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PubMedDate not supplied

Reactive arthritis.

Reactive arthritis (ReA) was known as Reiter's disease or Fiessinger-Leroy disease for nearly 100 years. However, during the past 30 years the disease has been known as reactive arthritis, a member of the spondyloarthritis family. Despite knowing the initiating event (infection) and genetic constitution (many patients have HLA-B27) of ReA, a model of interplay between environment and genetics, its pathogenesis is still incompletely known. This review covers the epidemiology, clinical features, treatment, and prognosis of ReA.

Adult↗

PubMed1993

The possible role of Shigella in sporadic enteric reactive arthritis.

Reactive arthritis (ReA) occurs after a urogenital infection usually with Chlamydia trachomatis or an enteritis due to Yersinia, Salmonella, Campylobacter or Shigella, Shigella, except during epidemics, is not considered to be a frequent cause of enteric reactive arthritis. However this might be due to the lack of a reliable antibody test, which makes diagnosis difficult. We compared synovial and peripheral blood lymphocyte proliferation to various bacterial antigens in 19 consecutive patients with ReA or undifferentiated oligoarthritis. In five patients Shigella was identified as the causative microbe by a specific synovial lymphocyte proliferation. All five patients had a history of symptomatic diarrhoea and had negative stool cultures by the time arthritis developed. Four of the five were HLA B27 positive. We conclude that Shigella may be underestimated as a cause of non-epidemic ReA.

Adult↗

PubMed1994

Role of bacteria-specific T cells in the immunopathogenesis of reactive arthritis.

Reactive arthritis is a usually self-limited sterile inflammation of joints that follows certain bacterial gastrointestinal or urogenital infections. The immunopathogenesis involves CD4+ T cells, which mediate an antigen-specific TH1 response to bacterial constituents within the joint. Properties of the arthritogenic bacteria and the physicochemical characteristics of the bacterial antigens may contribute to the development of reactive arthritis.

Animals↗

PubMed2004

Reactive arthritis.

Reactive arthritis is an infectious disease which may be initiated by several microbes in genetically susceptible hosts. The best known predisposing genetic factor is HLA-B27, but the mechanisms behind its action are still elusive. Worldwide agreement exists regarding the general guidelines in the diagnosis, differential diagnosis and management, even though official diagnostic criteria are not yet available. Several studies indicate that antibiotics are effective only if started before the immunological mechanisms of pathogenesis have been turned on. However, recent observations suggest that a 3-month course of antibiotics may diminish the late risk of chronic sequelae, especially in HLA-B27-positive patients with reactive arthritis.

Anti-Bacterial Agents↗

PubMed1997

[Toxocara infections in childhood in relation to reactive arthritis].

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.

Animals↗

PubMed2004

Disease mechanisms in reactive arthritis.

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.

Arthritis, Reactive↗

PubMed2005

Recent advances in reactive arthritis.

Reactive arthritis (ReA), one of the spondyloarthropathies, is an infectious related disease that occurs in a genetically predisposed individual, characterized by an immune-mediated synovitis with intra-articular persistence of viable nonculturable bacteria and/or immunogenic bacterial antigens. ReA long term prognosis is not as good as it was earlier believed. Two-thirds of patients develop prolonged joint discomfort, low back pain, or enthesopathies after acute ReA, and 15% to 30% of them develop chronic symptoms. The therapeutic options for patients with the more severe forms of the disease have been rather limited. The efficacy of tumor necrosis factor antagonists in other spondyloarthritis suggested that anticytokine therapy could also be effective for ReA. This paper reviews the latest concepts in urogenital and postenteric human leukocyte antigen-B27-associated ReA.

Anti-Bacterial Agents↗

PubMed1993

Current perspectives in reactive arthritis.

Reactive arthritis (ReA) is an inflammatory arthritis triggered by infection, usually urethritis or gastroenteritis, and is strongly associated with the MHC class I antigen HLA-B27. Two recent observations have excited interest: first, antigen and DNA from the triggering bacteria have been identified in the joint and, second, ReA synovial T cells have been found to respond specifically to the bacterium that caused the initiating infection. Because the trigger of ReA, its onset and the MHC association are all clearly defined, we can investigate hypotheses that are impossible to study in other forms of human arthritis. Here, Gabrielle Kingsley and Jochen Sieper review the topic in the light of a recent workshop.

Animals↗

PubMed2006

Infection and musculoskeletal conditions: Reactive arthritis.

Reactive arthritis (ReA) has been recognized as a clinical disease entity for nearly 100 years. The prevalence is estimated to be 30-40/100,000 adults. The HLA-B27-associated form is part of the spondyloarthritis concept. According to the current hypothesis the arthritis follows a primary extra-articular infection and is characterized by the presence of bacterial antigen and/or of viable but non-culturable bacteria persisting within the joint. Pathogenesis involves the modification of host cells by pathogen-associated molecular patterns (PAMPs, e.g. lipopolysaccharide), bacterial effector proteins, the adaptive immune system, and the genetic background. Up to 30% of patients develop chronic symptoms, and therapeutic options for these patients are still limited. Data for recommendations to apply conventional disease-modifying anti-rheumatic drugs (DMARDs) are rare; however, sulfasalazine seems to be effective, and first reports on agents that block tumour necrosis factor (TNF) are promising. Combination therapy of several antibiotics might open the window to curing the disease; however, controlled clinical studies are needed.

Anti-Bacterial Agents↗

PubMed1996

Aetiological agents and immune mechanisms in enterogenic reactive arthritis.

Reactive arthritis is triggered by an infection, either of the genitourinary or gastrointestinal tracts; the common triggering bacteria in enteric ReA include salmonella, shigella, yersinia, and campylobacter. It is still not clear how such different bacteria can lead to a similar clinical picture and have a similar association with the MHC class I antigen HLA-B27. Common both to enterogenic and urogenic bacteria is the type of peripheral joint involvement. However, this is not so different from other bacteria-associated arthritides and is probably the consequence of bacteria persistent inside the joint. What is unique to these bacteria is the HLA-B27-association and the nearly exclusively B27-linked clinical manifestations as sacroiliitis and iritis. Shigella-induced ReA has the highest B27-association while in salmonella- and chlamydia-induced ReA a lower association can be found. Mucosal entry of enterogenic bacteria give easy access to macrophages which might be important for the transport into the joint. Although bacteria-specific antibodies are of diagnostic value, the humoral immune response does not explain the immunopathogenesis and MHC-association of this disease. Bacteria-specific T-cells have been constantly found in the synovial fluid from ReA patients and have been further analysed. The identification of immunodominant antigens of these bacteria is of great importance to understand the pathogenesis. Although an antigen shared by all bacteria has not been identified until now progress is being made in this field. We have also to consider the possibility that these bacteria are not only driving the immune response themselves but rather work as a trigger for autoimmunity.

Arthritis, Reactive↗

PubMed1994

A longitudinal study of peripheral blood mononuclear cell proliferative responses to bacterial antigens in reactive arthritis.

Reactive arthritis (ReA) is a sterile inflammatory arthritis which usually occurs after an enteric or genitourinary infection. In recent years it has been recognized that synovial fluid mononuclear cells from an affected joint demonstrate marked proliferative responses if incubated with preparations of the organism triggering the arthritis; peripheral blood mononuclear cell (PBMC) responses are typically much smaller. One interpretation of this finding is that recognition of the triggering organism is enhanced within the joint compared to peripheral blood, but it could also be argued that the PBMC responses are actually depressed during acute arthritis. We have examined this possibility in a longitudinal study of PBMC proliferative responses in patients with ReA. In this study we have demonstrated that PBMC proliferative responses to the triggering organism were indeed depressed during acute ReA, and showed a significant increase after recovery from the arthritis. These findings also applied to PBMC recognition of the recall antigen PPD, and to the response to IL-2.

Adult↗

PubMedDate not supplied

Reactive arthritis.

Reactive arthritis (ReA) develops after an infection elsewhere in the body, generally in the genitourinary or intestinal tract. Chlamydia trachomatis, Yersinia enterocolitica, salmonella, shigella, and campylobacter are frequent triggering agents. Between 60% and 90% of patients are positive for HLA-B27. The arthritis occurs within 4 weeks of the primary infection and is oligoarticular and asymmetric. Extra-articular manifestations include mucocutaneous symptoms, ocular inflammation, and urethritis. The average duration of arthritis is 4 to 5 months but two-thirds of patients have symptoms for more than a year. Bacterial antigens have been found in synovial specimens from patients with ReA, but cultures are sterile. The treatment of ReA comprises non-steroidal anti-inflammatory drugs, intra-articular steroid injections, and physical treatment. Short-term antibiotic treatment has no effect in manifest ReA, whereas a tendency to improvement has been seen with treatment over months, at least after chlamydia infection.

Arthritis, Reactive↗

PubMed2004

Management of reactive arthritis.

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.

Adrenal Cortex Hormones↗

PubMed2001

Reactive arthritis.

Reactive arthritis is a disease affecting mostly young adults. Owing to a greater general awareness the diagnosis has become more common during recent years. It is well established that ReA is caused by an infection, mostly in genetically susceptible individuals. The pathogenetic mechanisms are still poorly understood, and the treatment rests mainly on anti-inflammatory drugs or steroids. Vigorous and early treatment of the triggering infection may prevent the development of ReA but this is rarely possible in everyday clinical practice. Despite its name, the disease should be considered as a general disorder that affects not only the joints. The prognosis is not as good as earlier believed, and relapses or chronic development are not unusual.

Adult↗

PubMed2006

[Reactive arthritis].

Reactive arthritis is a disease closely related to the presence of the HLA-B27 antigen and characterized by sterile joint inflammation secondary to infection. Arthritis is only one of the clinical manifestations of this systemic disease. Its diagnosis rests on history, clinical examination and various serologies. The prognosis is generally good, but recurrences are frequent, in particular in HLA-B27 positive patients. Treatment is mainly symptomatic, and antibiotics should be prescribed only in the event of an active infection. A 3 months course of antibiotics could be beneficial on the long-term evolution in HLA-B27 positive patients, but this practice deserves to be confirmed by additional randomized controlled studies.

Anti-Bacterial Agents↗

PubMedDate not supplied

Reactive arthritis: a paradigm for inflammatory arthritis.

Reactive arthritis (ReA) is an inflammatory arthritis which follows either chlamydia-induced non-specific urethritis or gastroenteritis due to yersinia, salmonella, shigella or campylobacter. It is distinguished from other infection-induced arthritides by its association with the MHC class I antigen HLA-B27, the pattern of arthritis (a lower-limb oligoarthritis often associated with sacroiliitis) and its systemic features (conjunctivitis, circinate balanitis and skin rash). ReA is unique among inflammatory arthritides in the clear definition of its trigger, its onset, its HLA association, and the demonstrating of a triggering antigen-specific cell-mediated immune response in the joint. Clear delineation of these factors makes it possible to test pathogenetic hypotheses which cannot be analysed in other more common forms of arthritis. However, since there are many similarities between these and ReA, the mechanisms established in ReA may have general relevance in understanding synovitis.

Antibody Formation↗

PubMed1989

[The study of intra-articular infectious agents in reactive arthritis].

Reactive arthritis is differentiated from infectious arthritis by the lack of intraarticular infectious agents. Recently 2 groups, using different techniques have demonstrated intra-articular antigens in cases of reactive arthritis associated with Chlamydia and Yersinia infections. In this article we report the preliminary results of screening cells from synovial fluid for DNA of certain microorganisms by in situ hybridization. Our findings provide complementary evidence of the intra-articular presence of at least parts of microbes.

Antigens, Bacterial↗

PubMed1991

Intracellular pathogens and professional phagocytes in reactive arthritis.

Reactive arthritis is a postinfectious complication which develops after certain infections, mostly gastrointestinal or urogenital. Antigenic structures of the causative microbes, but no live organisms, have been demonstrated in inflamed joints. The host factors as well as the microbial antigens responsible for the initiation of the arthritic process are unknown. The pathogenesis of reactive arthritis is discussed here with special reference to the intracellular life of the causative microbes and to monocytes/macrophages, which may be involved in early events of the arthritic process as well as in maintenance of the autoimmune type of responses.

Antigens, Bacterial↗