P222 Purely fibrostenotic Crohn’s disease without chronic inflammation is uncommon – a histopathologic study of resected intestine

Rationale: Crohn's disease is characterized by continuous severe course, and in a half of the patients is associated with formation of strictures that are difcult to treat and signifcantly decrease quality of life. Difculties during the diﬀerentiation between inﬂammation-related and fbrostenotic strictures and divergent approaches to their treatment in patients with Crohn's disease indicate the need in precise diagnostics and systematization of the radiological semiotics of strictures.Aim: To propose radiological semiotics of the small and large intestine strictures based on the results of multiaxial computed tomography (MACT) and magnetic resonance imaging (MRI).Materials and methods: MACT and MRI visualization was performed in 40 patients with a stenotic type of Crohn's disease.Results: The radiological signs of the strictures were classifed into two main groups: intestinal and extra-intestinal. They were systematized according to nine criteria, such as character of formation, etiology, number, inﬂammation grade, extension, shape, and location, presence of ileus and presence of other complications. The inﬂammation activity in the intestinal wall was evaluated during the postcontrast assessment: active inﬂammation in the arterial phase (at 25 seconds after administration of the contrast agent), chronic inﬂammation in the delayed phase (at 10 minutes). The MRI results were cross-checked with those of MACT. At the precontrast stage, MRI was more informative as per the width of the intestinal lumen, whereas MACT was preferential in the diagnosis of fat infltration of the intestinal wall. Post-contrast MACT and MRI were diagnostically equivalent. The most indicative for active inﬂammation were diﬀuse weighed MRI images, arterial phase MACT and MRI, whereas chronic inﬂammation and wall fbrosis were better diagnosed at the delayed phase (at 10 minutes) of MACT and MRI. Both methods (MACT and MRI) could not diﬀerentiate between the submucous and muscular layers of the intestinal wall. Mixed type of inﬂammation was seen in the walls of intestinal strictures: chronic inﬂammation dominated in the intermediate, most extensive part of a stricture and remained stable during the dynamic follow-up, whereas active inﬂammation was found in the marginal parts of the strictures, which were most susceptible to changes during the follow-up.Conclusion: Based on a set of certain signs obtained by radiological visualization, we propose a registry for stricture assessment based on evaluation of the inﬂammation activity.

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Ileocolic anastomotic inflammation after resection for Crohn’s disease indicates disease recurrence: a histopathologic study

Scandinavian Journal of Gastroenterology ◽

10.1080/00365521.2020.1780305 ◽

2020 ◽

Vol 55 (7) ◽

pp. 795-799

Author(s):

Robert P. Hirten ◽

Simran Mashiana ◽

Benjamin L. Cohen ◽

Bruce E. Sands ◽

Jean Frederic Colombel ◽

...

Keyword(s):

Crohn’S Disease ◽

Crohn's Disease ◽

Disease Recurrence ◽

Histopathologic Study

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Dietary factors in chronic inflammation: Food tolerances and intolerances of a New Zealand Caucasian Crohn's disease population

Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis ◽

10.1016/j.mrfmmm.2010.01.020 ◽

2010 ◽

Vol 690 (1-2) ◽

pp. 123-138 ◽

Cited By ~ 47

Author(s):

Christopher M. Triggs ◽

Karen Munday ◽

Rong Hu ◽

Alan G. Fraser ◽

Richard B. Gearry ◽

...

Keyword(s):

Crohn’S Disease ◽

New Zealand ◽

Crohn's Disease ◽

Chronic Inflammation ◽

Dietary Factors

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Role of MutS homolog 2 (MSH2) in intestinal myofibroblast proliferation during Crohn's disease stricture formation

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.90311.2008 ◽

2008 ◽

Vol 295 (3) ◽

pp. G581-G590 ◽

Cited By ~ 5

Author(s):

Martin Floer ◽

David G. Binion ◽

Victoria M. Nelson ◽

Sharon Manley ◽

Michael Wellner ◽

...

Keyword(s):

Crohn’S Disease ◽

Crohn's Disease ◽

Chronic Inflammation ◽

Tissue Remodeling ◽

Mesenchymal Cell ◽

Stricture Formation ◽

Muscularis Mucosa ◽

Cell Accumulation ◽

Tnf Α ◽

Intestinal Remodeling

Tissue remodeling and mesenchymal cell accumulation accompanies chronic inflammatory disorders involving joints, lung, vasculature, and bowel. Chronic inflammation may alter DNA-mismatch repair (MMR) systems in mesenchymal cells, but is not defined in Crohn's disease (CD) and its associated intestinal remodeling and stricture formation. We determined whether DNA-MMR alteration plays a role in the pathogenesis of CD tissue remodeling. Control and CD bowel tissues were used to generate primary cultures of muscularis mucosa myofibroblasts, which were assessed directly or following stimulation with TNF-α/LPS or H2O2. MutS homolog (MSH)2, MSH3, and MSH6 expression in tissues and myofibroblasts was determined. Immunohistochemical staining revealed an increased expression of MSH2 in CD muscularis mucosa and submucosal tissues compared with controls or uninvolved CD tissue, and MSH2 expression was increased in CD myofibroblasts compared with control cells. TNF-α/LPS and H2O2 further enhanced MSH2 expression in both control and CD cells, which were decreased by simvastatin. There were no significant changes in MSH3 and MSH6 expression. Proliferating cell nuclear antigen and Ki67 staining of CD tissue revealed increased proliferation in the muscularis mucosa and submucosa of chronically inflamed tissues, and enhanced proliferation was seen in CD myofibroblasts compared with controls. Simvastatin reversed the effects of inflammatory stress on the DNA-MMR and inhibited proliferation of control and CD myofibroblasts. Gene silencing with MSH2 siRNA selectively decreased CD myofibroblast proliferation. These data demonstrate a potential role for MSH2 in the pathogenesis of nonneoplastic mesenchymal cell accumulation and intestinal remodeling in CD chronic inflammation.

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Genetic factors in chronic inflammation: Single nucleotide polymorphisms in the STAT-JAK pathway, susceptibility to DNA damage and Crohn's disease in a New Zealand population

Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis ◽

10.1016/j.mrfmmm.2010.01.017 ◽

2010 ◽

Vol 690 (1-2) ◽

pp. 108-115 ◽

Cited By ~ 71

Author(s):

Lynnette R. Ferguson ◽

Dug Yeo Han ◽

Alan G. Fraser ◽

Claudia Huebner ◽

Wen Jiun Lam ◽

...

Keyword(s):

Dna Damage ◽

Crohn’S Disease ◽

New Zealand ◽

Crohn's Disease ◽

Single Nucleotide Polymorphisms ◽

Chronic Inflammation ◽

Genetic Factors ◽

Nucleotide Polymorphisms ◽

Single Nucleotide ◽

Zealand Population

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Mycobacteria in Crohn’s disease: how innate immune deficiency may result in chronic inflammation

Expert Review of Clinical Immunology ◽

10.1586/eci.10.29 ◽

2010 ◽

Vol 6 (4) ◽

pp. 633-641 ◽

Cited By ~ 20

Author(s):

Jean-Daniel Lalande ◽

Marcel A Behr

Keyword(s):

Immune Deficiency ◽

Crohn’S Disease ◽

Crohn's Disease ◽

Chronic Inflammation ◽

Innate Immune

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Differential prevalence of pathobionts and host gene polymorphisms in chronic inflammatory intestinal diseases: Crohn’s disease and intestinal tuberculosis

PLoS ONE ◽

10.1371/journal.pone.0256098 ◽

2021 ◽

Vol 16 (8) ◽

pp. e0256098

Author(s):

Imteyaz Ahmad Khan ◽

Baibaswata Nayak ◽

Manasvini Markandey ◽

Aditya Bajaj ◽

Mahak Verma ◽

...

Keyword(s):

Crohn’S Disease ◽

Crohn's Disease ◽

Chronic Inflammation ◽

Gene Polymorphisms ◽

Intestinal Tuberculosis ◽

Host Gene ◽

Disease Models ◽

Study Cohort ◽

Intestinal Diseases ◽

Significant Difference

Background and objectives Crohn’s disease (CD) and Intestinal tuberculosis (ITB) are chronic inflammatory ulcero-constrictive intestinal diseases with similar phenotype. Although both are disease models of chronic inflammation and their clinical presentations, imaging, histological and endoscopic findings are very similar, yet their etiologies are diverse. Hence, we aimed to look at differences in the prevalence of pathobionts like adherent-invasive Escherichia coli (AIEC), Listeria monocytogenes, Campylobacter jejuni and Yersinia enterocolitica in CD and ITB as well as their associations with host-associated genetic polymorphisms in genes majorly involved in pathways of microbial handling and immune responses. Methods The study cohort included 142 subjects (69 patients with CD, 32 with ITB and 41 controls). RT- PCR amplification was used to detect the presence of AIEC, L. monocytogenes, C. jejuni, and Y. enterocolitica DNA in colonic mucosal biopsies. Additionally, we tested three SNPs in IRGM (rs13361189, rs10065172, and rs4958847), one SNP in ATG16L1 (rs2241880) and one SNP in TNFRSF1A (rs4149570) by real-time PCR with SYBR green from peripheral blood samples in this cohort. Results In patients with CD, AIEC was most frequently present (16/ 69, 23.19%) followed by L. monocytogenes (14/69, 20.29%), C. jejuni (9/69, 13.04%), and Y. enterocolitica (7/69, 10.14%). Among them, L. monocytogenes and Y. enterocolitica were significantly associated with CD (p = 0.02). In addition, we identified all the three SNPs in IRGM (rs13361189, rs10065172, and rs4958847), one SNP in ATG16L1 (rs2241880) and TNFRSF1A (rs4149570) with a significant difference in frequency in patients with CD compared with ITB and controls (p<0.05). Conclusion Higher prevalence of host gene polymorphisms, as well as the presence of pathobionts, was seen in the colonic mucosa of patients with CD as compared to ITB, although both are disease models of chronic inflammation.

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