Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0009319 (colitis)
 19,384 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Histocompatibility (HLA) antigen phenotypes have been studied in 100 patients with ulcerative colitis, 100 with Crohn's disease, and 283 normal controls. In addition the incidence of ankylosing spondylitis, sacroiliitis, and "enteropathic" peripheral arthropathy was determined in the patients with inflammatory bowel disease (IBD). There was no significant difference in antigen frequency between patients and controls. However, the incidence of HLA-B27 was increased in the patients complicated by ankylosing spondylitis and/or sacroiliitis in both ulcerative colitis and Crohn's disease. In contrast, none of the 29 IBD patients with "enteropathic" peripheral arthropathy had B27 antigen. Furthermore, ankylosing spondylitis was found more frequently in ulcerative colitis bearing HLA-B27 compared with non-B27 patients (P less than 0-01). The same was found in Crohn's disease, although this difference was not statistically significant. In addition, 12 of 14 ulcerative colitis patients and five out of six Crohn's patients with HLA-B27 had total colitis, compared with the frequency of total colitis in non-B27 patients (P less than 0-024 and less than 0-03 respectively). The data suggest that B27 histocompatibility antigen could be a pathogenetic discriminator between the arthropathies in IBD and may be of prognostic significance with respect to extension and severity of the disease.
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PMID:Histocompatibility antigens in inflammatory bowel disease. Their clinical significance and their association with arthropathy with special reference to HLA-B27 (W27). 100 80

Seventy-nine consecutive patients with active ulcerative colitis were studied to establish the prevalence and clinical features of articular involvement. HLA typing for A and B loci was performed. Forty-nine patients showed an articular involvement (62%). Three different clinical patterns were identified: ankylosing spondylitis occurring in 20 subjects; peripheral arthritis in 15; unclassifiable spondylitis in 14. When compared to the general population in our area, patients with colitis showed a significantly higher prevalence of the HLA-A1 (p less than 0.005), B21 (p less than 0.001) and B27 (p less than 0.05); among patients with colitis, those with arthritis revealed higher frequency of HLA-B27 (p less than 0.05). Our study reveals a high prevalence of unclassifiable spondylitis during ulcerative colitis, and suggests a new approach to the classification of seronegative spondarthritis.
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PMID:The arthritis of ulcerative colitis: clinical and genetic aspects. 157 50

We describe a patient with recurrent Clostridium difficile-associated colitis who suffered severe arthritis and urethritis with each of three episodes of diarrhea. Although immune complex formation was demonstrated in synovial fluid, neutralizing antibodies to C. difficile cytotoxin A and B were not found in either serum or synovial fluid. Cholestyramine did not prevent a third episode of colitis which followed the use of amikacin. This patient was HLA-B27 positive; she developed sacroiliitis, tenosynovitis, oligoarthritis, culture negative urethritis, and cervicitis. With the successful treatment of each episode of diarrhea, these additional symptoms resolved. The close temporal correlation between recurrences of C. difficile-associated colitis and these other symptoms strengthens evidence from other reports which suggests that colonic infections with C. difficile may precipitate the Reiter's syndrome. Evidence from this case does not support the contention that antibodies to C. difficile toxins are implicated in producing joint inflammation.
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PMID:Relapsing Clostridium difficile colitis and Reiter's syndrome. 235 99

The place of inflammatory bowel disorders in the spondarthritis matrix has been discussed and aetiopathological and clinicoradiological features of their individual arthropathies described. Particular emphasis has been placed on the arthropathies of ulcerative colitis and Crohn's disease, but a comment is also included on the much rarer condition, Whipple's disease. The position of reactive arthritis resulting from enteric infection in relation to the spondarthritis concept is examined in the light of Reiter's-like clinical features and the association with HLA-B27. More 'peripheral' ideas of possible relevance to the spondarthritis idea (drug-induced colitis, intestinal-bypass syndrome) are included, together with a final section on experimental models of inflammatory bowel disease and of their arthropathies. It is concluded that certain inflammatory bowel disorders deserve a continuing place within the spondarthritis complex. Although their aetiopathogenesis is still imperfectly understood, it is likely that a blend of genes of small effect (polygenic inheritance) and environmental factors (e.g. microorganisms and/or their products) trigger disease processes which are enabled to manifest themselves by intermediary immunological processes. The precise way in which this is achieved is not yet known, but there is evidence that microorganisms (presumably in the gut of individuals genetically predisposed and suitably exposed environmentally) generate the formation of immune complexes. It is likely that these not only damage or further damage the mucosal lining of the bowel but also result in arthropathy and features of the disease 'distant' from bowel and joint (e.g. ocular inflammation, oral ulceration and skin manifestations). This concept is summarized in Figure 5.
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PMID:Inflammatory bowel disease. 258 32

We examined all available data on HLA-A and -B antigen distributions in patients with Crohn's disease and ulcerative colitis. The risk of Crohn's disease was significantly increased in individuals with HLA-A2, having a relative risk of 1.25, in 730 pooled Caucasoid patients compared with 10 863 pooled controls, and decreased in individuals with HLA-A11, having a relative risk of 0.62. The risk of ulcerative colitis was also significantly increased in individuals with HLA-B27 and -Bw35, having a relative risk of 1.81 and 1.41 respectively, in 560 pooled Caucasoid patients compared with 6151 pooled controls, whilst in 144 pooled Japanese patients who were compared with 442 pooled controls, the risk of colitis was increased in individuals with HLA-B5 with a relative risk of 2.79. All differences remained significant after correction for the number of antigens examined. The bases for these genetic associations are unclear.
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PMID:HLA-A and -B antigens in inflammatory bowel disease. 346 Sep 39

The abrupt onset of a sterile inflammatory oligoarthritis developed in a patient with active Clostridium difficile pseudomembranous colitis. The arthritis affected a hip and a knee. Leukocyte counts of synovial fluid obtained from the patient's left hip and knee were elevated. He was haplotyped as HLA-B27 antigen-positive. The colitis and arthritis promptly abated after treatment with oral vancomycin hydrochloride. Three other cases of arthritis associated with antibiotic-induced colitis were reviewed. It seems as if treatment of the colitis leads to resolution of the arthritis.
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PMID:Acute oligoarthritis associated with Clostridium difficile pseudomembranous colitis. 660 28

Recent rodent models have been exploited to explore mechanisms of intestinal and joint inflammation. HLA-B27 transgenic rats develop colitis, gastritis, and arthritis when raised in a conventional environment, but have no evidence of inflammation under germfree (sterile) conditions. Metronidazole treatment attenuates gastrointestinal inflammation, suggesting that anaerobic bacteria are important. Experimental bacterial over-growth of predominantly anaerobic bacteria reactivates arthritis in Lewis rats which have been previously injected intra-articularly with bacterial cell wall polymers. Reactivation arthritis is mediated by interleukin-1, tumour necrosis factor-alpha, and can be blocked by metronidazole. Intramural injection of the bacterial cell wall polymer, peptidoglycan-polysaccharide, leads to biphasic, chronic granulomatous enterocolitis and peripheral arthritis in Lewis rats, but only transient intestinal inflammation and no arthritis in Buffalo or MHC-matched Fischer rats. Chronic granulomatous inflammation is mediated by T lymphocytes and interleukin-1 and is dependent on persistent antigenic stimulation by poorly biodegradable bacterial polymers. Results in these models firmly incriminate resident normal enteric flora (especially anaerobes), bacterial products, and host genetic susceptibility in the pathogenesis of spondyloarthropathies. We suggest that increased uptake of luminal bacterial components across the inflamed mucosa leads to systemic distribution of these arthropathic products. The genetically susceptible host develops reactive arthritis due to defective downregulation of inflammation in response to immunologically active bacterial components.
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PMID:Animal models of intestinal and joint inflammation. 867 49

Genetic and environmental factors are important in the pathogenesis of clinical and experimental chronic intestinal inflammation. We investigated the influence of normal luminal bacteria and several groups of selected bacterial strains on spontaneous gastrointestinal and systemic inflammation in HLA-B27 transgenic rats. Rats maintained germfree for 3-9 mo were compared with littermates conventionalized with specific pathogen-free bacteria. Subsequently, germfree transgenic rats were colonized with groups of five to eight bacteria that were either facultative or strictly anaerobic. Transgenic germfree rats had no gastroduodenitis, colitis, or arthritis, but developed epididymitis and dermatitis to the same degree as conventionalized rats. Colonic proinflammatory cytokine expression was increased in transgenic conventionalized rats but was undetectable in germfree and nontransgenic rats. Colitis progressively increased over the first 4 wk of bacterial exposure, then plateaued. Only transgenic rats colonized with defined bacterial cocktails which contained Bacteroides spp. had colitis and gastritis. Normal luminal bacteria predictably and uniformly induce chronic colonic, gastric and systemic inflammation in B27 transgenic F344 rats, but all bacterial species do not have equal activities.
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PMID:Normal luminal bacteria, especially Bacteroides species, mediate chronic colitis, gastritis, and arthritis in HLA-B27/human beta2 microglobulin transgenic rats. 877 Aug 66

We report two cases of rheumatoid arthritis (RA) associated with Crohn's disease (CD). The first case was a 60-year-old man with longstanding CD who next developed a seropositive, nodular RA. This patient also had bilateral sacroiliitis, but without positive HLA B27. The second was a 65-year-old female with a 15-year history of seropositive RA who presented secondarily a CD. No sacroiliitis or nodules were found in this patient. Both patients were DR1 (DRB1* 0101). Gold salts were only given in the second case and were stopped many years before the gastrointestinal symptoms. A similar case report has been previously described consisting in an ulcerative colitis complicating a seronegative HLA-B27 RA with sacroiliitis. The gastrointestinal involvement in RA may be broad and includes many causes: drug-induced colitis (including gold enterocolitis) vasculitis and amyloidosis located in the gut, associated bowel disease such as collagenous colitis, and also infectious agents. In addition, erosive polyarthritis associated with gastrointestinal manifestations can present a problem in the differential diagnosis between RA and an enteropathic arthritis. Finally, the coexistence by chance of inflammatory bowel disease and RA is suggested by the low occurrence of these two conditions in the same patient.
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PMID:Crohn's disease associated with seropositive rheumatoid arthritis. 917 28

Over the past few years, application of targeted gene deletion and transgenic approaches has led to the often unanticipated development of rodent lines which develop inflammatory bowel disease. While none of these lines recapitulate the histopathological and clinical features usually associated with human inflammatory bowel disease (IBD) in their entirety, many exhibit key features comprising the development of "spontaneous" chronic and acute inflammation. These models include targeted deletion of the genes encoding IL-2, IL-10, TGF beta, T-cell receptor alpha/beta, keratin 8, and Gi2 alpha. In addition, animals expressing transgenes for the human WA-B27 (with beta-2 microglobulin) as well as a dominant negative construct which functionally blocks N-cadherin have also been observed to result in chronic inflammatory bowel disease. Most of the mutant murine lines experience a diffuse colitis, but some (HLA-B27 transgenic and IL-10-deficient) also experience small bowel inflammation. The variety of manipulations provides some important broad insights: (1) IBD can result from dysregulation of mucosal immune responses or impairment of epithelial barrier function, and (2) the natural history of inflammation resulting from mutation at a single genetic loci is substantially modulated by other genetic factors. With the rapidly-increasing variety of mutant mice, comparison of the residual components of immune system in lines developing IBD with those of lines not developing IBD, it is possible to deduce a requirement for TCR gamma/delta CD4+ lymphocytes as well as pivotal role of IFN gamma and (as a suppressive factor) IL-10. Study of a number of models has demonstrated the important interaction between environmental factors and genetic predisposition. Thus, in at least some of the lines (IL-2-deficient and HLA-B27) the inflammatory bowel disease is not observed when the mutant mice are maintained in a germ-free environment but does develop after reconstitution with a pathogen-free flora. In the TCR alpha/beta deficient mice, appendectomy in the neonatal period prevents the subsequent development of colitis. In still other models, inflammation may not occur without some challenge by an exogenous external agent, e.g., mice deficient in intestinal trefoil factor (ITF) exposed to dextran sodium sulfate (1). These models offer great promise to permit further dissection of the various constituents of the intestinal epithelium and mucosal immune response systems which are necessary for maintaining normal homeostasis and which can contribute to the development of inflammatory bowel disease. Further, they offer powerful tools for exploring the interaction between genetic and environmental factors to explicate the pathogenesis of inflammatory bowel disease and to develop new therapeutic intervention strategies.
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PMID:Lessons from genetic models of inflammatory bowel disease. 926 Mar 28


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