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PubMed2006

Reactive arthritis or post-infectious arthritis?

The term 'reactive arthritis' was first used in 1969 to describe the development of sterile inflammatory arthritis as a sequel to remote infection, often in the gastrointestinal or urogenital tract. The demonstration of antigenic material (e.g. Salmonella and Yersinia lipopolysaccharide), DNA and RNA, and, in occasional cases, evidence of metabolically active Chlamydia spp. in the joints has blurred the boundary between reactive and post-infectious forms of arthritis. No validated and generally agreed diagnostic criteria exist, but the diagnosis of reactive arthritis is mainly clinical based on acute oligoarticular arthritis of larger joints that develops within 2-4 weeks of the preceding infection. In about 25% of patients, the infection can be asymptomatic. Diagnosis of the triggering infection is very helpful for the diagnosis of reactive arthritis. This is mainly achieved by isolating the triggering infection (stools, urogenital tract) by cultures (stool cultures for enteric microbes) or ligase reaction (Chlamydia trachomatis). However, after the onset of arthritis, this is less likely to be possible. Therefore, the diagnosis must rely on various serological tests to demonstrate evidence of previous infection, but, these serological tests are unfortunately not standardized. Treatment with antibiotics to cure Chlamydia infection is important, but the use of either short or prolonged courses of antibiotics in established arthritis has not been found to be effective for the cure of arthritis. The long-term outcome of reactive arthritis is usually good; however, about 25-50% of patients, depending on the triggering infections and possible new infections, subsequently develop acute arthritis. About 25% of patients proceed to chronic spondyloarthritis of varying activity.

Arthritis, Reactive↗
PubMed1999

p53 overexpression in synovial tissue from patients with early and longstanding rheumatoid arthritis compared with patients with reactive arthritis and osteoarthritis.

OBJECTIVE: The p53 tumor suppressor gene is overexpressed in synovial tissue (ST) from patients with longstanding rheumatoid arthritis (RA), and may contain somatic mutations. The aim of this study was to determine p53 expression in ST from RA patients in different stages of the disease, compared with disease controls. METHODS: ST biopsy specimens were obtained from the knee joints of 31 RA patients in varying disease phases, 8 patients with reactive arthritis (ReA), 10 patients with inflammatory osteoarthritis (OA), and 6 control patients (4 with meniscus pathology, 2 with vascular insufficiency). ST was also obtained from the clinically uninvolved knee joints of 9 RA patients. Expression of p53 was determined by immunohistology with DO1 monoclonal antibody (mAb) in all patients and by Western blot analysis with DO7 mAb in a subgroup of the patients. RESULTS: The p53 protein was detected by immunohistology in 10 of the 13 patients with early RA (duration <6 months) and in 12 of the 14 patients with longstanding RA (duration >5 years). The p53 protein was also demonstrated in clinically uninvolved knee joints. Western blots revealed immunoreactive p53 in ST extracts from all RA patients. Expression of p53 was about twice as high in ST from patients with longstanding RA as in early RA samples, but the difference did not reach statistical significance. Small amounts of p53 were also detected in ST from ReA and OA patients, although the expression in RA synovium was significantly higher. Immunohistologic analysis of normal ST gave negative results for p53. CONCLUSION: This study shows that p53 overexpression is specific for RA, compared with OA and ReA. This phenomenon is probably secondary to increased production of wild-type p53 protein in response to DNA damage and secondary to somatic mutations caused by the genotoxic local environment in inflamed ST. Of interest, p53 overexpression can also be found in the earliest stages of RA and in clinically uninvolved joints.

Aged↗
PubMed1990

Tropical arthritis in Papua New Guinea: a reactive arthritis.

An idiopathic, asymmetrical oligoarthritis affecting young adults is prevalent in the tropical regions of Africa, Asia and Melanesia. A serological study was undertaken in 23 consecutive patients with polyarthritis. Each patient was assigned two paired control subjects. A standardized history, physical examination and investigations were performed. Acute and convalescent sera were examined for evidence of recent infection. The presence of HLA-B27 was determined. Twelve (52%) of the 23 patients had more than one of the clinical features of a reactive arthritis. No serological evidence was found of acute infection with viruses (arboviruses, enteroviruses, mumps, rubella, adenoviruses, Epstein-Barr virus and hepatitis B), Chlamydia, Mycoplasma, Yersinia or syphilis. HLA-B27 was found in 14 (61%) of the 23 patients in contrast with in seven (17%) of the 41 control subjects (P less than 0.001). In two patients with HLA-B27, diagnostic titres of antibodies to Campylobacter jejuni-Campylobacter coli indicated recent infection. The presence of HLA-B27 antigen was significantly (P less than 0.05) associated with the presence of the clinical features of reactive arthritis. This study suggests that "tropical arthritis" commonly is a reactive arthritis that is associated with the presence of HLA-B27.

Acute Disease↗
PubMed2003

Reactive arthritis: newer developments.

Reactive arthritis (ReA) is characterized by an aseptic inflammatory articular involvement occurring in a genetically predisposed individual secondary to an infectious process localized outside the joint. ReA usually refers to an acute or insidious oligoarthritis process after enteric (enteroarthritis) or urogenital (uroarthritis) infection. Conventional antirheumatic therapeutic modalities based on nonsteroid anti-inflammatory drugs, sulfasalazine, and steroids are effective in the majority of patients. In more refractory cases, the use of second-line agents including methotrexate and more recently biological agents such as etanercept and infliximab has been found highly effective. The role of antibiotics remains not well established, although they appear to be effective in acute ReA of urogenital origin.

Adult↗
PubMed2003

Role of bacteria and HLA-B27 in the pathogenesis of reactive arthritis.

Strictly speaking, "reactive arthritis" is a conventional term with no study-verified definition. This review will focus on the type of arthritis that is induced by the following species: Chlamydia, Shigella, Salmonella, Yersinia, and Campylobacter. The types of arthritis caused by these pathogens share a clinical pattern that is common in the spondyloarthropathies, especially undifferentiated spondyloarthropathy and Reiter's syndrome. All these diseases, including ankylosing spondylitis, must also share major pathogenetic pathways.

Arthritis, Reactive↗
PubMed1998

Analysis of T cell subsets present in the peripheral blood and synovial fluid of reactive arthritis patients.

OBJECTIVE: Reactive arthritis (ReA), a HLA-B27 associated arthropathy, develops in susceptible people after infection with certain bacteria. T cells have been implicated in the pathogenesis of the arthritis but which of the different subsets is involved is still debated. This study has further elucidated the role of the CD4+ and CD8+ T cells by examining the expression of various surface markers associated with activation. METHODS: Three colour flow cytometry was used to examine the phenotype of the T cells within the synovial fluid (SF) and peripheral blood (PB) of ReA patients. RESULTS: ReA SF, compared with paired PB, contained a higher percentage of CD69+, CD25+, and HLA-DR+ CD3+ T cells. The majority of SF T cells also expressed the putative memory marker CD45RO. Within the T cell subsets, CD25 was expressed primarily on the CD4+ T cells; however more CD8+ T cells were HLA-DR+. CONCLUSION: The results show that both CD4+ and CD8+ T cell populations demonstrate evidence of recent activation. Whether these cells are involved in inducing inflammation, regulating the inflammation, or have become active as a result of migration through the endothelium, remains to be determined by functional studies.

Adult↗
PubMed1983

[The outcome of reactive arthritis].

Cases of reactive arthritis generally have a favourable short-term outcome, within 1 to 6 months in 50 to 70 per cent of cases. The curable nature of the disease and its short clinical course mean that the therapeutic approach should be devoid of risks. Antibiotics, which are necessary for the mucosal lesion, are ineffective in the joint involvement. Non-steroidal anti-inflammatory agents, sometimes in combination with intra-articular steroid injections, seem to be sufficient in the simple forms. In the more chronic, polyarticular forms, gold therapy would appear to be preferable to the use of drugs which act on the immune system. However, the favourable short-term course is overshadowed by the incidence of relapse (30 to 50%), which are sometimes multiple, and by the subsequent development of pelvispondylitis (30% of cases) after an average of about 6 years. Permanent or recurrent peripheral joint manifestations can be seen. The clinical course of these conditions is very similar, whatever the causative agent.

Anti-Inflammatory Agents↗
PubMed1994

[Principles of therapy in reactive arthritis].

The diagnosis of reactive arthritis relies mainly on the presence of clinical symptoms caused by the initiating infection in the urogenital or enteral tract. An oligoarthritis mainly of the lower limbs occurs 1-6 weeks later. Chlamydia trachomatis and Yersinia enterocolitica are the most frequent triggers of reactive arthritis. Since the infections caused by these microbes are clinically often asymptomatic diagnostic evaluation can be difficult; serology is often nonspecific and cultures are mostly negative. The microscopic detection of bacterial antigens in the joint and the determination of a bacteria specific lymphocyte proliferation in the synovial fluid have changed the pathogenetic concept of reactive arthritis. However, these methods are technically difficult and not suitable for daily routine. There is no indication for short-term antibiotic treatment, as is often prescribed, except in the case of Chlamydia-induced urethritis, which should be treated in any case to prevent the onset or a relapse of reactive arthritis; the sexual partner must also be treated. Long-term therapy with various antibiotic regimens is now being tested in clinical trials. The symptomatic therapy of arthritis comprises physical methods and the use of nonsteroidal anti-inflammatory drugs; intra-articular administration of corticosteroids is of benefit in some cases. If the arthritis takes a chronic course disease modifying drugs such as sulfasalazine are partly successful; in refractory cases arthroscopic synovectomy may become necessary.

Anti-Bacterial Agents↗
PubMed2003

Identification of HLA-B27-restricted peptides in reactive arthritis and other spondyloarthropathies: computer algorithms and fluorescent activated cell sorting analysis as tools for hunting of HLA-B27-restricted chlamydial and autologous crossreactive peptides involved in reactive arthritis and ankylosing spondylitis.

The illustrated clinical and experimental results demonstrate the strong relationship between the MHC class I antigen HLA-B27 and synovial CD8+ T cells with specificity for bacterial and possible self-antigen in SpA. These new aspects obtained in recent experimental and clinical studies might also provide clues to the pathomechanisms of joint inflammation in SpA. In particular, the newly developed techniques will be of great relevance in the near future. New and more precise bioalgorithms reflecting new insights in the biology and biochemistry of proteins as recently presented [98, 99] can be helpful (e.g., a program with an improved prediction of the features of immunoproteasomes). Intracellular and secreted cytokine staining by FACScan allows examination of a great number of cells expressing certain antigens in response to certain stimuli. The analysis of T-cell responses with tetramer/peptide complexes can be useful to screen tissue sections for TCR, recognizing foreign or self-derived epitopes on those complexes loaded with selected (e.g., bacterial) peptides. Identification of arthritogenic peptides and a further understanding of the immunology of the pathomechanisms in SpA might open ways to design new peptide vaccines to prevent inflammation, autoimmunity, and other diseases by early intervention [100].

Algorithms↗
PubMedDate not supplied

The presence and significance of some anti-enzyme antibodies (anti-plasminogen, anti-trypsin, anti-phospholipase C) in rheumatoid arthritis (RA) and reactive arthritis (rA).

It is a well known fact that during the course of RA and rA, due to some cellular and molecular mechanisms, a number of proteolytic enzymes and membranal phospholipases are either activated or their concentration rises significantly. With this aim in view in the present work we have aimed to investigate if, in an inflammatory process associated to RA and rA, the human organism produces or not anti-enzyme antibodies. Using an enzyme-linked immunosorbent assay (ELISA), in the sera of 19 patients of RA and 19 of rA, the presence of the following antibodies has been ascertained: antiplasminogen (antiPAb), antitrypsin (antiTAb) and antiphospholipase C (antiPLCAb). Out of RA cases, 47.3% presented antiPAb, 36.8% antiTAb and 26.3% antiPLCAb. As it was expected, in the rA cases, these antibodies were found in a higher proportion of cases, i.e.: 85.7%, 71.4% and 57.1% respectively. When following the same cases before and during or after the treatment with nonsteroidal antiinflammatory agents (NSAIAs), the antibodies levels were significantly decreased especially in the RA cases. The results obtained indicated a significant rise of seric concentration of antiPAb, antiTAb and antiPLCAb, as well in RA as in rA. While the rise of antiPLCAb in RA and especially in rA could be explained due to microbial infections, the rise of the antiproteolytic enzymes antibody levels as well as the decrease of the antibody titres during or after NSAIAs treatment could be explained, in our opinion, on the basis of some autoimmune processes.

Antibody Specificity↗
PubMed2001

Clinical trials for post-streptococcal reactive arthritis.

Post-streptococcal reactive arthritis is a frequently observed entity that has an uncertain relationship with acute rheumatic fever. Although different criteria have been suggested for delineating these two conditions, none have been validated. In the absence of a clear definition, it has been impossible for investigators to carry out meaningful studies. Some children who were initially labeled as having post-streptococcal reactive arthritis later suffered from carditis and definite rheumatic fever with subsequent streptococcal infections. Some physicians now recommend that all children with post-streptococcal reactive arthritis receive penicillin prophylaxis. However, the proper duration of treatment and appropriate guidelines for patient selection have not been determined. It will be impossible to answer these questions until collaborative efforts are made to accurately define this illness and then begin a careful analysis of its etiopathogenesis and natural history. In the interim, each physician must evaluate the potential risks and benefits of penicillin prophylaxis in view of the risk of rheumatic fever in the community.

Adolescent↗
PubMed2003

Lower level of synovial fluid interferon-gamma in HLA-B27-positive than in HLA-B27-negative patients with Chlamydia trachomatis reactive arthritis.

OBJECTIVES: To compare the synovial fluid (SF) concentrations of various cytokines in rheumatoid arthritis (RA) and in reactive arthritis, and to look for a correlation between cytokine levels and the presence of HLA-B27 antigen in reactive arthritis patients. METHODS: Concentrations of interleukin (IL) 10, IL-12, IL-18, interferon gamma (IFN-gamma) and tumour necrosis factor alpha (TNF-alpha) were determined by commercially available enzyme-linked immunosorbent assays (ELISA) in the SF from 48 patients with reactive arthritis, 33 with RA and 13 with osteoarthritis (non-inflammatory controls). RESULTS: The SF concentrations of IL-10 were significantly lower in patients with reactive arthritis (median 2.3 pg/ml) than in RA patients (median 14.6 pg/ml). The SF levels of IFN-gamma were not significantly different but the ratios of IFN-gamma to IL-10 were significantly higher in patients with reactive arthritis (median 9.2) than in RA patients (median 0.83). When the subset of patients with Chlamydia trachomatis reactive arthritis was considered, the SF concentration of IFN-gamma was significantly lower in HLA-B27-positive (median 2.9 pg/ml) than in HLA-B27-negative patients (median 42.4 pg/ml). After 2 yr of follow-up, two HLA-B27-positive patients, who had low SF levels of IFN-gamma, had a chronic course of arthritis, whereas after 1 yr all HLA-B27-negative patients had complete resolution of arthritis. CONCLUSIONS: The lower IFN-gamma concentrations in HLA-B27-positive patients with C. trachomatis reactive arthritis could be related to the tendency of these patients to have more severe or chronic arthritis.

Adolescent↗
PubMed1994

The evolutionarily conserved ribosomal protein L23 and the cationic urease beta-subunit of Yersinia enterocolitica O:3 belong to the immunodominant antigens in Yersinia-triggered reactive arthritis: implications for autoimmunity.

BACKGROUND: Reactive arthritis (ReA) is a T cell mediated inflammatory process. The immune response is primarily directed against a triggering organism, although autoimmunity has been invoked in long-lasting, antibiotic-resistant disease. Although a variety of different species are known to trigger Reactive arthritis, the clinical manifestations are strikingly similar as well as closely associated to the HLA-B27 (70%). MATERIALS AND METHODS: Various antigenic fractions and single antigens of Yersinia enterocolitica were prepared, and their immunological activity was assessed by proliferation of synovial fluid mononuclear cells from 10 Reactive arthritis patients. The gene encoding one hitherto unknown antigen has been sequenced. Nonapeptides deduced from sequences of the target antigens were tested in an assembly assay. RESULTS: Two immunodominant proteins of Yersinia enterocolitica were found, one being the urease beta-subunit and the other the 50 S ribosomal protein L23. The latter has been sequenced and belongs to the evolutionarily conserved ribosomal proteins with homology to procaryotes and eucaryotes. One nonapeptide derived from the urease beta-subunit was identified as a possible epitope for HLA-B27-restricted cytotoxic T cells by its high affinity. This epitope is also highly conserved. CONCLUSION: Sharing of conserved immunodominant proteins between different disease triggering microorganisms could provide an explanation of the shared clinical picture in Reactive arthritis. Moreover, autoimmunity in Reactive arthritis might be mediated by antigen mimicry between evolutionarily conserved epitopes of ribosomal proteins and their host analogs.

Adolescent↗
PubMed1997

Increase of HLA-DRB1*0408 and -DQB1*0301 in HLA-B27 positive reactive arthritis.

OBJECTIVE: To study HLA class II association in reactive arthritis. METHODS: 63 patients with reactive arthritis and 46 with rheumatoid arthritis were included in the study. HLA-DR alleles were determined by using a sequence specific PCR method. Oligonucleotide hybridisation was used for definition of DRB1*04 subtypes and DQB1 alleles. HLA-B27 was determined by standard microcytotoxity test or by PCR. HLA-B27 subtyping was made by sequencing. RESULTS: 46 (73%) of 63 patients with reactive arthritis were HLA-B27 positive and 24 (38%) were HLA-DRB1*04 positive. When haplotypes were inferred according to the known associations between DRB1 and DQB1 alleles, the frequency of DRB1*04-DQB1*0301 haplotype was found to be 13% (12/92) in HLA-B27 positive reactive arthritis patients, in contrast to 0% in HLA-B27 negative reactive arthritis (P = 0.04) and 1% in random controls (P = 0.0009). However, this combination was also found in 5% of 84 HLA-B27 positive control haplotypes, showing a linkage disequilibrium between B27 and this particular class II haplotype. HLA-DRB1*0408 subtype was found in 8/24 (33%) of the HLA-DRB1*04 alleles in patients with reactive arthritis, accounting for most DQB1*0301 haplotypes, but only in 5/55 (9%) of the DRB1*04 alleles in random controls (P = 0.017). All reactive arthritis patients with this subtype were positive for HLA-B27. DRB1*04-DQB1*0302 haplotype was increased in patients with rheumatoid arthritis (28/92, 30%) compared with reactive arthritis (12/126, 10%) or with the controls (12/100, 12%; P = 0.003). HLA-B*2705 was by far the dominant B27 subtype both in reactive arthritis patients with the particular DRB1*0408-DQB1*0301 haplotype and in controls. It was found in 11 out of 12 DR analysed patients, as well as in 10 out of 11 randomly selected B27 positive controls. CONCLUSIONS: Although no single class II allele was found to be increased among patients with reactive arthritis, HLA-B27, DRB1*0408, and DQB1*0301 might exert a haplotypic effect in the pathogenesis of reactive arthritis, or they may be markers of a subset of B27 haplotypes conferring susceptibility.

Arthritis, Reactive↗
PubMed1988

Phagocyte function in reactive arthritis.

The pathogenesis of reactive arthritis is multifactorial. The possible pathogenetic mechanisms include the role of microbial antigens which cross-react with the host tissue or trigger cytotoxic immune response. In addition an exaggerated inflammatory response of the host may contribute to the clinical picture of the acute arthritis and its late sequels. In this review, we present data showing that HLA-B27 positive subjects show enhanced neutrophil (PMN) migration and their sera support PMN migration more than HLA-B27 negative sera. Enhanced PMN function is persistent in patients with previous severe reactive arthritis or with late inflammatory sequels. In addition to hyperreactive PMNs, monocytes from patients with previous yersinia arthritis, but also from healthy HLA-B27 positive subjects, respond to stimulation with lipopolysaccharide by enhanced production of inflammatory monokines compared with HLA-B27 negative healthy controls. Thus, hyperreactive phagocytes can contribute to the severe inflammatory complications seen in patients with reactive arthritis. The primed phagocytes can also respond vigorously when stimulated either with endogenous mediators of inflammation or with endotoxin released during a new infection or as a sequel of change in the mucosal permeability described in patients with spondyloarthropathy.

Arthritis, Infectious↗