Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0003864 (arthritis)
 69,039 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twenty-three of 81 intestinal bypass patients with episodes of bypass enteropathy had papulopustular or nodular skin lesions. Histologic examination of the dermal lesions showed various forms of vasculitis in nine of 14 subjects. In six of 11 patients examined by immunofluorescent microscopy, both the lesions and uninvolved sun-exposed skin areas had immunoglobulin and complement deposits in linear or granular patterns in the dermoepidermal line, giving the appearance of a positive lupus band test. Skin lesions resolved with spontaneous improvement of bypass enteropathy or in response to metronidazole therapy. After the bypass was dismantled, the eruptions disappeared permanently, and previously positive lupus band tests became negative. The skin lesions were frequently observed in association with arthritis, suggesting an immune-complex mechanism, probably originating in "blind loop" bacterial overgrowth.
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PMID:Cutaneous lesions after intestinal bypass. 700 72

Fifteen consecutive patients with PG have been studied during the period 1971-78. Systemic disease was found in 13 of the patients and preceded the skin disease in 10 patients by 1-25 years. Only two patients had ulcerative colitis. One patient had paroxysmal nocturnal hemoglobinuria and three patients had an IgA myeloma. Eight patients had polyarthritis; this was classical seropositive rheumatoid arthritis in two patients, and a seronegative inflammatory polyarthritis in six patients. Four patients had an unusual progressive erosive seronegative polyarthritis without evidence of granulomatous bowel disease, psoriasis, genital, urinary tract or eye disease. In three of these four patients the arthritis preceded the PG. Synovial fluid analysis showed depressed complement levels and in one patient deposits of immunoglobulins and complement were demonstrated in the synovial membrane. The course of the arthritis was progressive with development of disabling joint deformities and erosive destruction of joints, despite treatment with penicillamine, corticosteroids and nonsteroidal anti-inflammatory drugs. One other patient had severe degenerative joint disease and chondrocalcinosis in association with a seronegative inflammatory polyarthritis, and another patient had ulcerative proctitis and severe degenerative joint disease secondary to chronic seronegative inflammatory polyarthritis. None of the patients had colitic arthritis, but in view of the association between PG and ulcerative colitis, some patients previously reported with PG and joint disease may have been suffering from the arthritis of ulcerative colitis. PG developed at the site of skin trauma in six patients. The natural history of the skin disease ran one of two courses: an acute, progressive course in which the ulcers rapidly enlarged until arrested by treatment; and a chronic course in which the lesions extended slowly and which after a period of weeks began to show signs of spontaneous healing. In only the patients with ulcerative colitis was there any correlation between the activity of the associated disease and the onset and progression of the skin disease. Serum complement levels were normal and no circulating cryoprecipitable immune complexes were found. Skin histology showed no evidence of vasculitis and direct immunofluorescence examination of involved skin was negative for IgG, IgM, IgA and C3. No consistent abnormality of cell-mediated immunity or neutrophil function was found and no significantly increased prevalence of any HLA antigen type was noted. Twelve patients have been treated with systemic corticosteroids. Six of these patients developed serious steroid complications and four patients have died, all from complications of steroid therapy.
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PMID:Pyoderma gangrenosum: clinical and laboratory findings in 15 patients with special reference to polyarthritis. 736 40

Lymphocytes continuously migrate throughout the body in search of antigens. Virgin lymphocytes recirculate freely between the blood and different lymphatic organs, whereas immunoblasts extravasate preferentially into sites similar to those where they initially responded to antigen. Tissue-specific extravasation of lymphocytes is largely controlled by distinct lymphocyte surface receptors that mediate lymphocyte binding to high endothelial venules (HEV). In the present study, the molecular mechanisms determining the specificity of human mucosal (lamina propria) lymphocyte binding to different endothelial recognition systems were analyzed. Mucosal immunoblasts adhered five times better than small mucosal lymphocytes to mucosal HEV. Importantly, mucosal immunoblasts also bound to synovial HEV almost as efficiently as to mucosal HEV, but they did not adhere to peripheral lymph node HEV. To study the impact of different homing-associated molecules in this dual endothelial binding, we used a gut-derived T cell line and freshly isolated mucosal immunoblasts. Both cell types expressed integrins alpha 4, beta 1, beta 7, and lymphocyte function associated antigen 1 (LFA-1), and were CD44 positive, but practically L-selectin negative. Binding of mucosal immunoblasts to mucosal HEV was almost completely abolished by pretreatment with anti-beta 7 monoclonal antibodies, but it was independent of alpha 4/beta 1 function. In contrast, alpha 4/beta 1 partially mediated immunoblast adherence to synovial HEV, whereas alpha 4/beta 7 had only a minor role in adherence of blasts at this site. CD44 and LFA-1 contributed to HEV-binding both in mucosa and synovium. Taken together, this is the first report that demonstrates a critical role for alpha 4/beta 7 in the binding of gut lymphocytes to mucosal venules in humans. Moreover, a hitherto unknown interaction between mucosal effector cells and synovial endothelial cells was shown to be only partially mediated by the currently known homing receptors. The dual endothelial binding capacity of mucosal blasts may help to explain the pathogenesis of reactive arthritis not uncommonly associated with inflammatory and infectious bowel disease.
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PMID:Dual binding capacity of mucosal immunoblasts to mucosal and synovial endothelium in humans: dissection of the molecular mechanisms. 752 65

Five adults had inflammatory rheumatic disorders 6 to 20 years before the diagnosis of coeliac disease. It is known that joint inflammation occurs in certain patients with adult coeliac sprue who develop either a specific inflammatory rheumatic disease or an atypical progressive polyarthropathy, sometimes as the first manifestation of the intestinal disorder. The diagnosis of adult coeliac sprue should be entertained in these cases even in absence of major digestive disorders or malabsorption. IgA anti-reticulin antibodies and atrophy of the duodenojejunal villosities are the best indicators for diagnosis. There are two important reasons for making the diagnosis of "asymptomatic adult coeliac sprue". First a gluten-free diet can improve or even cure the inflammatory joint disease, a rare situation which emphasizes the causal relationship between these two diseases. Second, the risk of developing lymphoma (especially in the small bowel) is apparently lower in patients on gluten-free diet. Pathogenesis is unclear. Frequently the two autoimmune disorders simply appear to coincide in the same patient; more rarely, arthritis is a symptom of coeliac disease. The immunological mechanisms probably begin when antigens cross an excessively permeable intestinal mucosa.
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PMID:[Inflammatory rheumatism and celiac disease in adults. Coincidence or pathogenic relationship?]. 776 62

Uveitis may be an asymptomatic ocular process when it occurs in association with chronic inflammatory bowel disease (IBD). However, the frequency of uveitis in pediatric IBD is not known, as few patients have eye examinations on a routine basis. Experience with a child with Crohn's disease, who had asymptomatic uveitis identified by routine screening initiated because of associated arthritis, prompted us to undertake this evaluation. The purpose of this cross-sectional prospective study was to ascertain the point-prevalence of uveitis in pediatric IBD patients, including 97 with Crohn's disease and 50 with ulcerative colitis. Each child underwent an ophthalmologic assessment, including slit-lamp examination. In Crohn's disease, inflammatory cells and/or flare were observed in the anterior chamber of six (6.2%) patients. These changes were mild in all six patients and required no treatment. In the group with ulcerative colitis, there were no cases of asymptomatic uveitis. There was a higher frequency of asymptomatic transient uveitis in patients with Crohn's colitis (four of 22, 18.2%) than in those of other anatomic subgroups (two of 75, 2.7%; p < 0.05). Frequency of uveitis was also higher in IBD patients having other extraintestinal manifestations (15.0%) than in those without (3.1%; p < 0.10). There was no relationship observed between the activity of bowel disease and presence of ocular inflammation.
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PMID:Asymptomatic uveitis in children with chronic inflammatory bowel diseases. 814 95

Idiopathic inflammatory bowel disease include basically two disorders: ulcerative colitis and Crohn's disease. Both diseases are chronic and of unknown etiology and extraintestinal manifestations are seen in a high number of these patients. We studied 18 patients (7 female, 11 male) with previous diagnosis of inflammatory bowel disease (14 ulcerative colitis, 2 Crohn's disease, 1 pancolitis, 1 ulcerative proctitis) in order to search for extraintestinal manifestations with emphasis on osteoarticular and ocular involvement. The mean age at the time of diagnosis of the inflammatory bowel disease was 44 years (range 20 to 71 years). Mean time duration of the inflammatory bowel disease was 7 years (range 1 to 24 years) and of the articular manifestations 3.2 years (range 1 to 8 years). The osteoarticular manifestations developed after the diagnosis of the bowel disease in all but one patient (simultaneously) 17/18 patients had artralgias, 7/18 lumbalgia, 3/18 talalgia, 1/18 knee arthritis. (table I) Only six of the 17 patients with orteoarticular involvement has simultaneous activity of the underlying bowel disease. All the 18 patients were taking 2 g/day of sulfasalazine. Radiographic screening in all patients revealed sacroiliitis in 10. (table II) Of the 10 radiographic sacroiliitis 4 were grade I (confirmed by technetium phosphate scans, 2 were grade II and 4 grade III-IV. Three of the ten patients with radiographic sacroiliitis were asymptomatic (table II). Axial computed tomography was performed done in two patients: a) in one case to exclude osteitis condensens ilii, and b) in the other case to exclude septic arthritis. The severity of the sacroiliac damage was related with a longer duration of the inflammatory bowel disease.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Articular and extraarticular involvement in inflammatory bowel diseases]. 829 15

Yersinia enterocolitica infection in humans causes a broad spectrum of diseases ranging from acute bowel disease to extraintestinal manifestations such as reactive arthritis, erythema nodosum and uveitis. During the last decade a fascinating part of the molecular biology of the pathogenicity of human pathogenic Yersinia species has been unraveled. Pathogenicity factors such as protein tyrosine phosphatase, protein kinase, thrombin- and collagen-binding factors have been identified and characterized on the molecular level. In contrast to many animal models for human enteropathogenic microorganisms, experimental Y. enterocolitica infection in rodents resembles yersiniosis in humans and thus offers extraordinary opportunities to study the sequential steps of the infectious process. Rabbits are suitable animals in which to study Yersinia-induced enteritis (enterotoxin-mediated) and the humoral immune response after oral infection. The role of Peyer's patches (PP) in the entry of enteropathogenic Yersinia species has been elucidated in mice and rabbits. M cells are probably the primary target cells of invading Yersiniae. Surprisingly, after penetration of the mucosal epithelial cell layer Yersinia bacilli were visualized to be exclusively extracellular in PP tissue. Obviously neutrophils within PP were unable to phagocytize the invading microorganisms. Presently, it is not clear how the microorganisms disseminate from PP into lymph nodes, spleen, liver and lung of mice where they form abscesses and granuloma-like lesions. Immunohistologically the involvement of macrophages and T cells could be demonstrated in Yersinia-induced lesions of mice. Direct evidence for the role of T cells and cytokine-activated macrophages in the host defense reaction against a primary Yersinia infection in mice could be obtained from experiments including adoptive transfer of Yersinia-specific T cells and in vivo neutralization of TNF-alpha and IFN-gamma. The experimental rat model turned out to be a suitable model for studying Yersinia-induced aseptic arthritis. Lewis- and SHR rats proved to be arthritis-susceptible. Arthritogenicity of Yersinia for rats appeared to be restricted to Y. enterocolitica of serotype 08 and correlated with the virulence potential of this serotype. Surprisingly, expression of YadA, the collagen-binding factor, was not necessary for arthritis induction. A close association between both susceptibility to arthritis induction and Yersinia infection could be demonstrated in various rat strains. Depletion of alpha/beta T-cell receptor (alpha beta-TCR)-positive T cells by treatment with alpha beta-TCR-specific antibody revealed that T cells were required for clearance of the pathogen.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Experimental Yersinia enterocolitica infection in rodents: a model for human yersiniosis. 836 22

Inflammatory bowel disease may be associated with a variety of rheumatologic abnormalities. The patterns of described enteropathic arthritis, not associated with the HLA B27 antigen, include non-deforming peripheral arthritis, bilateral, symmetric sacroiliitis, an on occasion, destructive monoarthritis. We report three patients with Crohn's disease and patterns of joint disease that have not been previously described. The patients ranged in age from 16 to 31 yr. In all cases, both joint and bowel disease were present since childhood. Antinuclear antibody, rheumatoid factor, and HLA B27 antigen determinations were negative. The distribution and pattern of joint disease were similar to that seen in rheumatoid arthritis. We propose that these cases do not represent coincident rheumatoid arthritis and Crohn's disease, but, rather, atypical manifestations of enteropathic arthritis.
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PMID:Atypical arthropathy associated with Crohn's disease. 850 95

There is great interest in the association between intestinal inflammation and the various arthropathies. However, most studies assessing intestinal function in these diseases are confounded by the fact that non-steroidal anti-inflammatory drugs (NSAIDs) have profound effects on the small intestine. Hence NSAIDs cause quite distinct and severe biochemical damage during drug absorption (uncoupling of mitochondrial oxidative phosphorylation proving to be most important) which results in increased intestinal permeability. All commonly used NSAIDs, apart from aspirin and nabumetone, are associated with increased intestinal permeability in man. Whilst reversible in the short term, it may take months to improve following prolonged NSAID use. Increased intestinal permeability appears to be the central mechanism of converting the biochemical damage to an inflammatory tissue reaction (NSAID enteropathy). The inflammatory enteropathy is not, however, unique to NSAIDs but similar changes are found with other permeability breakers. In intestinal infections and in diseases associated with reduced mucosal defence, suggesting that the small intestinal inflammation represents a common final pathway for a number of intestinal injuries. Spondylarthropathies are associated with a high prevalence of terminal ileitis, but as most patients have been receiving NSAIDs it has been difficult to dissociate the effects of NSAIDs on intestinal function from that of the ileitis itself. Nevertheless, two studies suggest that increased intestinal permeability in spondylarthropathies occur independently of NSAID ingestion. Whilst these findings may have implications for the development of arthritis, the permeability changes in spondylarthropathy do not differ quantitatively or qualitatively from that of NSAIDs or other permeability breakers. NSAID enteropathy can be differentiated from spondylarthropathic enteropathy by differences in location of disease and lack of predilection of certain HLA types. However, as the two may coexist both enteroscopy and ileocolonoscopy may be necessary for this distinction.
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PMID:Influence of anti-rheumatic drugs on gut permeability and on the gut associated lymphoid tissue. 867 46

The four seronegative spondyloarthropathies can be divided into two main groups by their pattern of sacroiliitis and spondylitis (Table 1). The axial skeletal changes of ankylosing spondylitis and enteropathic arthropathy are often indistinguishable, as are those of psoriatic arthritis and Reiter's syndrome. Early proximal appendicular joint involvement in ankylosing spondylitis is a poor prognostic sign except in women where peripheral arthritis is more common, but has a more benign course. Peripheral joint destruction in enteropathic arthropathy is rare because treatment of the bowel disease also treats the arthritis. Distal appendicular involvement is characteristic of psoriatic arthritis and Reiter's syndrome. Proliferative erosions and enthesitis, periostitis, and normal mineralization aid in differentiating psoriatic arthritis and Reiter's syndrome from rheumatoid arthritis. The distribution of arthritis also differs from that seen in classic rheumatoid arthritis, with asymmetry and involvement of the distal interphalangeal joints more common in psoriatic disease and Reiter's syndrome.
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PMID:The seronegative spondyloarthropathies. 882 66


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