scholarly journals Relevance of Segmental Colitis with Diverticulosis (SCAD) to Other Forms of Inflammatory Bowel Disease

2009 ◽  
Vol 23 (6) ◽  
pp. 439-440 ◽  
Author(s):  
Hugh J Freeman
Keyword(s):  
Older Adults ◽  
Inflammatory Bowel Disease ◽  
Inflammatory Process ◽  
Colonic Mucosa ◽  
Clinical Course ◽  
Normal Colonic Mucosa ◽  
Endoscopic Evaluation ◽  
Inflammatory Bowel ◽  
Definition Of ◽  
Segmental Colitis

A well localized inflammatory process involving only the sigmoid colonic segment associated with diverticulosis (SCAD), has become increasingly recognized as a distinct clinical and pathological disorder, usually described in older adults, often with rectal bleeding. Although some resolve spontaneously, most patients appear to respond to treatment only with 5-aminosalicylate. Endoscopic evaluation reveals a nonspecific inflammatory process localized in the sigmoid colon that usually completely resolves with histologically normal colonic mucosa. Recurrent symptoms with evidence of recurrent segmental colitis may occur, but most have an entirely benign clinical course. Further definition of the underlying molecular signalling that occurs in this apparently distinctive disorder may be critically important to understand the elements of a colonic inflammatory process that can completely and spontaneously resolve.

scholarly journals Expression of interleukin 1β and interleukin 1β converting enzyme by intestinal macrophages in health and inflammatory bowel disease

Gut ◽  
1998 ◽  
Vol 42 (2) ◽  
pp. 214-219 ◽  
Author(s):  
M E McAlindon ◽  
C J Hawkey ◽  
Y R Mahida
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Colonic Mucosa ◽  
Peripheral Blood Monocyte ◽  
Interleukin 1Β ◽  
Enzyme Linked Immunosorbent Assay ◽  
Normal Colonic Mucosa ◽  
Converting Enzyme ◽  
Inflammatory Bowel ◽  
Targeted Inhibition

Background—In the lipopolysaccharide (LPS) stimulated peripheral blood monocyte, the precursor form of interleukin 1β (IL-1β, 31 kD) is processed by IL-1β converting enzyme (ICE) to the mature, bioactive form (17 kD). IL-1β is a proinflammatory cytokine which is likely to have a role in the pathogenesis of inflammatory bowel disease (IBD).Aims—To investigate the expression and processing of IL-1β and ICE by tissue macrophages from normal and IBD colonic mucosa.Methods—Mucosal biopsy specimens and lamina propria cells from normal and IBD colons were studied by reverse transcription polymerase chain reaction (RT-PCR), western blot analysis, and ELISA (enzyme linked immunosorbent assay).Results—Normal colonic macrophages synthesised only the precursor form of IL-1β whereas in IBD the mature form was also produced. Similarly, cells from normal colonic mucosa synthesised ICE as the precursor (p45) only, whereas macrophages from IBD colons produced active (p20) ICE. Ac-Tyr-Val-Ala-Asp-CHO, a specific peptide aldehyde inhibitor of ICE, significantly reduced the amount of mature IL-1β released by isolated IBD macrophages (from a median of 1.2 (range 0.78–4.42) ng/ml to 0.43 (0.21–1.6) ng/ml; p<0.01).Conclusions—Exposure of normal colonic macrophages to LPS only induces the production of the precursor form of IL-1β, because the cells fail to activate ICE. In contrast, IBD colonic macrophages are able to activate ICE and hence release mature IL-1β in a manner similar to circulating monocytes. This is consistent with IBD macrophages being recently recruited from the circulating monocyte population. Targeted inhibition of ICE may represent a novel form of therapy in IBD.

Inflammation and Cancer IV. Colorectal cancer in inflammatory bowel disease: the role of inflammation

2004 ◽  
Vol 287 (1) ◽  
pp. G7-G17 ◽  
Author(s):  
Steven H. Itzkowitz ◽  
Xianyang Yio
Keyword(s):  
Colorectal Cancer ◽  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Colonic Mucosa ◽  
Normal Colonic Mucosa ◽  
Sporadic Colorectal Cancer ◽  
Increased Risk ◽  
Inflammatory Bowel ◽  
Repair Genes

Patients with ulcerative colitis and Crohn's disease are at increased risk for developing colorectal cancer. To date, no known genetic basis has been identified to explain colorectal cancer predisposition in these inflammatory bowel diseases. Instead, it is assumed that chronic inflammation is what causes cancer. This is supported by the fact that colon cancer risk increases with longer duration of colitis, greater anatomic extent of colitis, the concomitant presence of other inflammatory manifestations such as primary sclerosing cholangitis, and the fact that certain drugs used to treat inflammation, such as 5-aminosalicylates and steroids, may prevent the development of colorectal cancer. The major carcinogenic pathways that lead to sporadic colorectal cancer, namely chromosomal instability, microsatellite instability, and hypermethylation, also occur in colitis-associated colorectal cancers. Unlike normal colonic mucosa, however, inflamed colonic mucosa demonstrates abnormalities in these molecular pathways even before any histological evidence of dysplasia or cancer. Whereas the reasons for this are unknown, oxidative stress likely plays a role. Reactive oxygen and nitrogen species produced by inflammatory cells can interact with key genes involved in carcinogenic pathways such as p53, DNA mismatch repair genes, and even DNA base excision-repair genes. Other factors such as NF-κB and cyclooxygenases may also contribute. Administering agents that cause colitis in healthy rodents or genetically engineered cancer-prone mice accelerates the development of colorectal cancer. Mice genetically prone to inflammatory bowel disease also develop colorectal cancer especially in the presence of bacterial colonization. These observations offer compelling support for the role of inflammation in colon carcinogenesis.

scholarly journals Macrophage heterogeneity in normal colonic mucosa and in inflammatory bowel disease.

Gut ◽  
1988 ◽  
Vol 29 (11) ◽  
pp. 1531-1538 ◽  
Author(s):  
M C Allison ◽  
S Cornwall ◽  
L W Poulter ◽  
A P Dhillon ◽  
R E Pounder
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Colonic Mucosa ◽  
Normal Colonic Mucosa ◽  
Inflammatory Bowel

scholarly journals Mo1343 Inflammatory Bowel Disease Unclassified in Real Practice: Prevalence, Clinical Course and Therapy Requirements

2013 ◽  
Vol 144 (5) ◽  
pp. S-642
Author(s):  
Fernando Bermejo ◽  
Alicia Algaba ◽  
José Luis Cuño ◽  
Belén Botella ◽  
Carlos Taxonera ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Clinical Course ◽  
Inflammatory Bowel ◽  
Real Practice

scholarly journals Influence of a Positive Family History on the Clinical Course of Inflammatory Bowel Disease

2016 ◽  
Vol 10 (9) ◽  
pp. 1024-1032 ◽  
Author(s):  
Sung Wook Hwang ◽  
Min Seob Kwak ◽  
Wan Soo Kim ◽  
Jeong-Mi Lee ◽  
Sang Hyoung Park ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Family History ◽  
Bowel Disease ◽  
Clinical Course ◽  
Positive Family History ◽  
Inflammatory Bowel

Altered Leukotriene B4Metabolism in Colonic Mucosa with Inflammatory Bowel Disease

1995 ◽  
Vol 30 (1) ◽  
pp. 44-49 ◽  
Author(s):  
A. Ikehata ◽  
N. Hiwatashi ◽  
Y. Kinouchi ◽  
H. Yamazaki ◽  
K. Ito ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Colonic Mucosa ◽  
Inflammatory Bowel

Chronic Nonspecific Inflammatory Bowel Disease of the Cecum and Proximal Colon in Children With Grossly Normal-Appearing Colonic Mucosa: Diagnosis by Colonoscopic Biopsies

PEDIATRICS ◽  
1987 ◽  
Vol 80 (2) ◽  
pp. 255-261
Author(s):  
Melvin B. Heyman ◽  
Jay A. Perman ◽  
Linda D. Ferrell ◽  
M. Michael Thaler
Keyword(s):  
Inflammatory Bowel Disease ◽  
Abdominal Pain ◽  
Bowel Disease ◽  
Colonic Mucosa ◽  
Disease Process ◽  
Proximal Colon ◽  
Chronic Abdominal Pain ◽  
Medical Attention ◽  
Inflammatory Bowel ◽  
Inflammatory Changes

The diagnosis of inflammatory bowel disease rests on radiologic, endoscopic, and histologic creteria. Five patients, 2 to 17 years of age, sought medical attention because of chronic abdominal pain, diarrhea, and heme-positive stools. Rectal biopsies, visual inspection of colonic mucosa through the colonoscope, and contrast radiographs of the large and small intestine yielded nonspecific results. Serial endoscopic biopsies demonstrated a gradient of inflammatory changes diminishing in severity distally from the ileocecal valve and cecum. The disease process was most evident in specimens from the cecum, whereas biopsies distal to the transverse colon had a normal histologic appearance in all five patients. Biopsies from the proximal colon may provide evidence of inflammatory bowel disease not detectable using standard techniques. The combination of chronic abdominal pain, diarrhea, and heme-positive stools associated with inflammatory changes in biopsy specimens obtained from the proximal colon, but normal findings on radiologic, colonoscopic, and rectal biopsy examinations, may represent an early stage in the evolution of chronic nonspecific inflammatory bowel disease, including ulcerative colitis or regional enteritis (Crohn disease).

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