesions. Management of dysplasia, timing of surveillance, chemoprevention, and the surgical approaches are all areas that stimulate various discussions. The aim of this review is to provide an up-to-date focus on CRC in IBD, from laboratory to bedside.

scholarly journals Intestinal Permeability in Inflammatory Bowel Disease: Pathogenesis, Clinical Evaluation, and Therapy of Leaky Gut

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Andrea Michielan ◽  
Renata D’Incà
Keyword(s):  
Inflammatory Bowel Disease ◽  
Intestinal Permeability ◽  
Bowel Disease ◽  
Intestinal Inflammation ◽  
Mucosal Barrier ◽  
Mucosal Inflammation ◽  
Confocal Laser Endomicroscopy ◽  
Confocal Laser ◽  
Sugar Absorption ◽  
Inflammatory Bowel

The pathogenesis of inflammatory bowel disease (IBD) is multifactorial with data suggesting the role of a disturbed interaction between the gut and the intestinal microbiota. A defective mucosal barrier may result in increased intestinal permeability which promotes the exposition to luminal content and triggers an immunological response that promotes intestinal inflammation. IBD patients display several defects in the many specialized components of mucosal barrier, from the mucus layer composition to the adhesion molecules that regulate paracellular permeability. These alterations may represent a primary dysfunction in Crohn’s disease, but they may also perpetuate chronic mucosal inflammation in ulcerative colitis. In clinical practice, several studies have documented that changes in intestinal permeability can predict IBD course. Functional tests, such as the sugar absorption tests or the novel imaging technique using confocal laser endomicroscopy, allow anin vivoassessment of gut barrier integrity. Antitumor necrosis factor-α(TNF-α) therapy reduces mucosal inflammation and restores intestinal permeability in IBD patients. Butyrate, zinc, and some probiotics also ameliorate mucosal barrier dysfunction but their use is still limited and further studies are needed before considering permeability manipulation as a therapeutic target in IBD.

scholarly journals Microevolution infimHGene of Mucosa-Associated Escherichia coli Strains Isolated from Pediatric Patients with Inflammatory Bowel Disease

2012 ◽  
Vol 80 (4) ◽  
pp. 1408-1417 ◽  
Author(s):  
Valerio Iebba ◽  
Maria Pia Conte ◽  
Maria Stefania Lepanto ◽  
Giovanni Di Nardo ◽  
Floriana Santangelo ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Pediatric Patients ◽  
Environmental Changes ◽  
Mucosal Inflammation ◽  
Content Type ◽  
E Coli ◽  
Inflammatory Bowel ◽  
Tract Infections

ABSTRACTSeveral studies reported increased numbers of mucosa-associatedEscherichia colistrains in patients with inflammatory bowel disease (IBD), encompassing Crohn's disease (CD) and ulcerative colitis (UC). The majority ofE. colistrains possess type 1 fimbriae, whose tip fibrillum protein, FimH, naturally undergoes amino acid replacements, an important process in the adaptation of commensalE. colistrains to environmental changes, like those observed in IBD and urinary tract infections. In this study, we analyzed mutational patterns in thefimHgene of 52 mucosa-associatedE. colistrains isolated from IBD and non-IBD pediatric patients, in order to investigate microevolution of this genetic trait. FimH-positive strains were also phylogenetically typed and tested for their adhesive ability on Caco-2 cells. Specific FimH alleles for each grouping feature were found. Mutations G66S and V27A were related to CD, while mutations A242V, V163A, and T74I were attributed to UC. Otherwise, the G66S, N70S, and S78N mutations were specifically attributed to B2/D phylogroups. The N70S and A119V mutations were related to adhesiveE. colistrains. Phylogroup B2, adhesive, and IBDE. colistrains showed a higher site substitution rate (SSR) in thefimHgene, together with a higher number of mutations. The degree of naïve mucosal inflammation was related to specific FimH alleles. Moreover, we could suggest that the V27A mutation is pathoadaptive for the CD intestinal habitat, while we could also suggest that both the N70S and S78N mutations are related to the more virulentE. coliB2 phylogroup. In conclusion, we found some FimH variants that seem to be more involved than others in the evolution of IBD pathogenesis.

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