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

More than fifty years after the clinical syndrome was described by Reiter, Fiessinger and Leroy, the diagnostic criteria of what has now been termed reactive arthritis are still under debate. Reactive arthritis can be defined as an aseptic inflammatory joint disease occurring either in a patient with a bacterial infection located in a distant organ or with a particular genetic predisposition. The lack of specific criteria has led to a certain degree of liberty in interpreting the three basic elements of reactive arthritis: clinical presentation, "distant" infection, genetic predisposition. It is generally accepted that limiting the diagnosis of reactive arthritis only to patients with the classic oculo-uretro-synovial manifestations is unsatisfactory. The question remains open as to whether only patients presenting both inflammatory joint disease and spondylarthropathy have reactive arthritis or whether any undetermined etiology of arthritis is sufficient if the patient also has a "distant" infection and a specific genetic predisposition (HLA B27). Two new elements further complicate the situation. The first is the recent demonstration that the synovial fluid in patients with reactive arthritis might contain microbial antigens. The second is that longterm antibiotics (more than 3 months) could have a beneficial effect. Asking when the diagnosis should be entertained is thus not a moot question. Although we still have no clear answer, it is reasonable to state that the diagnosis of reactive arthritis should be retained only in patients with both inflammatory joint disease and criteria compatible with spondylarthropathy. Clinical research is required to determine whether the germ is actually present or not within the joint and to assess the effect of long-term antibiotherapy.
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PMID:[The concept of reactive arthritis]. 912 8

Reactive arthritis belongs to a group of rheumatoid diseases known as seronegative spondylarthritis or spondarthropathies. Of many reactive arthritis-evoking agents, the authors focused on larval toxocarosis. The authors describe a child with high anti-Toxocara antibody and circulating antigen titres in combination with acute Chlamydia infection, which may have caused reactive arthritis in this immunologically impaired organism. This is evidence of the coincidence of different pathological factors manifested by reactive affection of the knee joint.
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PMID:[Toxocara infections in childhood in relation to reactive arthritis]. 916 57

Reactive arthritis (ReA) is one of the most common arthritides affecting young adults. In most cases it follows urogenital or enteric bacterial infection, but its pathogenesis is not fully understood. It is generally considered a sterile arthritis which appears to involve immune response to bacterial organisms and genetic host susceptibility associated with the presence of HLA-B27 antigen. New findings suggest that in some ReA cases, viable bacteria are present inside the joints, and these organisms may cause the disease and trigger the inflammatory response. ReA manifests clinically as a rheumatoid factor negative oligoarthritis associated with enthesopathy and certain mucosal and skin lesions. Laboratory findings in ReA are non-specific. Although concepts of its pathogenesis are still evolving, so-called ReA remains an important condition to be distinguished from rheumatoid arthritis. Prognosis is generally better. Treatments with known effects in some cases include non-steroidal anti-inflammatory drugs, intra-articular corticosteroids, oral tetracyclines and sulphasalazine. The occasional chronic and severe ReA may be very difficult to treat.
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PMID:Reactive arthritis: is it a useful concept? 929 60

Reactive arthritis is triggered by certain microbes that cause primary infections mainly on the gastrointestinal or urogenital mucosa. The disease is strongly associated with HLA-B27. Long persistence of causative microbes or their structures in the body has been thought to have an important role in the pathogenesis of reactive arthritis. This suggests that the elimination of the microbes causing reactive arthritis is ineffective or disturbed in HLA-B27-positive individuals developing this complication. We examined the role of the HLA-B27 antigen in microbe-host interaction in vitro by monitoring the invasion and intracellular survival of Salmonella enteritidis in mouse fibroblasts transfected with HLA-B27, HLA-B7, or beta2-microglobulin only. S. enteritidis invaded into all the three transfectants with the same efficiency. However, at 6 and 10 days after incubation, there were more living intracellular Salmonella organisms in HLA-B27 transfectants than in the other transfected cell lines (P < 0.05), suggesting that the bactericidal effect is impaired in these cells. Impaired NO production in HLA-B27-transfected cells was indicated as a possible mechanism, since the amount of nitrite in the supernatants of the Salmonella-infected HLA-B27-transfected cells was smaller than that in the supernatants of the Salmonella-infected HLA-B7- or beta2-microglobulin-transfected cells (P < 0.001). The inhibition of NO synthesis by N-monomethyl-L-arginine resulted in impaired elimination of Salmonella also in HLA-B7and beta2-microglobulin-transfected cells. The inverse correlation between intracellular survival of Salmonella and the amount of nitrite detected in culture supernatants supports the hypothesis that the L-arginine-dependent NO pathway plays an important role in the murine fibroblast response against Salmonella. We suggest that a major histocompatibility complex class I antigen, HLA-B27, may contribute to the intracellular persistence of Salmonella by a mechanism which involves the NO pathway.
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PMID:HLA-B27 modulates the survival of Salmonella enteritidis in transfected L cells, possibly by impaired nitric oxide production. 931 32

Reactive arthritis is an acute form of arthritis apparently caused by a combination of bacterial infection and genetic influences. Recent experiments using an animal model suggest that certain bacterial cell wall polymers originating from endogenous enteric bacteria may be responsible for the condition.
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PMID:Role of endogenous enteric organisms in the reactivation of arthritis. 941 85

Reactive arthritis was originally defined as a sterile joint inflammation after infection elsewhere in the body, but this view has been challenged in the past decade since different antigens and DNA and RNA of various triggering microbes have been shown to exist at the sites of inflammation in the joints. It has been suggested that microbial antigens, or intact pathogens, are important for the pathogenesis of reactive arthritis, at least in the early phase of the disease, but the exact mechanism of how the pathogens contribute to the development of this usually self-limiting polyarthritis has not been discovered. This article reviews the theories on the role of infectious agents as triggers of reactive arthritis.
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PMID:Infectious agents as triggers of reactive arthritis. 976 88

Reactive arthritis is usually a self-limiting polyarthritis which develops after certain gastrointestinal or urogenital infections. Microbial antigens found in the inflamed joints are thought to play a key role in the development of this disease. It is not known how antigens of the pathogenic organisms migrate from the mucosal tissues into the joints. The data presented here show that mononuclear phagocytes which mediate the dissemination of several intracellular pathogens acquire an enhanced capacity to bind to nonstimulated vascular endothelial cells after phagocytosis of Yersinia enterocolitica O:3, one of the causative organisms of reactive arthritis. The increased binding to previously nonstimulated endothelial cells was mediated by P-selectin, whose translocation to the endothelial cell surface was induced by monocytes with intracellular Yersinia bacteria. These results suggest that mononuclear phagocytes may be responsible for the dissemination of bacterial antigens and the initiation of the joint inflammation in reactive arthritis.
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PMID:Monocytes that have ingested Yersinia enterocolitica serotype O:3 acquire enhanced capacity to bind to nonstimulated vascular endothelial cells via P-selectin. 991 83

Reactive arthritis is a member of the spondyloarthropathy. Bacteria which cause reactive arthritis infect the mucosal surfaces. Either the whole bacteria or their fragments are subsequently carried to the joints inside which are induced a TH1 lymphocyte response in which oligoclonal T lymphocytes as well peptide-specific CD8+ T lymphocytes participate. Human lymphocyte antigen (HLA)-B27 is a predisposing gene. Besides being determinants for the CD8+ T lymphocyte response it can also modify the response of other cells to the invasive bacteria. This would lead to alteration of the fate of the bacteria as well as release of arthritis-causing cytokines.
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PMID:Pathogenesis of reactive arthritis. 1022 63

Reactive arthritis, also called Reiter's syndrome, is the most common type of inflammatory polyarthritis in young men. It is sometimes the first manifestation of human immunodeficiency virus infection. An HLA-B27 genotype is a predisposing factor in over two thirds of patients with reactive arthritis. The syndrome most frequently follows genitourinary infection with Chlamydia trachomatis, but other organisms have also been implicated. Treatment with doxycycline or its analogs sometimes shortens the course or aborts the onset of the arthritis. Reactive arthritis may also follow enteric infections with some strains of Salmonella or Shigella, but use of antibiotics in these patients has not been shown to be effective. Reactive arthritis should always be considered in young men who present with polyarthritis. Symptoms may persist for long periods and may, in some cases, cause long-term disability. Initial treatment consists of high doses of potent nonsteroidal anti-inflammatory drugs. Patients with large-joint involvement may also benefit from intra-articular corticosteroid injection.
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PMID:Reactive arthritis (Reiter's syndrome). 1046 25

Reactive arthritis is one of the spondyloarthropathy family of clinical syndromes. The clinical features are those shared by other members of the spondyloarthritis family, though it is distinguished by a clear relationship with a precipitating infection. Susceptibility to reactive arthritis is closely linked with the class 1 HLA allele B27; it is likely that all sub-types pre-dispose to this condition. The link between HLA B27 and infection is mirrored by the development of arthritis in HLA B27-transgenic rats. In this model, arthritis does not develop in animals maintained in a germ-free environment. Infections of the gastrointestinal, genitourinary and respiratory tract appear to provoke reactive arthritis and a wide range of pathogens has now been implicated. Although mechanistic parallels may exist, reactive arthritis is distinguished from Lyme disease, rheumatic fever and Whipple's disease by virtue of the distinct clinical features and the link with HLA B27. As in these conditions both antigens and DNA of several micro-organisms have been detected in joint material from patients with reactive arthritis. The role of such disseminated microbial elements in the provocation or maintenance of arthritis remains unclear. HLA B27-restricted T-cell responses to microbial antigens have been demonstrated and these may be important in disease pathogenesis. The importance of dissemination of bacteria from sites of mucosal infection and their deposition in joints has yet to be fully understood. The role of antibiotic therapy in the treatment of reactive arthritis is being explored; in some circumstances, both the anti-inflammatory and anti-microbial effects of certain antibiotics appear to be valuable. The term reactive arthritis should be seen as a transitory one, reflecting a concept which may itself be on the verge of replacement, as our understanding of the condition develops. Nevertheless it appropriately describes arthritis that is associated with demonstrable infection at a distant site without traditional evidence of sepsis at the affected joint(s). Although several forms of disease could be described as "reactive", particularly acute rheumatic fever, post-meningococcal septicaemia arthritis and Lyme disease, in clinical practice the term is restricted to an acute spondyloarthritis, usually, but not exclusively, linked to acute genitourinary or gastrointestinal infection. A proportion of patients fulfil criteria for Reiter's Syndrome [1].
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PMID:Reactive arthritis. 1059 44


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