Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P50583 (asymmetrical)
 12,197 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Reactive arthritis following infection with Yersinia is endemic in Scandinavian countries; the prevalence is low in the UK, however. We have reviewed the literature pertaining to Yersinia-related reactive arthritis in the UK and describe 12 patients who presented over a 3-year period with an asymmetrical seronegative polyarthropathy and serological evidence of recent Yersinia infection. Five patients recalled having a diarrhoeal illness prior to the onset of the arthropathy. None had a prior history of psoriasis, inflammatory bowel disease or ankylosing spondylitis. A history of urethral discharge was elicited from one patient. Extra-articular manifestations were seen in three patients (iritis in two, erythema nodosum in another). Four patients developed chronic joint disease after periods of 4, 6, 8, and 18 months, respectively. The prevalence of Yersinia-related arthritis in the UK may be higher than previously thought.
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PMID:Yersinia-related arthritis in the United Kingdom. A report of 12 cases and review of the literature. 148 36

In an open study, sulfasalazine was given to 15 HLA-B27 positive patients with asymmetrical pauciarticular arthritis and enthesopathies resistant to nonsteroidal antiinflammatory drugs (NSAID). In 11 patients, long lasting remission of inflammatory and biological variables was obtained after 3 to 12 months of treatment. In the other 4 patients significant improvement of the clinical and biological variables was observed. In the 7 patients on whom ileocolonoscopy was performed, inflammatory signs were seen in the terminal ileum or ileocecal valve, suggestive of inflammatory bowel disease (IBD). It is generally accepted that sulfasalazine improves the intestinal symptoms of IBD; our study suggests that it is also beneficial in HLA-B27 related arthropathies resistant to NSAID. No significant adverse reactions were encountered. These findings are encouraging but have to be confirmed in a double blind controlled study.
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PMID:HLA-B27 related arthritis and bowel inflammation. Part 1. Sulfasalazine (salazopyrin) in HLA-B27 related reactive arthritis. 286 76

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

Mild arthritis/arthralgia is the most frequent extraintestinal manifestation in inflammatory bowel disease (IBD) and has been reported to occur in 10-35% of patients in different studies. A classification of peripheral arthropathy in relation to inflammatory bowel disease has recently been proposed. Type 1: pauciarticular, asymmetrical, preferably large joints, and related to IBD activity. Type 2: polyarticular, symmetrical, preferably small joints, and occurring independently of IBD activity. While this classification requires the presence of synovitis, arthralgia without swelling or other objective signs are of equal frequency but are not covered by this system. In this issue of the journal, Thomas et al. report a prospective study, incorporating strict endoscopic and histological criteria for pouchitis, which elucidates the correlation to arthropathy. Both pouchitis and symptoms of the joints occurred more frequently in ulcerative colitis patients than in patients with familial polyposis. Surprisingly, arthropathy was not more frequent among patients with pouchitis than among patients without pouchitis in this study. Extraintestinal manifestations of the joints are thus not likely to be a reactive arthritis secondary to pouchitis, which would have been an obvious explanation. Preoperative occurrence of extraintestinal manifestations from the joints does not seem to be predictive for the outcome of an ileo-anal pouch anastomosis and especially development of pouchitis. The arthritic symptoms were generally mild and not disabling.
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PMID:Arthritis and the gut. 1050 37

Spondyloarthropathies are important and common inflammatory arthropathies that occur in approximately 2% of the population. They are often underrecognized. The diagnosis features the presence of asymmetrical, predominately lower limb arthritis and/or inflammatory back pain. The spondyloarthropathies can be subdivided into several disease subcategories, including ankylosing spondylitis, Reiter's/reactive arthritis, psoriatic arthritis, inflammatory bowel disease-associated arthritis and a large group of undifferentiated spondyloarthritis. The interactions between infectious agents and the individual's genetic background are important aetiological factors. Therapies for these conditions include physical therapy, non-steroidal anti-inflammatories and disease-modifying drugs.
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PMID:Spondyloarthropathies: an overview. 1178 74

Peripheral involvement of the joints, including pauciarticular, asymmetrical, transitory and migrating synovitis and enthesiopathy, is observed in 10-20% of affected inflammatory bowel disease patients. Recurrence is common and frequently coincides with a flare-up of intestinal disease. The true prevalence of axial involvement is less well established. Sacroiliitis is a hallmark of spondylitis, but is under-reported due to its insidious onset and sometimes asymptomatic nature. Radiographic evidence of sacroiliitis is present in about 20-25% of patients. Ankylosing spondylitis, as defined by the Rome criteria, is present in 3-10% of inflammatory bowel disease patients, and is thought to have a different genetic predisposition in these patients compared with 'classic' ankylosing spondylitis: whereas the human leucocyte antigen B27 phenotype is present in 90% of patients with 'classic' ankylosing spondylitis, the prevalence decreases to only 30% in patients with ankylosing spondylitis secondary to Crohn's disease. Polymorphisms involving CARD15 appear to be a possible genetic trigger: 78% of patients with Crohn's disease and symptomatic or asymptomatic sacroiliitis carry at least one mutation, compared with only 48% of control Crohn's disease patients. Moreover, in other forms of spondyloarthropathy, a similar association has been reported: 42% of patients with spondyloarthropathy and associated asymptomatic chronic gut inflammation, who are considered likely to develop Crohn's disease and ankylosing spondylitis, are carriers of at least one CARD15 mutation, compared with only 7% of patients with normal histology. In addition to genetic markers, clinical features support the relationship between gut and joint pathophysiology. In cases of spondyloarthropathy, a very rapid, substantial and sustained improvement in symptoms has been reported following treatment with infliximab, suggesting an essential role for tumour necrosis factor-alpha in spondyloarthropathy, similar to that observed in Crohn's disease.
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PMID:Review article: joint involvement in inflammatory bowel disease. 1535 92

The term 'spondyloarthritides' (SpA) comprises ankylosing spondylitis (AS), reactive arthritis, arthritis/spondylitis with inflammatory bowel disease, and arthritis/spondylitis with psoriasis. The main links between these diseases are an association with HLA-B27 and a similar clinical picture. Patients normally present with chronic low back pain or asymmetrical arthritis, predominantly of the lower limbs, and an overlap of these symptoms often occurs. AS is regarded as the most severe subtype. Recent attention has focused on earlier diagnosis of AS among patients with chronic low back, and this is becoming more important as effective therapies for early treatment have become available. AS is a disease of young people, normally starting in the third decade of life. The incidence and prevalence rates of AS, and of SpA as a whole, are strongly dependent and are directly correlated to the prevalence of HLA-B27 in a given population. Incidence rates of 0.5-8.2/100 000 population and prevalence rates of 0.2-1.2% have been described for AS, and about double these figures have been reported for SpA.
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PMID:Concepts and epidemiology of spondyloarthritis. 1677 73

Chronic inflammation ofmusculoskeletal structures is the most prominent disease manifestation of SpA. More specifically, the axial disease affects the spine, the sacroiliac joints and the hips. Peripheral disease includes peripheral arthritis, with a preference for asymmetrical inflammation ofjoints of the lower limbs and enthesitis, which is the presence of inflammation at the sites were ligaments and tendons attach to the bone. Additionally, SpA is often characterized by subclinical inflammation of the gut which partially resembles inflammatory bowel disease. Here, we will review the immunopathology of these different disease manifestations and relate them to clinical applications as well as emerging pathogenic concepts.
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PMID:Synovial and mucosal immunopathology in spondyloarthritis. 1973 21

Joint involvement associated with inflammatory bowel disease (IBD) belongs to the concept of spondyloarthritis (SpA) and includes two types of arthritis: a peripheral arthritis characterized by the presence of pauciarticular asymmetrical arthritis affecting preferentially joints of lower extremities and an axial arthropathy including inflammatory back pain, sacroiliitis and ankylosing spondylitis (AS). Treatment of arthritis includes a short-term use of NSAIDs associated with optimized treatment of gut inflammation. Safety concerns mean that long-term treatment with NSAIDs is best avoided if possible. Salazopyrine can be recommended for treatment of peripheral arthritis. Methotrexate and azathioprine are generally ineffective. Finally, efficacy of anti-TNF therapy (infliximab and adalimumab) is well established. However, use of etanercept is not recommended because of the increased risk for intestinal disease relapse. Pathogenesis of gut-joint iteropathy is not elucidated. Both inflammations are tightly related as suggested by human evidence of gut inflammation in patients with other forms of SpA and animal evidence of gut and joint inflammation in HLA-B27/human beta(2)-microglobulin transgenic rat model and TNF(DeltaARE) mice. Several clues for the linkage between gut and joint inflammation have been put forward including an altered recognition and handling of bacterial antigens, an aberrant trafficking of CD8+ T cells with an impaired T-helper type 1 cytokine profile and expression of aEb7 integrin, an altered trafficking of macrophages expressing CD163 and evidence of an increased angiogenesis. A transcriptome analysis of mucosal biopsies identified a set of 95 genes that are differentially expressed in both CD and SpA as compared with healthy controls suggesting common pathways. TNF plays a key role in the pathogenesis of various arthritic diseases and IBD. Mesenchymal/myofibroblast-like cells may represent the local primary targets of TNF in the induction of gut and joint pathology. Selective expression of TNFRI on these cells seems to be sufficient to orchestrate the complete development of SpA-related pathologies at least in TNF(DeltaARE) mice. Finally, genetic susceptibility is probably required to develop these pathologies. Genotyping of AS patients provided evidence for an important overlap between determinants of inherited predisposition to CD and AS. The best documented common association is with an IL-23R polymorphism, although the exact role remains unexplored. In addition, evidence suggests that a number of recently identified CD-susceptibility loci are associated with AS. Clinical, genetical, immunological and therapeutic evidence support the tight junction between gut and joint inflammation in two linked diseases, IBD and SpA, belonging to the 'immune-mediated inflammatory diseases'.
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PMID:Joint involvement associated with inflammatory bowel disease. 1989 67

Stem cell research is a innovative technology that focuses on using undifferentiated cells able to self-renew through the asymmetrical or symmetrical divisions. Three types of stem cells have been studied in laboratory including embryonic stem cell, adult stem cells and induced pluripotent stem cells. Embryonic stem cells are pluripotent stem cells derived from the inner cell mass and it can give rise to any fetal or adult cell type. Adult stem cells are multipotent, have the ability to differentiate into a limited number of specialized cell types, and have been obtained from the bone marrow, umbilical cord blood, placenta and adipose tissue. Stem cell therapy is the most promising therapy for several degenerative and devastating diseases including digestive tract disease such as liver failure, inflammatory bowel disease, Celiac sprue, and pancreatitis. Further understanding of biological properties of stem cells will lead to safe and successful stem cell therapies. (Korean J Gastroenterol 2011;58: 125-132).
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PMID:[Stem cell properties of therapeutic potential]. 2196 99


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