Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0021390 (inflammatory bowel disease)
 23,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study has identified a group of patients with inflammatory chronic, or relapsing acute arthritis who even in the absence of gastrointestinal symptoms have histological evidence of ileocolitis. At colonoscopy simultaneous biopsies of the terminal ileum and colon were taken from 108 patients with reactive arthritis (n = 55) or ankylosing spondylitis (n = 53), 47 patients with other rheumatic diseases and 19 control patients suffering from colonic polyps, adenocarcinoma, or chronic constipation. All control patients and all but one patient with rheumatoid arthritis, juvenile chronic arthritis, systemic lupus erythematosus, lumbar back ache, and psoriatic arthritis did not have histological evidence of acute or chronic inflammatory bowel disease. In contrast, in 30 of 35 (56.6%) patients with ankylosing spondylitis, and in 37 of 55 (67%) patients with reactive arthritis, regardless of HLA B27 phenotype, there was histological evidence of inflammatory bowel disease with features either of acute enterocolitis, or early Crohn's disease. Only 18 of 67 (27%) of the patients with histological gut inflammation, however, had intestinal symptoms.
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PMID:Histopathology of intestinal inflammation related to reactive arthritis. 349 71

The prevalence of HLA-A, B, C and DR antigens was determined and compared in 94 patients with reactive arthritis, 54 patients with ankylosing spondylitis (AS), 37 patients with inflammatory bowel disease (IBD) and in 1,010 apparently normal blood donors. The 185 patients all underwent ileocolonoscopy with biopsy of ileum, ileocecal valve and cecum. HLA-B27 was found elevated in the groups with reactive arthritis (48%, chi 2 = 82, p less than 0.0005) and the AS groups (78%, chi 2 = 157, p less than 0.0005), compared to healthy controls. HLA-Bw62 was significantly raised in the patients with reactive arthritis (34%, chi 2 = 73, p less than 0.0005) (particularly the HLA-B27 negatives (48%, chi 2 = 90, p less than 0.0005) and in the HLA-B27 negative patients with AS (25%, chi 2 = 5.5, p less than 0.02). This did not apply to the other patients with AS (4.7% NS). HLA-Bw62 could be associated with a specific clinical picture of asymmetrical pauciarticular arthritis, accompanied by enthesopathies and sacroiliitis classified as idiopathic reactive arthritis, especially when the disease is of enterogenic origin. The frequency of HLA-Bw62 was very high in patients with reactive arthritis and in patients with AS with active chronic (n = 39, 23%, chi 2 = 13, p less than 0.0005) and Crohn-like lesions (n = 14, 50%, chi 2 = 35, p less than 0.0005) on gut biopsy, normal in patients with acute lesions (n = 35, 11%, NS).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:HLA antigens in seronegative spondylarthropathies. Reactive arthritis and arthritis in ankylosing spondylitis: relation to gut inflammation. 349 33

The study of sixty-five children with antigen HLA B27 associated chronic rheumatism was performed. There was a male preponderance, and mean age at onset was ten. A family history was available in half patients. After a 5-year follow up study, 32% of the patients were diagnosed as having ankylosing spondylitis or Reiter's syndrome or psoriatic arthritis or arthritis associated to inflammatory bowel disease. The other patients should be considered as having an HLA B27 associated juvenile chronic arthritis with special features such as enthesopathy, acute joint pain or sausage-like digits. Three patients had a very severe outcome with considerable joint lesion seen on X Ray.
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PMID:HLA B27 associated chronic arthritis in children: review of 65 cases. 350 11

An adaptation of the sib pair method is given for testing the independence of transmission of Gm and the disease, using variable X (which gives information on the phenotypic identity of a sib pair for Gm). Then the joint distribution of IBD for HLA and X for Gm among affected sib pairs was derived under different two-locus models (multiplicative and other) in which one locus is strictly linked to HLA and the other to Gm. We also propose a test for a joint effect of HLA and Gm and whether this effect is multiplicative or not.
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PMID:Two-disease locus model: sib pair method using information on both HLA and Gm. 378 Dec 39

We studied the in vitro effect of indomethacin, hydrocortisone, sulphasalazine, and its metabolites sulphapyridine (SP) and 5-amino salicylic acid (5-ASA) on peripheral blood mononuclear cells (PBMC) from 49 patients with inflammatory bowel disease and 34 controls. Indomethacin caused a highly significant increase in the PBMC response to the mitogen PHA-P compared with controls (P less than 0.01), indicating increased activity of a prostaglandin-producing suppressor cell system. On the contrary, sulphasalazine resulted in a reduced response which was significantly greater for the group with inflammatory bowel disease than the control group (P less than 0.05). This reduction was also produced by 5-ASA (P less than 0.05) but not by sulphapyridine. Addition of indomethacin to PBMC incubated with sulphasalazine significantly reduced the effect of sulphasalazine (P less than 0.001). Hydrocortisone resulted in a reduced response which was similar to that of controls and was not altered by the addition of indomethacin. The response to indomethacin, hydrocortisone, sulphasalazine, sulphapyridine, and 5-ASA was not dependent on the HLA type of the patients, disease activity, or drug therapy. The results suggest that increased suppression by a population of prostaglandin-producing suppressor cells plays a role in the immunopathology of inflammatory bowel disease, but that sulphasalazine does not exert its therapeutic effect by acting on this step of the immunoregulatory system. Any trials of indomethacin therapy in inflammatory bowel disease should take into account that, in vitro, sulphasalazine and indomethacin have opposing mechanisms of action in this system.
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PMID:Increased suppressor cell activity in inflammatory bowel disease. 611 75

The case is described of a young woman with Crohn's disease of the rectum and terminal ileum in whom systemic lupus erythematosus syndrome was diagnosed after 3 yr of symptoms and 4 yr treatment with sulfasalazine. Polyarthralgias and pleuritic chest pains resolved and leucopenia, anemia, and high titers of antinuclear and DNA antibodies returned to normal after withdrawal of the drug. No HLA antigen association was found but a slow acetylation phenotype was present. Consideration should be given to this complication of sulfasalazine therapy in patients with inflammatory bowel disease in whom arthropathy or other features of lupus syndrome appear after treatment is instituted.
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PMID:Sulfasalazine-induced lupus syndrome in a patient with Crohn's disease. 612 17

Peripheral blood T lymphocytes and T lymphocyte subsets have been quantified in 28 patients with ulcerative colitis and 26 with Crohn's disease by an indirect immunofluorescence technique using monoclonal antibodies: OKT3, which detects all peripheral blood T lymphocytes; OKT4 (T cells of helper phenotype); and OKT8 (T cells of supressor-cytotoxic phenotype). Eighteen normal subjects and 16 patients with a variety of non-inflammatory gastrointestinal disorders were studied as controls. No significant differences were found between patient and control groups in the proportions of circulating T lymphocytes or their subsets. When compared with normal subjects, absolute numbers of T lymphocytes were reduced in patients with active ulcerative colitis or Crohn's disease (p less than 0.05). OKT4+ T cell numbers were reduced in ulcerative colitis, whether active (p less than 0.02) or inactive (p less than 0.05) and in active Crohn's disease (p less than 0.05) Numbers of OKT8+ T cells were reduced in active Crohn's disease (p less than 0.01). There were no differences in T lymphocyte numbers between the patient groups and the disease control subjects. The OKT4+:OKT8+ ratio in patients with inflammatory bowel disease did not differ from that in controls. No relation was found between any of the parameters studied and disease activity, site, or extent of disease, or treatment with sulphasalazine or corticosteroids. The presence of Ia-like, HLA-DR antigens on T cells was detected using a double marker immunofluorescence technique. In control subjects up to 7% of OKT3+ cells were HLA-DR+. In only three patients was the proportion of HLA-DR+ cells greater than in controls. These results indicate that the pathogenesis of ulcerative colitis or Crohn's disease does not depend upon an alteration in the proportion of circulating T lymphocytes nor upon an imbalance of T lymphocyte subsets as defined by monoclonal antibodies. The reduction in T lymphocyte numbers may result from mucosal infiltration. The findings also suggest that circulating T lymphocytes are not activated.
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PMID:T lymphocyte subsets in inflammatory bowel disease: peripheral blood. 622 76

HLA-DR-positive histiocytes in the lamina propria of the human intestine have been characterised using combined histochemical and immunohistological techniques. In the small intestine, 80-90% of the HLA-DR+ histiocytes had irregular surfaces with stellate processes, and exhibited strong membrane adenosine triphosphatase (ATPase) activity, but weak acid phosphatase (ACP) and non-specific esterase (NSE) activities (HLA-DR+ ACP+/- NSA+/- ATP++; type 1 cell). In contrast, in the lamina propria of the colon the majority (60-70%) of HLA-DR+ cells were large, round cells with strong ACP and NSE activities but no detectable ATPase activity (HLA-DR+ ACP++ NSE++ ATP+/-; type 2 cell). The colon also contained a population of type 1 cells (30-40%). In active inflammatory bowel disease affecting the colon a third population of HLA-DR+ histiocytes was seen. These cells were irregular in outline, with many processes, and were ACP++ NSE+ ATP+/- (type 3 cell). The type 3 cells appeared to replace type 2 cells. After treatment, the appearances returned to normal. These findings suggest that the different populations of HLA-DR+ histiocytes in the human intestine may have several functions, reflecting the different forms of antigen present in the intestine. The alterations in inflammatory bowel disease may represent activation in response to an invading antigen.
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PMID:Heterogeneity of HLA-DR-positive histiocytes in human intestinal lamina propria: a combined histochemical and immunohistological analysis. 633 64

Of 12 patients with inflammatory bowel disease (IBD) and ankylosing spondylitis (AS) or sacroiliitis (SI), only 4 (32%) had HLA-B27. Family studies revealed 3 B27-negative relatives with AS, 1 with SI, 1 with SI and IBD, and 1 with IBD alone. HLA haplotypes did not segregate with disease. These data suggest a non-HLA linked genetic predisposition to IBD which also confers susceptibility to spondylitis, even in the absence of expression of bowel disease.
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PMID:The spondylitis of inflammatory bowel disease. Evidence for a non-HLA linked axial arthropathy. 645 May 95

The expression of HLA-DR and HLA-A,B,C antigens by human colonic epithelium has been examined in tissue sections of patients with inflammatory bowel disease using an immunohistological technique. Colonic epithelial cells from all 21 control subjects with histologically normal colonic mucosa were HLA-DR-. In contrast, in nine of 13 patients with active ulcerative colitis and 11 of 12 with active Crohn's disease the epithelium of involved colonic mucosa was HLA-DR+. HLA-DR antigens were found on the epithelium of only one of six patients with ulcerative colitis in remission and one of three with inactive Crohn's disease. Moreover, these antigens were not present on the epithelium of non-inflamed colonic mucosa in two patients with Crohn's disease in whom adjacent involved mucosa showed strong epithelial reactivity. This difference between patients with active and those with inactive disease is highly significant (P less than 0.005). These findings provide further evidence of the importance of cell-mediated immune mechanisms in the pathogenesis of inflammatory bowel disease.
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PMID:Expression of HLA-DR antigens by colonic epithelium in inflammatory bowel disease. 657 96


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