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)

The majority of ankylosing spondylitis (AS) patients not only possess HLA-B27, but during active phases of the disease have elevated levels of total serum IgA, suggesting that a microbe from the bowel flora is acting across the gut mucosa. Biochemical studies have revealed that Klebsiella bacteria, not only possess 2 molecules carrying sequences resembling HLA-B27 but increased quantities of such microbes are found in fecal samples obtained from AS patients and such patients have Crohn's like lesions in the ileo-caecal regions of the gut. Furthermore AS patients from 10 different countries have been found to have elevated levels of specific antibodies against Klebsiella bacteria. It has been suggested that these Klebsiella microbes, found in the bowel flora, might be the trigger factors in this disease and therefore reduction in the size of the bowel flora could be of benefit in the treatment of AS patients. Microbes from the bowel flora depend on dietary starch for their growth and therefore a reduction in starch intake might be beneficial in AS patients. A "low starch diet" involving a reduced intake of "bread, potatoes, cakes and pasta" has been devised and tested in healthy control subjects and AS patients. The "low starch diet" leads to a reduction of total serum IgA in both healthy controls as well as patients, and furthermore to a decrease in inflammation and symptoms in the AS patients. The role of a "low starch diet" in the management of AS requires further evaluation.
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PMID:The use of a low starch diet in the treatment of patients suffering from ankylosing spondylitis. 883 6

The association of HLA-B27 with ankylosing spondylitis (AS), first described more than 20 years ago, triggered intensive research all over the world. AS is a disease model to study the interplay between genetic, immunologic, and environmental factors in the induction of rheumatic disease. Over the past years, substantial advances have taken place in the area of the molecular and cellular immunology of the HLA-B27 molecule, HLA-B27 subtype polymorphism, peptide binding and presentation to cytotoxic T cells, and their relevance to disease. New insights into the pathogenesis of the spondylarthropathies come from the development of animal models, namely HLA-B27/human beta 2-microglobulin transgenic rats, and HLA-B27 transgenic, beta 2-microglobulin knock-out mice. The role of gram-negative bacteria and gut inflammation in the development of ankylosing spondylitis continues to be the focus of interest in many studies. In this review, recent hypotheses of the pathogenesis of AS and its relationship to HLA-B27 are discussed.
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PMID:[New aspects in the pathogenesis of Bechterew disease]. 886 46

To determine the prevalence of morphologic bowel lesions in patients with inflammatory rheumatic diseases and to better define the interactions between intestinal and articular pathology, 177 patients [39 with reactive arthritis (ReA), 40 with psoriatic arthritis (PsA), 23 with ankylosing spondylitis (AS), 21 with undifferentiated spondyloarthropathy (USpA) and 54 with rheumatoid arthritis (RA)] underwent ileocolonoscopy followed by multiple biopsies of the large bowel and the ileum and ileocecal valve. Biopsies were then examined with light and electron microscopy. During the endoscopic examination various degrees of gut inflammation were observed in 13% of ReA, 5% of PsA, 26% of AS, 14% of USpA and 11% of RA patients. At the histological examination those percentages were respectively 51%, 45%, 48%, 38%, and 15%, and at the electron microscopic examination 76%, 53%, 90%, 60%, and 50%. Our results show that an involvement of the gut is a factor in a large percentage of patients with spondyloarthropathy and, to a lesser extent, with RA. The involvement of the intestine in RA manifests itself mainly in ultrastructural lesions, thus this involvement is not so obvious as in the spondyloarthropathies; however, it could nonetheless play an important role in the etiopathogenesis of this disease.
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PMID:Intestinal histological and ultrastructural inflammatory changes in spondyloarthropathy and rheumatoid arthritis. 913 22

We investigated the frequency of gut inflammation and the role of gut lesion in the pathogenesis of the ankylosing spondylitis (AS) in Korean patients. Ileocolonoscopy and biopsy of the colon and terminal ileum were performed on 24 Korean patients with AS. Endoscopic lesions were observed in 7 patients (29.2%). The lesions were found more often in the terminal ileum (6/7) than in the colon (1/7). Histologic signs of gut inflammation were detected in 14 patients (58.3%), acute lesions in 2 patients (8.3%) and chronic lesions in 12 patients (50%). Gut inflammation were as frequently found in Korean patients with AS as in Western patients. These findings suggest that gut inflammation may play a role in the pathogenesis of AS in Korean patients as it does in Western patients.
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PMID:Ileocolonoscopic and histologic studies of Korean patients with ankylosing spondylitis. 943 10

In the pathogenesis of spondyloarthropathies, infection and gut inflammation are the most important external triggering factors. Early antimicrobial therapy to treat urethritis caused by Chlamydia trachomatis is effective in preventing a recurrent reactive arthritis. When the arthritis appear, a short term conventional antimicrobial therapy is unable to modify its course. In acute chlamydia arthritis, patients benefit from a prolonged (3-month) treatment with tetracycline, while such a treatment has not proved to be effective in enteroarthritis or in chronic forms of reactive arthritis. The role of sulfasalazine in the treatment of patients with spondyloarthropathies is controversial. It might modify the disease course during acute and chronic reactive arthritis, and is working for patients with ankylosing spondylitis, especially patients with peripheral arthritis. Data showing an effect of sulfasalazine in the prevention of chronic spondyloarthropathy or in modification of the long-term prognosis of ankylosing spondylitis are, however, lacking.
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PMID:Therapeutic aspects of spondyloarthropathies -- a review. 980 93

Prognosis in the majority of patients with acute reactive arthritis is usually good, with most patients recovering in a few months. In about 15% to 30% of such patients, the disease progresses, and spondyloarthropathy and even ankylosing spondylitis develop in the following 10 to 20 years. A recurrent attack of reactive arthritis is common in patients with chlamydia-triggered arthritis, but it is rare in patients who have had enteroarthritis. In patients with chronic spondyloarthropathy without evidence of preceding infection, the disease can progress slowly into ankylosing spondylitis. When reactive chlamydia arthritis is indicated, a prolonged course of antibiotics is needed. For other forms of reactive arthritis, solid evidence in favor of antibiotic therapy is still lacking. Presence of hip pain, decreased mobility of thoracic cervical or thoracic spine, heel pain, inflammatory gut lesions, high erythrocyte sedimentation rate, positive family history, and presence of human leukocyte antigen B27 are indicators for chronicity. Sulfasalazine might be of use in chronic arthritis and ankylosing spondylitis, especially if the patient has peripheral arthritis.
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PMID:Prognosis, course of disease, and treatment of the spondyloarthropathies. 989 8

Eye inflammation, especially uveitis, is a prominent feature of spondyloarthropathies. Uveitis associated with ankylosing spondylitis and Reiter's syndrome usually is a unilateral acute anterior uveitis with a high tendency to recur sometimes in the contralateral eye. Uveitis associated with undifferentiated spondyloarthropathy, inflammatory bowel disease, and psoriasis may be less characteristic in its presentation, with a higher tendency to posterior pole involvement, bilaterality, and chronicity. Although acute anterior uveitis is grouped into the spectrum of human leukocyte antigen B27-related disease, other genetic and environmental factors including infections by gram-negative bacteria and gut inflammation can play a role in its pathogenesis. The prognosis of uveitis usually is excellent with topical treatment, and only those with posterior pole involvement or a high tendency to recur or to chronicity might benefit from immunosuppressive therapy.
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PMID:Eye involvement in the spondyloarthropathies. 989 10

A growing body of evidence suggests that T lymphocytes play an important role in initiating and maintaining the inflammatory process characteristic of the human leukocyte antigen (HLA)-B27-associated spondyloarthropathies. T cells seem to be involved in the primary defense reaction against arthritis-triggering gram-negative bacteria at the site of extra-articular infection, in determining the systemic cytokine pattern, in the recirculation process between gut mucosa and the joint, and in mediating secondary autoimmune joint inflammation. The factors involved in disease chronicity (namely in ankylosing spondylitis and psoriatic arthritis) are still unknown. Autoreactive T cells may contribute to this process by recognition of cross-reactive self-epitopes (ie, molecular mimicry between bacterial and self-antigens). Autoreactive T cells may as well be inappropriately upregulated by bacterial superantigens, or by local inflammatory reactions leading to the uncovering of former cryptic self-epitopes. In this paper, we review recent studies on peripheral blood and synovial T cells in patients with reactive arthritis, enteropathic spondyloarthropathy, psoriatic arthritis, and ankylosing spondylitis.
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PMID:T-cell studies in the spondyloarthropathies. 1112 74

Spondyloarthropathies (SpA) are a group of related disorders. The hallmark symptoms include spondylitis, pauci-articular synovitis and enthesiopathy. In an important number of cases, subclinical gut inflammation with pathological findings resembling Crohn's disease can be found. Some of these patients may eventually develop overt Crohn's disease. Conventional medical therapy in patients with SpA consists of non-steroidal anti-inflammatory drugs (NSAIDs). Sulphasalazin can be co-administered, especially in cases of chronic synovitis or enthesiopathy. Recently, experience with anti-TNF-alpha monoclonal antibodies (infliximab), a new class of biological compounds, has opened new avenues for treating patients with SpA. In particular, infliximab used in two open studies gave significant benefit on the locomotor manifestations in patients with Crohn's disease, in patients with ankylosing spondylitis, undifferentiated SpA and psoriatic arthritis. Etanercept, another TNF-alpha antagonist (soluble receptor), was shown to induce benefit in a placebo-controlled study in patients with psoriatic arthritis. The relationship between SpA and inflammatory bowel disease lead to the hypothesis that interfering with gut inflammation in patients with SpA would yield a potential target for modulating the synovitis in these patients. Thus, besides TNF-alpha blockade, other strategies with potential efficacy can be envisioned, such as IL-10, ICAM-1 antisense or anti-(4)beta(7) antibodies.
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PMID:Current use of biologicals for the treatment of spondyloarthropathies. 1133 71

Tumor necrosis factor-alpha is a major effector and regulatory cytokine, which seems to have an outstanding position in rheumatic and other inflammatory states. Because TNF-alpha has been detected in the inflamed gut and sacroiliac joints of patients with chronic inflammatory bowel diseases and spondyloarthritides, like ankylosing spondylitis, there was need for studies of the efficacy of the modern biologic anti-TNF agents infliximab and etanercept in these diseases. Infliximab is approved for the treatment of Crohn disease. In addition, there are now also positive data for infliximab in the treatment of ankylosing spondylitis and for etanercept and infliximab in the treatment of psoriatic arthritis.
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PMID:New treatment options in spondyloarthropathies: increasing evidence for significant efficacy of anti-tumor necrosis factor therapy. 1155 23


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