Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01889 (ankylosing spondylitis)
 5,717 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Serum titres of IgA are raised in ankylosing spondylitis and increased titres of antibodies to klebsiella have also been reported. The humoral response was investigated in ankylosing spondylitis and other inflammatory disorders. IgA antibodies to klebsiella pneumoniae K43 were measured in patients with ankylosing spondylitis, Crohn's disease, ulcerative colitis, and rheumatoid arthritis and in controls. Significantly raised median titres of anti-klebsiella IgA, measured as optical density at 405 nm with an enzyme linked immunosorbent assay (ELISA), were seen among the patients with ankylosing spondylitis (0.7), Crohn's disease (0.8), rheumatoid arthritis (0.6), and ulcerative colitis (0.8) compared with controls (0.4). Activity of disease in ankylosing spondylitis and titres of anti-klebsiella IgA were not correlated. In contrast, titres of anti-klebsiella IgM were significantly lower in patients with ankylosing spondylitis and ulcerative colitis. The increase in the titres of anti-klebsiella IgA may be due to increased permeability of the gut to bacterial antigens, leading to an increased IgA response in the gut mucosa and permitting the release of IgA into the circulation. As the increased antibody titres were seen in Crohn's disease and rheumatoid arthritis as well as in ankylosing spondylitis the response may be nonspecific, occurring because of possible underlying inflammatory bowel disease in these conditions.
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PMID:Raised titres of anti-klebsiella IgA in ankylosing spondylitis, rheumatoid arthritis, and inflammatory bowel disease. 313 77

We measured the amount of plasma endotoxin in 95 patients with inflammatory rheumatic diseases (42 with ankylosing spondylitis; 12 with possible ankylosing spondylitis; 41 with rheumatoid arthritis) and in 16 patients with Crohn's disease with a quantitative Limulus assay. Significantly increased mean values were found in inflammatory rheumatic diseases and in Crohn's disease. Between 31% and 50% of the patients had endotoxin values higher than 10 pg/ml--none of the controls had such values. Patients on regular treatment with NSAIDS had higher amounts of endotoxin again. From our results we discuss an intestinal involvement in inflammatory rheumatic diseases. An inflammation of the gut with an increased permeability seems to be responsible for the raised plasma endotoxin levels compared to healthy controls. NSAIDs probably contribute to the increased permeability of the gut.
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PMID:[Determination of endotoxin in inflammatory rheumatic diseases--the effect of nonsteroidal anti-inflammatory agents on intestinal permeability]. 321 62

In 40 distal ileal and 40 colonic biopsies of arthritic patients mostly without gastrointestinal symptoms, but with histological evidence of acute or chronic inflammation of the gut, the number of immunoglobulin (Ig) containing plasma cells was studied morphometrically using a peroxidase antiperoxidase technique. Compared with controls, the ileal mucosal biopsies showed an increase of IgA and IgG in acute ileitis. In chronic ileitis there was an increase of IgA, IgG, and IgM similar to Crohn's disease. In colonic biopsies there was a significant increase of all immunoglobulin classes in acute inflammation. In chronic inflamed mucosa there was also an increase of all three Ig classes. The Ig distribution, however, was significantly different in acute and chronic colitis. These findings give immunohistochemical evidence of the existence of two different types of inflammation related to reactive arthritis or the peripheral joint involvement of ankylosing spondylitis. The Ig pattern in acute colitis is similar to that found in infectious colitis, suggesting an enterobacterial origin of the arthritis in this group of patients although bacteriological and serological investigations were negative. In the chronic type of arthritis related ileocolitis, the pattern of Ig containing cells is similar to that found in Crohn's disease but different from infectious and ulcerative colitis, which makes the hypothesis that a great number of these arthritis patients suffer from asymptomatic or subclinical Crohn's disease acceptable.
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PMID:Immunoglobulin containing cells in terminal ileum and colorectum of patients with arthritis related gut inflammation. 339 65

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

Ileocolonoscopy and microscopic examination of ileum biopsies were performed on 35 patients with reactive arthritis, with asymmetrical pauciarticular arthritis and enthesopathies. Ileocolonoscopy was also performed on 26 patients with ankylosing spondylitis (AS) and on 19 control patients with rheumatoid arthritis, juvenile chronic arthritis, systemic lupus erythematosus and psoriatic arthritis. In the reactive group, ileocolonoscopy showed macroscopic inflammation in 16 cases and abnormal microscopic examination in all but 2 cases, even in patients without gastrointestinal disorders. In the 2 patients with sexually acquired disease, the gut was normal. In the AS group, inflammation was observed in the B27 negative and positive patients with peripheral joint involvement. Occasionally, ileal signs were seen in the HLA-B27 positive patients without peripheral joint involvement. None of the controls showed signs of gut inflammation. Ilecolonoscopy may be of value in detecting subclinical forms of bowel inflammation.
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PMID:HLA-B27 related arthritis and bowel inflammation. Part 2. Ileocolonoscopy and bowel histology in patients with HLA-B27 related arthritis. 387 21

Forty-five strains of Y enterocolitica including eleven from ankylosing spondylitis patients were examined for their ability to invade Hep-2 cells in culture. Nineteen out of twenty pathogenic strains were invasive and the rest were non-invasive. Three pathogenic strains were invasive, and three non-pathogenic strains were not invasive to human foetal gut. Invasiveness was not found to be useful for differentiating ankylosing spondylitis from non-ankylosing spondylitis strains.
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PMID:Observations on the action of strains of Yersinia enterocolitica from various sources on Hep-2 cells and human foetal gut. 409 67

Ileocolonoscopy and microscopic examination of ileum biopsies have been performed on patients with reactive synovitis, ankylosing spondylitis (AS) and on a control group. Histological signs of gut inflammation were present in practically all patients with reactive synovitis, with the exception of the patients with sexually-acquired disease. In the AS group, inflammation of the ileum was observed in the HLA-B27 negative patients and in AS B27 positive patients with peripheral joint involvement. Occasionally, changes of the ileum were seen in the B27 positive AS patients without peripheral joint involvement. Signs of gut inflammation were absent in all controls. These data suggest that chronic inflammation of the ileum could be implicated in the pathogenesis of some cases of reactive synovitis and even in the peripheral joint involvement frequently seen in ankylosing spondylitis. In the second part of the study, sulfasalazine (Salazopyrin) was administered to 15 HLA-B27 positive patients with reactive synovitis, who had failed to respond to non-steroidal anti-inflammatory drugs. In 11 of the 15 patients, a clinical and biological remission occurred 3 to 11 months after the start of sulfasalazine treatment. The frequency of spontaneous remissions in reactive synovitis calls for confirmation of these encouraging results in double-blind controlled studies.
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PMID:Macroscopic and histological changes of the ileum HLA-B27 related diseases: therapeutic consequences. 615 38

Serum immunoglobulins were measured in 122 patients with ankylosing spondylitis (AS) during various phases of disease activity and compared to those in 58 healthy subjects. The mean serum IgA was 38% higher in patients (306.9 mg/dl) than in controls (222.7 mg/dl) (P < 0.005), but there was no significant difference in IgG and IgM levels. Increased IgA was associated with laboratory parameters of active inflammatory disease. The mean IgA in patients having an erythrocyte sedimentation rate (ESR) equal to or greater than 15 mm/h was 369 mg/dl, 65% higher than in controls (P < 0.001), whereas there was no significant difference between controls and patients with an ESR of less than 15 mm/h. The mean IgA in patients having a C-reactive protein (CRP) level equal to greater than 15 micrograms/ml (15 mg/l) was 387.8 mg/dl, 74% higher than in controls (P < 0.001), and again there was no significant difference between controls and patients with CRP levels less than 15 micrograms/ml. (SI conversion: g/l = mg/dl x 0.01). It is suggested that selective increase of serum IgA occurs predominantly during phases of active inflammatory disease in AS, and this finding is compatible with the concept of a microbial triggering agent acting across an IgA secreting organ such as the gut.
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PMID:Association of inflammation with raised serum IgA in ankylosing spondylitis. 745 30

An association between inflammatory bowel disease and enteroarthritis and the spondyloarthropathies has been known of for a while. Within the past few years, ileocolonic studies have expanded the diagnostic accuracy of asymptomatic gut inflammation, and it now seems evident that chronic gut inflammation is either associated with or is even the cause of chronicity of peripheral arthritis and the development of ankylosing spondylitis. This situation, previously studied in adult patients, now appears also to affect pediatric patients with spondyloarthropathies, who seem to have similar genetic and inflammatory bowel findings. Chronic infection in the gut has been demonstrated in Whipple's disease. Analogously, infection or immunologic aberrations probably contribute to chronicity in other forms of spondyloarthropathy. Infection also might be involved, at least partly in attacks of uveitis, but activation of immunologic mechanisms can mediate tissue destruction during eye inflammation.
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PMID:Enteropathic arthritis, Whipple's disease, juvenile spondyloarthropathy, and uveitis. 752 Jul 27


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