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Query: UMLS:C0021390 (inflammatory bowel disease)
 23,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Mast cell degranulation in the gut causes mucus secretion, mucosal edema, and increased gut permeability and may be responsible for some of the symptoms and signs of inflammatory bowel disease. We have used a novel monoclonal antibody (AAI) against tryptase expressed exclusively in the granules of mast cells to enumerate mast cells in rectal biopsies in order to study the effect of inflammatory bowel disease and drug treatment upon rectal mast cell numbers. Rectal mast cell numbers are significantly reduced in inflammatory bowel disease patients taking corticosteroids (mean 4.95 cells/mm2) when compared with control patients (10.1, P less than 0.001) and inflammatory bowel disease patients not taking corticosteroids (9.7, P less than 0.001 Wilcoxon rank sum test). The reduction in mast cell counts was independent of the degree of inflammation or architectural distortion. There was a negative correlation between the dose of corticosteroids and mast cell count (r = 0.53, P less than 0.05 Spearman rank correlation), and the mast cell count was reduced within a few days of treatment and remained low throughout steroid therapy. Mucosal mast cell depletion may be an important mechanism of action of corticosteroids in inflammatory bowel disease.
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PMID:Corticosteroid treatment reduces mast cell numbers in inflammatory bowel disease. 197 67

The spot-ELISA technique has been used to enumerate the frequency of cells secreting tumor necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma), isolated from biopsies of normal intestine and from biopsies of children with inflammatory bowel disease. TNF-alpha production was undetectable in six out of 12 biopsies from normal intestine and in the other six biopsies it ranged from 60 to 580 TNF-alpha-secreting cells/10(6) isolated intestinal cells. In contrast, cells isolated from biopsies of children with Crohn's disease (n = 9) all showed elevated frequencies of TNF-alpha-secreting cells (500-12,000 secreting cells/10(6) cells). In ulcerative colitis, four out of eight children had increased production of TNF-alpha and in children with indeterminate colitis two out of three had elevated levels. There was no correlation between plasma TNF-alpha levels and the number of intestinal cells secreting TNF-alpha. In controls and all groups of patients IFN-gamma-secreting cells were uncommon. These results suggest that TNF-alpha is an important mediator of inflammation in the human gut, and, furthermore, may play a role in the growth failure frequently seen in children with inflammatory bowel disease.
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PMID:Tumour necrosis factor-alpha and interferon-gamma production measured at the single cell level in normal and inflamed human intestine. 211 10

Immunologic abnormalities have been implicated in the etiology of inflammatory bowel disease (IBD). Defects of systemic immunity and of local (intestinal) immunity have been studied. The numbers of T and B lymphocytes and their characteristics seem to vary with the disease, but no cause-and-effect relationship has been established. The presence of anticolon antibodies in patients with ulcerative colitis suggests that these antibodies could be involved in IBD, but they have also been found in other conditions. In the peripheral blood, abnormalities of cell-mediated immunity are inconsistent and suggest that they are not fundamental defects of the disease. The hypothesis that the inflammatory process is a result of immune-mediated intestinal tissue damage is being extensively studied. The high familial incidence of the disease suggests a role of histocompatibility locus antigens, but no reproducible association can be established. In vivo and in vitro studies of mucosal mononuclear cells have revealed abnormalities of immunoglobulin production, some types of cytotoxicity against gut-derived antigens, and altered lymphokine production associated with the disease. Further studies of the intestinal immune system would seem to be the most fruitful line of research.
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PMID:Immune events associated with inflammatory bowel disease. 219 24

Ulcerative colitis and Crohn's disease both may occur in the elderly. In many populations, a second peak in the incidence of inflammatory bowel disease occurs near age 70. Clinical manifestations of inflammatory bowel disease in the elderly are generally similar to those seen in younger patients, although there is a tendency for both ulcerative colitis and Crohn's disease to involve more distal segments of the gut in older patients. Ischemic and infectious colitis, diverticulitis, and malignancy can all masquerade as inflammatory bowel disease in the elderly. Recent epidemiologic and clinical reports indicate that the outlook for older patients with inflammatory bowel disease is more favorable than previously suspected.
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PMID:Inflammatory bowel disease in the elderly. 219 50

We have attempted to confirm the claim by Dvorak and Silen that 'Crohn's disease is accompanied by a severe and extensive necrosis of gut axons...[which] may serve to differentiate Crohn's disease from other inflammatory conditions'. In this electron microscope study the diagnoses were withheld until the assessment of axonal damage was completed. We assessed the axonal damage in ileostomy biopsies in 13 cases of Crohn's disease, four cases of ulcerative colitis, and two 'controls'. In Crohn's disease we found a mean per cent of abnormal axons of 29.85, in ulcerative colitis of 21.25 per cent, and in the two 'controls' of 12.11 and 10.63 per cent, respectively. The difference between the 13 cases of Crohn's disease and the six cases of non-Crohn's disease is not significant. We found considerable numbers of abnormal, very small axons of uncertain nature but probably related to regeneration following surgery. Including or excluding such axons did not significantly alter the incidence of abnormal axons. We conclude that axonal damage is common in chronic inflammatory bowel disease and is not specifically related to Crohn's disease.
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PMID:Axonal damage in Crohn's disease is frequent, but non-specific. 221 71

The current treatment of inflammatory bowel disease (IBD), though improved over earlier therapies, remains variable rather than consistent and supportive rather than curative. The similar management of ulcerative colitis (UC) and Crohn's disease (CD), which are thought to be differing though related disorders, suggests that therapy is nonspecific. The variation in therapeutic practices results from the fact that the etiologies of the diseases are obscure, from limited knowledge of the biological and pharmacological actions of drugs commonly prescribed (sulfasalazine, 5-ASA compounds, steroids, 6-MP and azathioprine), from an inadequate understanding of genetic differences influencing drug metabolism, from insufficient awareness of the factors influencing drug efficiency (concurrent use of antimotility drugs, cigarette smoking, food combinations), from the variability of the patient groups studied (extent and severity of disease), and from incomplete documentation of the clinical status of patients at the time of therapeutic trial. Future advances in treatment will depend on gaining new information about the nature of IBD and of drug pharmacology and bioavailability, derived from collaborative studies by clinicians, clinical investigators, and basic scientists. Important areas for IBD research include the biology of intestinal epithelium, the nature of the IBD inflammatory reaction and of gut mucosal immune regulation (via the application of new biotechnologies) and more representative experimental animal models. Decisive multicenter therapeutic studies require agreement on definitions of ulcerative colitis and Crohn's disease, accurate characterization of patient groups, acceptable objective criteria of IBD severity and activity, and reliable indicators of therapeutic response.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Limitations in the evaluation of therapy in inflammatory bowel disease: suggestions for future research. 222 94

Ulceration anywhere in the gastrointestinal tract induces a novel cell lineage, which grows from the bases of existing crypts, ramifies to form a new gland, and ultimately emerges onto the mucosal surface. The lineage produces neutral mucin, shows a unique lectin-binding profile and immunophenotype, and secretes abundant immunoreactive epidermal growth factor/urogastrone (EGF/URO). All gastrointestinal stem cells can produce this cell lineage following mucosal ulceration, secreting EGF/URO to stimulate cell proliferation, regeneration and ulcer healing. This cell lineage is very commonly associated with gastrointestinal ulceration, and we propose that a major in vivo role for EGF/URO is to stimulate ulcer healing throughout the gut via induction of this cell lineage in the adjacent mucosa. EGF/URO should therefore be assessed in the conservative management of inflammatory bowel disease.
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PMID:Ulceration induces a novel epidermal growth factor-secreting cell lineage in human gastrointestinal mucosa. 226 47

In order to study local immunoregulatory mechanisms in patients with seronegative spondylarthropathy and histological evidence of asymptomatic intestinal inflammation, we determined mononuclear cells in distal ileal mucosa with an indirect immunoperoxidase technique using a panel of monoclonal antibodies. The number of intraepithelial lymphocytes in inflamed mucosa was not significantly increased. They carried mainly the suppressor-cytotoxic CD8 marker (greater than 80%), less frequently the helper T cell marker CD4 and lacked the pan T epitope CD3 in greater than 50%. There were no intraepithelial B cells or natural killer cells. The lamina propria lymphocytes were T and B cells, the former being more numerous. Helper T cells were more frequent than suppressor-cytotoxic T cells. There were no alterations in the proportion of T cells in inflamed mucosa. Natural killer cells were scarce. They occurred in small numbers in a minority of cases with gut inflammation and spondylarthropathy and rarely in inflammatory bowel disease. It is concluded that although there is an increase of lamina propria monocytes, there is no immunoregulatory imbalance in the ileal mucosa of patients with seronegative spondylarthropathy.
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PMID:Ileal mucosal mononuclear cells in patients with seronegative spondylarthropathy. 233 10

Major histocompatibility complex molecules act as non-specific receptors for antigenic proteins and present them to T-cells. Presented antigen together with class II molecules activates antigen specific T-helper cells and may trigger a cellular immune response. The expression of HLA-DR antigens by epithelial cells was examined with an indirect peroxidase technique in ileal biopsies from 38 patients with seronegative spondylarthropathy and features of acute or chronic gut inflammation on biopsy, 14 patients with chronic inflammatory bowel disease, 10 rheumatic and 10 non-rheumatic controls. In acute ileitis, there was more HLA-DR expression in villous and crypt epithelial cells than in non-inflamed controls (p less than 0.01). In chronic inflammation and in chronic inflammatory bowel disease, class II antigens were more expressed in villus (p less than 0.02) and crypt epithelium (p less than 0.01). Strong HLA-DR expression in crypt epithelial cells was connected with active inflammation (p less than 0.02). These findings suggest binding of unknown enterobacterial or nutritional luminal antigens to HLA-DR antigens normally present in enterocytes. The enterocytes act as antigen presenting cells causing a local increase of targets for activated T-cells and trigger the gut inflammation responsible for the clinical symptoms of the seronegative spondylarthropathy.
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PMID:Major histocompatibility complex class II antigen (HLA-DR) expression by ileal epithelial cells in patients with seronegative spondylarthropathy. 235 4

We have used 99Tcm-labelled nanocolloid in an attempt to locate areas of inflamed bowel wall or abscesses in five patients with ulcerative colitis and nine with Crohn's disease. The scintigraphic findings were evaluated by comparison with those of recent barium studies and, in three patients, with surgical findings at laparotomy. It proved difficult to localize segments of inflamed bowel accurately with 99Tcm-nanocolloid because of the accumulation of radioactivity in the gut lumen, especially 2 or more hours after injection. However, there was little uptake of the labelled nanocolloid by areas of inflamed gut wall in the period before 2 h. When 99Tcm-nanocolloid scans were compared with 111In-WBC scans in eight patients who had both investigations, 99Tcm-nanocolloid scintigraphy was considerably less sensitive than 111In-WBC scintigraphy. One abscess was located correctly; the other was obscured by nearby bladder and bone marrow radioactivity. We conclude that 99Tcm-nanocolloid scanning is neither sensitive nor reliable enough for assessing the location of inflamed bowel wall or the presence of abscess in patients with inflammatory bowel disease.
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PMID:99Tcm-nanocolloid imaging in inflammatory bowel disease. 235 67


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