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)

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

Ankylosing spondylitis and reactive arthritis are seronegative spondyloarthropathies, which are strongly associated with HLA-B27. Despite intensive investigation, the basis for this association is not clear. However, in recent years one favored hypothesis to explain this linkage has been that of molecular mimicry, i.e., sharing of linear or conformational epitopes common to microbial antigens and host structures. During the past few years several examples of molecular mimicry between HLA-B27 and microbial antigens have been described. Heat shock proteins, among others, have been considered as target candidates for autoimmune phenomena, because of the high degree of homology between bacterial and mammalian species. Reactive arthritis triggered by Yersinia or Salmonella provides a unique model for studying the pathogenetic mechanisms underlying human inflammatory joint diseases in general, because the arthritogenic microbes are known and well-characterized. We have described two bacterial proteins that share amino acid homology with HLA-B27, namely YadA (Yersinia adhesin) and OmpH, outer surface proteins of Yersinia and Salmonella, respectively. Notably, the area of identity of these amino acid sequences is located in the same place on the HLA-B27 molecule as a hexapeptide identical between Klebsiella nitrogenase and HLA-B27, and a pentapeptide shared by a Shigella flexneri protein and HLA-B27. We have investigated immune responses to a panel of synthetic peptides based on the HLA-B27-homologous portions of pathogen-specific antigens in patients with reactive arthritis and ankylosing spondylitis. One third of the patients have antibodies to the synthetic peptides. However, instead of recognizing the HLA-B27-homologous portion, the antibodies are directed against the flanking sequences of the synthetic peptides. The concept of the role of molecular mimicry between HLA-B27 and microbial antigens in the pathogenesis of spondyloarthropathies is discussed, with a conclusion that no convincing evidence for its significance exists at the present.
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PMID:Molecular mimicry: any role in the pathogenesis of spondyloarthropathies? 750 16

Reactive arthritis following infection with enteropathogenic bacteria is usually a self-limiting disease that disappears after a few months without sequela. We describe two girls who developed carditis shortly after the onset of reactive arthritis due to infection with Salmonella enteritidis. The carditis presented with fatigue and arrhythmia and involved the aortic valve in both patients leading to definite aortic regurgitation in one. A similar pattern of cardiac involvement is found in other spondyloarthropathies, including Reiter's syndrome and ankylosing spondylitis. We conclude that Salmonella reactive arthritis may be complicated by carditis.
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PMID:Reactive arthritis due to Salmonella enteritidis complicated by carditis. 784 47

Reactive arthritis is caused by an infection, and components of the triggering agent can be demonstrated at the site of inflammation. This fact has opened new views in studies regarding other rheumatic diseases, such as rheumatoid arthritis and ankylosing spondylitis. The possible role of infectious agents in their etiology and pathogenesis is being re-evaluated.
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PMID:Infection and arthritis. 794 42

The generally reported prevalence of 0.1% to 0.2% for ankylosing spondylitis in the white population is probably too low, because it is based almost entirely on hospital records. The incidence and clinical presentation of ankylosing spondylitis have not changed during the past few decades. For reactive arthritis, the list of microbes recognized as triggering agents is continuously increasing. Reactive arthritis is divided into urogenic, enterogenic, respiratory tract-associated, and idiopathic arthritides. In addition, several microbial diseases may be accompanied by reactive arthritis, even though the identity of the causative agent is not always known. In the diagnosis of the spondyloarthropathies, definite progress has been made in developing classification criteria. Intensive research is going on to evaluate new therapies, with special attention to the use of antimicrobial agents for the treatment of reactive arthritis.
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PMID:Epidemiologic aspects, clinical features, and management of ankylosing spondylitis and reactive arthritis. 806 6

Whereas it is clear that HLA-B27 is increased in many North American natives, the prevalence varies a great deal. There is still a paucity of data on a large number of tribes. There is, however, a suggestion that HLA-B27 positive prevalence follows cultural/linguistic groupings. Reactive arthritis, sacroiliitis, and ankylosing spondylitis also appear to be increased in these people, but their relationship to HLA-B27 and possibly additional genetic predisposing factors is far from clear. Given these data and the known association of infectious agents, more extensive studies are warranted, especially in those tribes with a large enough population to achieve statistical significance.
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PMID:Arthritis and HLA-B27 in native North American tribes. 972 93

Reactive arthritis (ReA) is an aseptic form of articular inflammation induced by infections mainly localised in the gastrointestinal (enteroarthritis) or urogenital (uroarthritis) tracts. The bacteria principally involved as causative agents are Chlamydia, Salmonella, Shigella, Campylobacter and Yersinia. The clinical picture is usually characterised by a mono-oligoarthritis of the lower limbs. Axial involvement is possible and extra-articular manifestations such as enthesitis, tenosynovitis, bursitis and dactylitis are frequent. NSAIDs and sulfasalazine are still the drugs most commonly used in the treatment of ReA. Steroids are administered when inflammatory symptoms are resistant to NSAIDs. Experiences with other DMARDs (disease modifying antirheumatic drugs) such as azathioprine, methotrexate and cyclosporin, have been sporadically reported and they can be employed in patients that are unresponsive to the more usual medicaments. The intake of antibacterials (tetracyclines) may be useful in uroarthritis but have not been so successful in enteroarthrits. In more aggressive cases, or when ReA evolves towards ankylosing spondylitis, TNF-alpha blockers could represent an effective choice.
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PMID:Management of reactive arthritis. 1468 Apr 36

Reactive arthritis (ReA) occurs after a preceding bacterial infection of the urogenital or gastroenteral tract. The bacteria triggering ReA persist in vivo and seem to be responsible for triggering an immune response. A cytokine imbalance with a relative lack of T-helper 1 cytokines may play an important role allowing these bacteria to survive. This seems to be relevant for manifestation and chronicity of the arthritis. For the chronic cases and cases evolving into ankylosing spondylitis, the interaction between bacteria and human leukocyte antigen B27 plays an additional crucial role. Among others, the arthritogenic peptide hypothesis is one way to explain this association. Human leukocyte antigen B27-restricted peptides from Yersinia and Chlamydia, which are stimulatory for CD8+ T cells derived from patients with ReA, have been identified. The exact role of such peptides for the pathogenesis of ReA and other spondyloarthritides still has to be defined.
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PMID:Disease mechanisms in reactive arthritis. 1501 41

Reactive arthritis are definied as steriles arthropathies using classic bacteriological techniques. They are due to extra articular infection and are often associated with HLA B27. The outcome of these arthritis is characterised by the recurrence of flares with sometimes appearition of ankylosing spondylitis. The pathogenesis of reactive arthritis is modified when bacterial antigens or alive micro-organisms are discovered in involved joints. Several current works have underlined the interest of antibiotic therapy in the chlamydial reactive arthritis. Chronic forms can justify the use of anti-rheumatic drugs such as salazopyrine.
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PMID:[Reactive arthritis]. 1582 6

Ankylosing spondylitis is the prototype of related diseases commonly called spondylarthropathies which include reactive arthritis, psoriatic arthritis, arthritis associated with inflammatory bowel diseases (enteropathic arthritis) and undifferentiated spondylarthropathies. Ankylosing spondylitis and spondylarthropathies are generally observed in young patients but can be observed later in life or in persons >50 years of age. All the spondylarthropathy subgroups are represented in the elderly with some features particular to this age group. Indeed, radiological aspects of ankylosing spondylitis may be difficult to interpret because of the radiological changes induced by aging. Late-onset peripheral spondylarthropathies are characterised by severe disease, marked elevation of laboratory parameters of inflammation, oligoarthritis involving the lower limbs and oedema of the extremities. Psoriatic arthritis is more severe in the elderly and is associated with worse outcomes than in young patients. The clinical presentation of undifferentiated spondylarthropathy is as varied in the elderly as in young and middle-aged adults. Reactive arthritis and enteropathic arthritis are observed in the elderly more rarely. The effects of aging on drug metabolism and pharmacokinetics, together with the existence of co-morbidities and polypharmacy, are responsible for difficulties in the therapeutic management of late-onset ankylosing spondylitis or spondylarthropathies. Indeed, NSAIDs should be used with caution in older patients because of the high risk of serious gastrointestinal complications. Sulfasalazine and methotrexate have been used as disease-controlling drugs but did not prove very effective. Pamidronate and tumour necrosis factor (TNF)-alpha antagonists offer a therapeutic alternative but have not been specifically tested in the elderly. Pamidronate has been tested in young-onset ankylosing spondylitis and spondylarthropathies with conflicting results but can be used in older patients without risk of major adverse effects. TNFalpha antagonists have been adequately evaluated in ankylosing spondylitis and spondylarthropathies and are associated with dramatic improvement in clinical and biological parameters of disease activity. However, the safety profile of these agents in the elderly is not currently known and careful surveillance, in particular for the risk of infection such as tuberculosis, and/or exacerbation of chronic heart failure, is thus required when using these drugs in this age group.
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PMID:Late-onset ankylosing spondylitis and related spondylarthropathies: clinical and radiological characteristics and pharmacological treatment options. 1597 37


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