Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0010346 (Crohn's disease)
 21,615 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have investigated the correlation of 24 h and 48 h faecal Indium-111 excretion with each other and with several clinical activity indices for Crohn's disease (CD): Crohn's disease activity index (CDAI), activity index (AI), simple index (SI), Oxford score, and laboratory parameters, such as ESR, serum albumin, orosomucoid, C-reactive protein, alpha-l-antitrypsin (alpha 1-AT) faecal concentration, and alpha 1-AT clearance in 58 CD patients (37 with small bowel and 21 with colonic disease). A significant correlation was found between 24 and 48 h faecal Indium-111 excretion for small bowel (r = 0.708, p less than 0.0001) and colonic disease (r = 0.994, p less than 0.0001). The median faecal Indium-111 excretion for colonic involvement (4%; 0.15-50% median and range) was significantly (p less than 0.005) higher than that for small bowel disease (0.45%; 0.03-2.9%). No significant correlation was found between faecal Indium-111 excretion and any activity index in the patients with small bowel disease, while in the group of patients with colonic localisation only the AI showed a significant correlation (r = 0.593, p less than 0.02). Faecal Indium-111 excretion was significantly correlated with alpha 1-AT clearance (r = 0.712, p less than 0.0001) and faecal alpha 1-AT concentration (r = 0.750, p less than 0.0001) in small bowel and in colonic localisation (r = 0.530, p less than 0.02 and r = 0.444, p less than 0.05). Serum albumin was significantly correlated only in the group of patients with colonic disease (r = -0.593, p less than 0.05). The present study shows poor agreement between activity indices, serum parameters of activity and faecal Indium-111 excretion. As a good correlation was found with the alpha1-clearance, which reflects losses into the gut, these results may suggest that faecal Indium excretion does not only reflect activity of inflammation, but my relate to the extent of intestinal ulceration.
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PMID:Are activity indices helpful in assessing active intestinal inflammation in Crohn's disease? 280 91

The pathogenesis of Crohn's disease may involve altered function of immunoregulatory T cells in the intestine. To investigate this hypothesis, lamina propria lymphocytes were isolated from intestinal specimens resected from patients with active Crohn's disease and control subjects (colon carcinoma and diverticular disease) using an enzymatic technique. The T-cell phenotypes and function of these lymphocytes were compared with that of peripheral blood lymphocytes. The proportion of Leu-2-positive (suppressor/cytotoxic) cells was similar in peripheral blood and isolated lamina propria lymphocytes, both in Crohn's disease and control patients. Although the proportion of Leu-3-positive (helper/inducer) lymphocytes was lower in lamina propria lymphocytes than peripheral blood lymphocytes, there was no difference comparing Crohn's disease and control patients. Helper T-cell function, as determined by measuring the ability of T cells to increase immunoglobulin synthesis by pokeweed mitogen-stimulated normal peripheral blood B cells, was similar in peripheral blood lymphocytes and lamina propria lymphocytes, and comparing Crohn's disease with control patients. Suppressor T-cell function, as determined by measuring the ability of T cells to inhibit immunoglobulin production by cultures containing pokeweed mitogen-stimulated normal peripheral blood T and B cells, was also similar comparing peripheral blood lymphocytes and lamina propria lymphocytes, and comparing Crohn's disease with control patients: neither peripheral blood lymphocytes nor lamina propria lymphocytes significantly suppressed immunoglobulin synthesis. OKT8 (suppressor/cytotoxic)-enriched lamina propria lymphocytes mediated only marginal suppression, whereas concanavalin A-activated intestinal T cells did mediate significant suppression, in both Crohn's disease and control patients. Thus, patients with active Crohn's disease have no alteration of immunoregulatory T-cell function for polyclonal mitogen-induced immunoglobulin synthesis at the gut mucosal level, despite the presence of an inflammatory process in the intestine.
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PMID:Immunoregulatory function of lamina propria T cells in Crohn's disease. 285 28

To study the effect of mucosal inflammation on tissue concentrations of somatostatin, the distribution and concentration of somatostatin in specimens of normal and abnormal (ulcerative colitis and Crohn's disease) ileum and colon were determined by a specific radioimmunoassay. Each tissue specimen obtained at surgery was separated by microdissection into the mucosa-submucosa and the muscularis externa. Immunoreactive somatostatin was acid-extracted from each layer before measurement. Gel chromatography was used to characterize immunoreactive somatostatin measured by radioimmunoassay; somatostatin-28 was the major immunoreactive species measured in human intestine. In normal colon, concentrations of somatostatin were not related to patient age. Concentrations of immunoreactive somatostatin in the mucosa-submucosa of the descending colon were significantly decreased in ulcerative colitis and in Crohn's colitis, compared with normal colon. There was no apparent relationship between concentrations of somatostatin and the duration of inflammatory bowel disease. However, somatostatin concentrations appeared to be lower in patients with severe colitis than in patients with minimal colitis. The decrease in mucosal-submucosal concentrations of somatostatin is in agreement with previous morphologic studies, which have suggested diminished populations of endocrine cells in ulcerative colitis. The possible role of somatostatin in the colon suggests that further studies of the alteration of this gut peptide may be useful in understanding a component of the pathophysiology of idiopathic inflammatory bowel disease.
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PMID:Somatostatin in the idiopathic inflammatory bowel diseases. 289 35

Crohn's disease (CD) is an idiopathic chronic inflammatory gut disease with frequent extragut inflammatory manifestations in the eyes, orbit, lungs, joints, and skin. A bacterial cause of CD is suspected, but cultivation of a specific pathogen has not been forthcoming. Mollicute-like organisms (MLOs) were recently reported to cause human chronic ocular inflammatory disease. Inoculation of this MLO into mouse eyelids produced chronic progressive granulomatous ocular and orbital inflammatory disease. In addition, MLOs disseminated to produce similar disease in the gut, heart, and lungs. MLOs are noncultivable cell wall-deficient bacterial pathogens. Because they also pass bacteria-retaining 0.450-micron filters, they can be overlooked or confused with viruses. Because MLOs have a characteristic ultrastructural appearance, they can be identified in diseased cells with the use of a transmission electron microscope. MLOs parasitize and destroy leukocytes. They alter the nucleus, replace the cytoplasm, and destroy organelles. MLO-caused disease is treatable by certain antibiotics. This report describes MLO-parasitized vitreous lymphocytes, monocytes, and polymorphonuclear leukocytes from three patients with CD who had chronic uveitis. The results indicate that MLOs probably caused the uveitis of these patients with CD. The gut as the possible source of the MLO is suggested. Rifampin therapy of Crohn's and MLO-caused disease is discussed.
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PMID:Crohn's disease uveitis. Parasitization of vitreous leukocytes by mollicute-like organisms. 292 94

Expression of the gp100 common acute lymphoblastic leukaemia antigen (CALLA) was studied in the mucosa of the gut by means of indirect immunofluorescence on cryostat tissue sections with a panel of eight monoclonal antibodies to common acute lymphoblastic leukaemia antigen (anti-CALLA antibodies) and two antibodies to non-CALLA leukaemic antigens. Expression of CALLA was absent from normal stomach epithelium, adult and fetal colonic epithelium of normal histology, and colonic epithelium from patients with Crohn's disease or ulcerative colitis. By contrast, all eight anti-CALLA antibodies gave a characteristic reaction in normal adult and fetal small bowel mucosa, with specific localisation to the entire brush border of jejunal epithelium. Whereas seven of these antibodies reacted both with normal jejunal epithelium and with the damaged epithelium of patients with coeliac disease, antibody RFAL-2 reacted strongly only with histologically normal small bowel but more weakly in patients with coeliac disease to a degree related to the amount of histological abnormality. Expression of the moeity like CALLA identified with RFAL-2 was strongest in crypt epithelium and proportionally diminished along the villi according to the amount of histological damage in coeliac disease, being essentially absent in patients with "subtotal villous atrophy."
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PMID:Expression of the common acute lymphoblastic leukaemia antigen (CALLA gp100) in the brush border of normal jejunum and jejunum of patients with coeliac disease. 293 54

Although the aetiology of ulcerative colitis and Crohn's disease remain unknown, immunological effector mechanisms become activated within the inflamed mucosa and may be responsible for the pathogenesis of chronic disease. There is an increased production of immunoglobulin within the mucosa, some of which has specificity for bacterial antigens, and complement activation occurs during exacerbation of the disease. Lymphocytes isolated from peripheral blood, or from the intestinal mucosa, are cytotoxic to colonic epithelial cells in vitro; a reaction which can be modulated by serum factors and bacterial antigens. Within the mucosa, there are increased populations of T lymphocytes although there is no change in the ratio of helper- to suppressor-cells as defined by phenotype. Studies of immunoregulatory control have shown that there may be alterations in the modulation of the local immune response, especially during active disease, although it is not clear whether these changes are primary or merely secondary to inflammation. It is posulated that many of the humoral and cellular responses to gut-associated antigens occur as a result of increased antigen absorption, increased presentation of antigen to the immune system due to the expression of Class II antigens by the inflamed epithelium and altered immuno-regulatory control.
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PMID:Immunology of inflammatory bowel disease. 293 26

The monoclonal antibodies (mAbs) WR16, UCHL1 and WR19 identify subsets of CD4+ lymphocytes that have been functionally characterized as suppressor inducer cells or helper inducer cells. These were applied as components of a panel of lymphocyte-specific mAbs for the phenotypic analysis of lymphocyte populations within biopsies taken from rheumatoid synovial membrane and normal and inflamed gut. The phenotype of peripheral blood lymphocytes from patients with rheumatoid arthritis were also compared to normal controls. The rheumatoid synovium was characterized immunohistologically by a lymphocytic infiltrate composed predominantly of CD4+ lymphocytes and a CD4:CD8 ratio of 2.4. The CD4+ population was composed of UCHL1+ cells to the exclusion of WR16+ cells. This finding was confirmed by double immunofluorescence staining using directly conjugated Leu-3a and WR16. The UCHL1+/WR16-/CD4+ phenotype was maintained in the synovial biopsies regardless of whether the patient had commenced treatment with disease modifying drugs. The absence of WR16+ cells within the rheumatoid synovium was shown to be a localized phenomenon as there was a slight elevation of circulating WR16+ lymphocytes in the peripheral blood of rheumatoids whilst the levels of UCHL1+ and WR19+ lymphocytes remained unchanged. As no appropriate normal control tissue is available for comparison to the rheumatoid synovium we also examined the lymphocytes present within Crohn's disease-involved bowel biopsies and compared them to normal gut tissue lymphocytes using WR16 and UCHL1 mAbs. The CD3+ lymphocytes present within normal tissue comprised a mixture of WR16+ and UCHL1+ cells. In contrast the CD3+ lymphocytes within Crohn's involved tissue were exclusively UCHL1+ as previously observed in the rheumatoid synovium. These data indicate that the CD4+ lymphocyte infiltrate present within inflammatory lesions of presumed distinct aetiology exhibit a localized selective loss of cells with the CD45R+/CD4+ suppressor inducer phenotype. This may be a consequence of the selective extravasation of CD4+ helper induced cells or more likely, in view of the previously documented loss of the p220 molecule identified by CD45R mAbs upon T-cell activation, the result of CD4+ T-cell activation at sites of inflammation.
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PMID:An immunohistological study of CD4+ lymphocyte subsets within inflammatory lesions with special reference to rheumatoid arthritis and inflammatory bowel disease. 297 33

Crohn's disease is a chronic relapsing inflammatory disease of the intestine of unknown cause. It has been suggested that the disease may result from an abnormality of the immunological functions of the gut. Recent advances in the study of the gastrointestinal immune system show that T cells in the intestinal mucosa are more activated, contain a higher proportion of T4 cells having the phenotypic and functional characteristics of helper-inducer cells, have greater capacity for IL-2 production, and have altered responsiveness to antigen stimulation. In the intestinal mucosa in Crohn's disease the predominance of T cells with helper-inducer function is maintained, and there is no evidence of augmented suppressor activity. Although natural killer cells are infrequent in the intestinal mucosa in Crohn's disease, lymphokine activated killer cell precursors and cytolytic T cell precursors are present and it is possible that these cells also play an important role in the disease. The failure to identify specific infections or environmental etiologies in Crohn's disease is consistent with the hypothesis that the disease is due to an inappropriate immunological hyper-responsiveness to ubiquitous components of the alimentary tract.
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PMID:Cellular immune mechanisms in the pathogenesis of Crohn's disease. 297 7

Vasoactive intestinal peptide (VIP), first isolated from the gut, was originally considered a candidate gastrointestinal hormone. Since about 1975, however, it has become increasingly clear that it is primarily a neurotransmitter or neuromodulator and that it exerts its functions mainly by local release from nerve endings. VIP plays a hormonal role only when it is released in large amounts from a tumor, with a consequent overflow into the circulation and grossly elevated plasma concentrations of the peptide. Moderately increased VIP plasma and tissue concentrations that cause mainly local effects are found in intestinal ischemia. Crohn's disease and some other chronic inflammatory diseases of the bowel. VIP is also measured in increased amounts in the normal fetus and neonate, where it may play an important physiological role. Such an increase of VIP levels in the circulation could enhance perfusion and metabolic activity of tissues during their rapid-growth period. On the other hand, disorders with a disturbed VIP function such as achalasia and Hirschsprung's disease and possibly also asthma and cystic fibrosis seem to be characterized mainly by a derangement of smooth muscle activity and/or exocrine secretion. Considering this list of disorders where VIP has either a proven or suspected role, it is easy to imagine the significance of this peptide in pediatric pathophysiology.
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PMID:[Vasoactive intestinal polypeptide (VIP)--possible importance in diseases of childhood]. 299 82

Ileocolonoscopy with biopsy of caecum, ileocaecal valve and terminal ileum were performed on 232 patients with seronegative spondylarthropathies and on 65 control patients. Inflammatory gut lesions were found in 65% of the patients with reactive arthritis (ReA) and in 57% of the patients with ankylosing spondylitis (AS), especially in those with peripheral arthritis. The controls had a normal gut. This finding would suggest that exogenous factors causing inflammation of the gut lead to a disturbed permeability of the gut wall or to a deficient local immunological defence mechanism permitting antigens to enter the circulation, inducing the joint and tendon inflammation. Support for this hypothesis was provided by the results of a repeat ileocolonoscopy, disclosing a strong association between the presence of gut inflammation on biopsy and the persistence of joint inflammation. Patients presenting some of the histological lesions found on biopsy (especially active chronic lesions) and patients with proven Crohn's disease were found to share a genetic marker (HLA-BW62). This would suggest that some of the patients with seronegative spondylarthropathies suffer from a subclinical form of Crohn's disease of which the joint symptoms are the unique clinical manifestation.
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PMID:Ileocolonoscopic findings in seronegative spondylarthropathies. 304 80


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