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Query: UMLS:C0003864 (arthritis)
 69,039 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Reactive arthritis is an abacterial form of arthritis that develops after infection at a site distant from the affected joint(s). The condition has long been recognised, often under the name of Reiter's syndrome. During recent years a number of research teams have published new findings concerning the pathogenesis of reactive arthritis which may also prove to be of importance for other rheumatic diseases. The clinical picture, treatment and prognosis of reactive arthritis are also discussed in the article.
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PMID:[Reactive arthritis]. 273 94

Reactive arthritis of one or more peripheral joints developed after an enteric infection with Clostridium difficile in 2 adult patients. Other reactive signs such as conjunctivitis, mucous membrane lesions and urethritis were absent. One patient had the HLA-B27 antigen. Short term followup showed a benign course of the arthritis. Three other cases of arthritis associated with C. difficile were reviewed.
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PMID:Reactive arthritis associated with Clostridium difficile enteritis. 325 87

Certain gastrointestinal tract infections can trigger reactive arthritis. The best known triggering agents are yersinia, salmonella, shigella, campylobacter jejuni, and possibly clostridium difficile. The clinical findings show a subacute onset of mono- or oligoarthritis, less often of asymmetric polyarthritis with predominance of the lower limbs. The clinical picture is somewhat modified by the genetic constitution (HLA type) of the patient. HLA-B27-positive patients appear to have more severe symptoms, extraarticular features and incomplete or complete Reiter's syndrome than HLA-B27-negative patients. Diagnosis of postenteritic reactive arthritis is based on bacteriological stool analysis and/or examination of serumantibodies to the corresponding agents. Reactive arthritis is usually self-limiting and therefore treatment of the disease has to be mainly symptomatic. Only more severe chronic or destroying arthritis is thought to be treated locally (i.e. by synoviorthesis) or by immunoregulatory drugs.
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PMID:[Reactive arthritis in enteral infections]. 332 61

Reactive arthritis is arthritis in which, although the nature of the responsible infection is known or suspected upon serological grounds, attempts at recovering the pathogen from the synovial fluid have failed. One of the main pathogenetic problems is the multiplicity of etiologic agents. Some are exogenous and may be related to the articular tropism of certain microorganisms, to immunologic depression due to an antecedent or coincident infection, and to successive reinfections by the same pathogen or by others which may promote an exacerbation of the disease. Others are endogenous and attention should be given to the local or systemic presence of an antigen as well as, in some instances, to the persistence of residual forms of infecting agents, which are more readily demonstrated with current bacteriological and serological methods. Although reactive arthritis is to be distinguished from septic arthritis, it can no longer be clearly differentiated from the classical post-infectious rheumatism. Once it has been produced, the antigenic stimulation is responsible for an immunologic response which tends to check systemic extension but may also produce tissue damage in the host. Some patients have circulating immune complexes which may bind to the joint, thereby damaging it. In other patients, particularly those who are HLA B27 positive, host-pathogen cross-reactions are demonstrated. Actually, the most frequent pathogenetic sequence seems to be a combination of two or more of these mechanisms, as there are reasons to believe that presence of the pathogen in situ is not required for the persistence of the inflammatory process. Reactive arthritis was first reported in adults following either sexually transmitted urethritis due to chlamydiae, mycoplasma or gonococci, or hepatitis B or an intestinal infection due to Yersinia, Campylobacter, Shigella, Klebsiella or Salmonella. Later, it was described in pediatric patients, particularly in Scandinavia where, for genetic reasons, the HLA B27 group is prevailing. Reactive arthritis seems less frequent in caucasian ethnic groups and above all in Latin Americans among whom HLA B27 carriers are more uncommon; however, it must be pointed out that they have not been as extensively studied and that other etiologic factors may still remain to be discovered. The course and etiology of the different forms of arthritis share certain characteristics which have been determined through a better knowledge of these conditions: onset occurs one or several weeks after a respiratory, urinary or, most often in children, digestive infection. This episode is unremarkable or latent and often overlooked.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Reactive arthritis in children]. 632 Apr 36

In 1982, 3370 cases of inflammatory rheumatism were declared. The geographical analysis of the distribution of these cases (departmental and regional) suggests that their distribution is not homogeneous throughout the country, with a predominance of psoriatic arthritis in the Midi and the Pyrenees and a predominance of rheumatic pelvispondylitis in Aquitaine. Based on the number of cases declared, we can calculate the distribution of each type of inflammatory rheumatism by age and by sex and the incidence per million inhabitants in each age group. These figures are only indicative, as the data from some departments was incomplete. The calculation of a "criterion of frequency" attempts to equalize this bias. Reactive arthritis (352 cases) represents 10.4 p. cent of all cases of inflammatory rheumatism. This large series collected over one year confirms the clinical data already established. The responsible organisms, by order of frequency, were: Chlamydia trachomatis, Yersinia enterocolitica, Shigella, Y. pseudotuberculosis and Ureaplasma urealyticum. 50 p. cent of these cases of arthritis were classified as reactive on the basis of clinical findings and history and the bacteria was not isolated. The HLA-B27 antigen is present in 68 p. cent of the 302 cases in which it was tested.
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PMID:[National survey on reactive arthritis by the French Society of Rheumatology]. 660 98

Over a 10-year period 37 children were hospitalized with infections of Yersinia enterocolitica III, IX or Yersinia pseudotuberculosis IA. The diagnosis was based on elevated antibody titres against these micro-organisms. Thirteen of the children had reactive arthritis caused by Yersinia. The duration of arthritis in the primary phase varied between 3 and 22 months, the average being 6.5 months. Two patients developed persistent arthritis. chemical synovectomy with osmic acid was performed in 3 children because of persistent synovitis in the knee joint. All 3 became asymptomatic after this therapy. The follow-up study of the patients with arthritis was performed after an average period of 4 years 7 months. The histocompatibility antigen HLA-B27 was found in 11 of the 13 children. This group included both patients with chronic arthritis and the 3 synovectomized children. Reactive arthritis in this material was a common, serious complication in an otherwise benign infection.
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PMID:Yersinia arthritis in children. 696 33

Reactive arthritis associated with Yersinia enterocolitis in adults has not been reported in this country. We are reporting a 26-year old female with a polyarticular arthritis, primarily of the large joints following an episode of diarrhea. She was also observed to have erythema nodosum and erythema multiforme. Yersinia enterocolitica grew in abundance in stool culture. The clinical picture is consistent with the reactive arthritis associated with Yersinia enterocolitis.
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PMID:Reactive arthritis associated with Yersinia enterocolitica gastroenteritis. 733 83

Reactive arthritis of 1 or more peripheral joints developed after an enteric infection with Campylobacter jejuni in 6 adult patients. Other reactive signs, such as conjunctivitis, aphthous stomatitis, stranguria and sterile leukocyturia occurred in 4 patients. Five of the 6 patients possessed the HLA-B27 antigen. The history indicated previous joint disease in 4 of the 6 patients. The short-term follow-up showed a benign course of the arthritis. When a reactive arthritis syndrome is clinically suspected, investigations should include a search for Campylobacter jejuni infection by culture of the stool and by serological tests to demonstrate antibodies against Campylobacter jejuni.
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PMID:Reactive arthritis after Campylobacter jejuni enteritis. 742 Mar 35

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

The term spondyloarthropathy, currently used to describe some forms of idiopathic arthritis of childhood, may be inappropriate because most children included in this category do not have arthritis of the spine, and inflammatory disease of the sacroiliac joints is an infrequent or late finding. Juvenile AS, the archetype, or "complete" disease may account for only one fifth of the so-called "spondyloarthropathies". "Incomplete" or "early" spondyloarthropathies are most frequent. Such children may not develop axial symptoms and signs for 5 to 10 years after onset, and they may be better characterized as having enthesitis-related arthritis, a term proposed by a recent task force of the International League Against Rheumatism (ILAR). Reactive arthritis, although etiologically linked with the spondyloarthropathies, uncommonly progresses to AS in childhood; most patients have peripheral arthritis with or without enthesitis resolving in the relatively short term. The arthritis associated with IBD is more commonly peripheral than axial. Although axial disease undoubtedly occurs in JPsA, in the authors' experience it is very uncommon.
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PMID:Spondyloarthropathies of childhood. 756 86


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