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PubMed1989

Increased expression of HLA-DQ antigens by interstitial cells and endothelium in the synovial membrane of rheumatoid arthritis patients compared with reactive arthritis patients.

We investigated cellular phenotypes and expression of class II major histocompatibility complex antigens on endothelium and cellular infiltrates in synovium from patients with rheumatoid arthritis (RA) or reactive arthritis, using an indirect immunoperoxidase technique. The RA specimens showed synovial lining layer hypertrophy and several focal accumulations of lymphocytes, both of which were absent in the reactive arthritis synovium. The percentage of cells expressing monocyte/macrophage markers was significantly higher in RA specimens. The percentages of cells expressing B and T cell markers were similar in both diseases. There was no significant difference in the expression of HLA-DR or DP by endothelium in the 2 diseases, but a marked increase in expression of HLA-DQ by endothelium was observed in the RA synovium versus that from patients with reactive arthritis. This overexpression of HLA-DQ was also seen in the interstitial cells of RA patients compared with reactive arthritis patients. In the reactive arthritis synovium, a significant population of cells (30%) was noted to be HLA-DR positive, and negative for macrophage and lymphocyte markers. Some of these cells had a dendritic morphology. The coexpression of HLA-DQ and HLA-DR may play an important role in antigen presentation and disease chronicity in RA.

Adult↗
PubMed1999

A clinical and serological comparison of group A versus non-group A streptococcal reactive arthritis and throat culture negative cases of post-streptococcal reactive arthritis.

OBJECTIVE: To identify clinical and serological differences of patients with reactive arthritis after infection with Lancefield group A beta-haemolytic streptococci (GAS), compared with non-group A-that is, group C or G streptococci (NGAS:GCS/GGS), and a group of culture negative or unidentified streptococci (GUS). METHODS: A prospective study of consecutive patients with reactive arthritis after serologically or culture confirmed infection with beta-haemolytic streptococci, presenting to the outpatient department of rheumatology from January 1992 until January 1998. Alternative causes for reactive arthritis were excluded. Main outcome measures were clinical and serological characteristics including antistreptolysine-O (ASO) and antideoxyribonuclease-B (antiDNase-B) antibody titres. RESULTS: 41 patients (female/male ratio 22/19; mean (SD) age 38 (13) years) with reactive arthritis were included. Culture of throat swab was positive in 13 cases (32%): 6 (15%) GAS, 7 NGAS (17%), that is, 5 (12%) GCS, 2 (5%) GGS. In 28 cases throat culture remained negative resulting in a group of unidentified streptococci; antibiotic pre-treatment had been given by the general practitioner in 18 cases (64%). Arthritis was non-migratory, the number of arthritic joints in GAS and NGAS was similar, whereas in NGAS patients fewer joints were involved than in GUS: mean (SEM) 36 swollen joint index: 3.3 (1.0) in NGAS v 5.6 (1.0) in GUS (p<0.005); 28 swollen joint index: 2.9 (1.0) in NGAS v 4.3 (0.8) in GUS (p<0.05). Extra-articular manifestations-that is, erythema nodosum/ multiforme, AV conduction block or hepatitis-were observed after GAS or GUS infection, but not after NGAS infection. ASO and/or antiDNase-B rose significantly in all patients. The maximal titres for ASO and antiDNase-B in 41 PSRA patients were: mean (SEM) 1242 (232) U/l and 890 (100) U/l respectively; the maximal ASO titres were similar in the three groups: mean (SEM) 1125 (185) in GAS, 625 (160) in NGAS (GAS v NGAS: p=0.17), and 1430 (320) U/l in GUS (NGAS v GUS: p=0.10). AntiDNase-B titres were: mean (SEM) 1075 (180) in GAS, 375 (105) in NGAS (GAS v NGAS: p<0.01), and 995 (125) U/l in GUS (NGAS v GUS: p<0.005). ASO: antiDNase-B ratios were: mean (SEM) 0.89 (0.21) in GAS, 2.60 (0.76) in NGAS (GAS v NGAS: p<0.05), and 1.43 (0.28) in GUS (NGAS v GUS: p=0.12). CONCLUSION: Post-streptococcal reactive arthritis occurs not infrequently. Differentiation of PSRA based on the causative streptococcal strain is frequently thwarted by negative throat cultures. Sometimes extra-articular manifestations are present that exclude NGAS as the causative organism. Serologically, lower antiDNase-B titres may be indicative for primary NGAS infection; the ASO/antiDNase-B ratio may be of additive value for differentiation in cases of a negative throat culture: the higher ASO/antiDNase-B ratios suggesting primary NGAS infection. In reactive arthritis, serological monitoring consisting of a simultaneous titration of antiDNase-B and ASO, seems to be of clinical importance to trace GAS induced cases, especially when throat cultures remain negative.

Adult↗
PubMed1995

Diagnostic value of synovial fluid analysis in children with reactive arthritis.

We report on three children with pauciarticular arthritis in whom the clinical picture and serology were compatible with both arthritis reactive to infection with Yersinia or Salmonella and with Lyme arthritis. Results of analysis of synovial fluid by polymerase chain reaction for enterobacterial or borrelial sequences were negative. Immunofluorescence with specific antibodies revealed the presence of amorphous enterobacterial antigens in synovial fluid cells. Since this staining did not reveal enterobacterial morphology, we infected synovial fluid cells of two children with juvenile rheumatoid arthritis in vitro with Yersinia or Salmonella. After 24 h typical rods were observed, but after about 1 week amorphous antigen similar to what had been found in the three patients was seen. In cases of reactive arthritis with ambiguous results of serological testing the diagnosis may be confirmed by demonstration of enterobacterial antigens in synovial fluid.

Adolescent↗
PubMed2002

Mass spectrometric proteome analyses of synovial fluids and plasmas from patients suffering from rheumatoid arthritis and comparison to reactive arthritis or osteoarthritis.

Differential proteome analysis is used to study body fluids from patients suffering from rheumatoid arthritis (RA), reactive arthritis (reaA) or osteoarthritis (OA). Mass spectrometric structure characterization of gel-separated proteins provided a detailed view of the protein-processing events that lead to distinct protein species present in the respective body fluids. (i) Fibrin(ogen) beta-chain degradation products, presumably plasmin-derived, appeared solely in synovial fluids (SF) from both patient collectives, (ii) calgranulin B (MRP14) was exclusively identified in SF samples derived from 5 out of 6 patients suffering from RA. Calgranulin B was not observed in synovial fluids from OA patients, nor in plasmas from either patient group. In all cases where calgranulin B was detected, calgranulin C was identified as well. (iii) Serum amyloid A protein spots were determined in plasmas and synovial fluids from patients with RA, but not in patients with OA. In addition to disease-relevant differences, interindividual differences in haptoglobin patterns of the patients under investigation were observed. Hence, in-depth proteome analysis of body fluids has proven effective for identification of multiple molecular markers and determination of associated protein structure modifications, that are thought to play a role for specifically determining a defined pathological state of diseased joints.

Adolescent↗
PubMed2002

Poststreptococcal reactive arthritis.

Poststreptococcal reactive arthritis (PSRA) refers to a poststreptococcal arthritic condition that does not fulfill the Jones Criteria for diagnosis of acute rheumatic fever. Clinical features include additive rather than migratory arthritis that responds relatively poorly to salicylates and nonsteroidals; persistence for mean of 2 months; elevated acute phase reactants; and laboratory (usually serologic) evidence of recent group A streptococcal infection. PSRA is not associated with HLA-B27 but rather with HLA-DRB1*01. Because up to 6% of PSRA patients develop mitral valve disease, it is recommended that antistreptococcal prophylaxis be administered for 1 year and then discontinued if there is no evidence of cardiac involvement.

Acute Disease↗
PubMed2003

[The role of diagnostic tests in the identification of Chlamydia trachomatis infection in reactive arthritis].

UNLABELLED: Reactive arthritis (ReA) is a sterile inflammation of the synovial membrane of one or more joints developing after urogenital or gastro-intestinal infection. The syndrome most frequently follows infection with Chlamydia trachomatis. Useful for the diagnosis can be the serological tests. At present there is the possibility to identify the specific antibodies (IgG, IgA, IgM) to Chlamydia trachomatis. The subject of the study was the group of 87 patients in age 19-78; 58 women and 29 men from whom urogenital smear and serum were tested. The control group were 30 people age 25-70 without rheumatological disorders. Chlamydia trachomatis was found in urogenital smear in 42 (48%), in 56 (64%) patients immunoglobulin IgG were positive, and immunoglobulin IgA in 16 (18%). The laboratory tests and clinical symptoms allow to make a diagnosis of ReA in 38 (43%) and possible ReA in 5 (5.7%) of patients. CONCLUSIONS: 1. There is no gold standard for the diagnosis of ReA. 2. None of the tests or the clinical symptoms alone are strong enough to make a definite diagnosis of ReA. 3. Tests to identify Chlamydia trachomatis, with respect of typical clinical symptoms are useful the diagnosis of ReA. 4. The diagnosis of ReA is most probable if we have typical clinical symptoms, clinical evidence of a preceding infection plus a positive result of serology or PCR plus positivity for HLA-B27.

Adult↗
PubMed1997

Antigen-dependent B cell differentiation in the synovial tissue of a patient with reactive arthritis.

BACKGROUND: Reactive arthritis (ReA) can develop as a consequence of a bacterial infection with organisms such as Chlamydia trachomata, Shigella flexneri, or Yersinia enterocolitica. Although the mechanism underlying the induction of a chronic synovitis is unknown, the expression of HLA-B27 seems to play a crucial role in the etiology of the disease. Bacterial antigens induce a humoral immune response, but little is know about the impact of B cells on the inflammatory processes developing in the synovial membrane. MATERIALS AND METHODS: Cryostat sections were prepared from the synovial tissue (ST) of patients with ReA and stained with antibodies specific for T, B, and follicular dendritic cells. Lymphoid infiltrates were directly isolated by microdisection and DNA was prepared from them. The rearranged V genes were amplified by polymerase chain reaction (PCR), cloned, and sequenced. RESULTS: Histological staining showed that germinal, center-like structures develop in the ST of patients with ReA. B cells with a heterogenous repertoire were isolated from these lymphoid infiltrates. The majority of V regions carried somatic mutations indicating that sequences are derived from memory B cells. Genealogical trees demonstrate clonal expansion and diversification of the B cell repertoire in the ST. CONCLUSIONS: The finding of local V-region diversification suggests that in the ST of patients with ReA, an antigen-driven, T cell-dependent differentiation of B cells occurs. This local B cell response may contribute to the progress of the disease. Whether B cells are specific for the bacteria inducing the synovitis or for self-determinants present in the ST remains to be determined.

Adult↗
PubMed2000

On the difficulties of establishing a consensus on the definition of and diagnostic investigations for reactive arthritis. Results and discussion of a questionnaire prepared for the 4th International Workshop on Reactive Arthritis, Berlin, Germany, July 3-6, 1999.

OBJECTIVE: There is no agreement on how to classify and diagnose reactive arthritis (ReA) and it is also unclear what kind of specific clinical and laboratory investigations are appropriate. We define relevant points of agreement and identify points of disagreement among an international group of experts in the field. METHODS: Prior to the 4th International Workshop on Reactive Arthritis, Berlin, July 1999, we sent questionnaires to 42 experts identified by personal knowledge and recent publications. RESULTS: The response rate was 81% (n = 34). There was agreement on the nomenclature and recommendation to use the term "reactive arthritis" only if the clinical picture and the microbes involved are HLA-B27 and spondyloarthropathy (SpA) associated, whereas the term "infection related arthritis" is used for all other arthritides related to or associated with infections. A differentiation between acute and chronic ReA with a cutoff of 6 months is recommended. The history of a preceding symptomatic infection is thought to be most relevant for a diagnosis of ReA. The minimal interval between preceding symptoms and arthritis is proposed to be 1-7 days, maximally 4 weeks. The joint pattern in ReA is asymmetrical, with predominance of the lower limbs. SpA related symptoms may contribute to the diagnosis. A search for chlamydia in urine/urethra/cervix is recommended, while in the case of diarrhea enterobacteria should be searched for in stool and antibodies against them in serum. There were also areas of disagreement, such as: Is arthritis essential for the diagnosis of ReA?, Is it oligoarthritis or any arthritis?, What are the role and value of polymerase chain reaction investigation?, The role and value of serology?, Is the diagnostic sensitivity of microbiological tests for ReA increased by HLA-B27 determination? CONCLUSION: The points of agreement will support better communication in this area, and clarification of the disagreements will lead to further studies and discussion.

Arthritis, Reactive↗
PubMedDate not supplied

[Reactive arthritis].

The term reactive arthritis was introduced to describe an acute non-purulent arthritis complicating an infection elsewhere in the body. Reactive arthritis can also be classified into HLA-B27 associated and non-associated forms. Rheumatic fever is an example of the HLA-B27 non-associated forms with genetic factors other than HLA-B27 involved. HLA-B27 associated reactive arthritis includes enteric, urogenic and idiopathic arthritides. The bacteria known to trigger post-enteritic reactive arthritis are: Yersinia, Salmonella, Shigella, Campylobacter, Clostridium difficile and Brucella; those known to trigger post-urethritic reactive arthritis are Chlamydia trachomatis and Ureaplasma urealyticum, but often the germ remains unidentified. Mechanisms through which susceptibility to reactive arthritis is linked to HLA-B27 antigen are still incompletely understood, but a clue could be cross-reactivity between B27 and a surface antigen of pathogenic germs. The clinical profile of the disease is characterized by an asymmetrical oligoarthritis with involvement particularly of the peripheral joints of the lower limbs. The arthritis generally recovers without sequelae within a few weeks or months. Accompanying features can be the involvement of enthesis and tendon sheets in form of a talalgia or dactylitis. In some cases the arthritis can relapse and chronicize. In some cases, in addition, involvement of the axial skeleton can occur (spondylitis and/or sacroiliitis). Another feature of the disease is the frequent association with typical extra-articular manifestations such as uveitis and muco-cutaneous lesions.

Arthritis↗
PubMed1993

T cells are responsible for the enhanced synovial cellular immune response to triggering antigen in reactive arthritis.

In reactive arthritis (ReA) there is specific proliferation of synovial fluid (SF) mononuclear cells (MNC) to the triggering bacterial antigen; comparatively little or no response is seen in peripheral blood (PB). To investigate the mechanism of this elevated local immune response, we examined patients with typical ReA who showed an enhanced antigen-specific synovial immune response in bulk culture. Using separated fractions of T cells and antigen-presenting cells (APC) from PB and SF we showed that the synovial T cells rather than SF APC are responsible for the specific proliferation. By limiting dilution analysis, the frequency of T cells responding to the specific antigen was found to be significantly increased compared with the frequency of irrelevant antigen-specific T cells. Furthermore, the frequency of T cells responding to the specific antigen was higher in SF (between 1/619 and 1/4846, mean 1/2389) than in PB (between 1/1286 and 1/16,279, mean 1/7350). We conclude that the specific synovial cellular immune response in ReA is mainly due to an expansion of antigen-specific T cells within the joint. However, the non-specific hyper-reactivity of SF T cells and differences between SF and PB APC may make a more minor contribution.

Adult↗
PubMed2006

Is the enthesitis-related arthritis subtype of juvenile idiopathic arthritis a form of chronic reactive arthritis?

OBJECTIVE: Enteric organisms are known to trigger reactive arthritis. The enthesitis-related arthritis (ERA) form of juvenile idiopathic arthritis (JIA) clinically resembles reactive arthritis. Therefore, we looked for a role of enteric bacteria in ERA. METHODS: Synovial fluid (SF) was obtained from 26 patients with ERA and 10 patients with rheumatoid arthritis (RA). Blood specimens were also obtained from patients with ERA and from 10 normal individuals. Lymphocyte proliferation assays were done on whole blood and SF mononuclear cells using as antigens crude lysates of the enteric bacteria Salmonella typhimurium, Yersinia enterocolitica, Shigella flexneri and Campylobacter jejuni. Crude lysate of Escherichia coli was used as a control antigen. HLA-B27 typing was done using the polymerase chain reaction. Homing of gut-specific T cells (CD103+) to the synovial compartment was studied using tri-colour flow cytometry. The antigen-specific cytokine profile was determined by flow cytometry. RESULTS: Antigen-specific lymphoproliferative responses were observed in 14 of 26 patients. Among these patients, 12 showed a response in SF (four each to S. typhimurium and C. jejuni, and in two each to S. flexneri and Y. enterocolitica), and two patients in blood (S. typhimurium in both). None of the healthy controls showed a response in the blood. Lymphoproliferative responses in SF were more frequent in patients with JIA (12/26) than in controls with RA (1/10, P < 0.05). Patients with an antigen-specific response had a higher ratio of SF/blood CD103+ T cells compared with those with no antigen-specific response (P < 0.01). Antigen-specific as well as mitogen-stimulated cytokine production showed a Th1 bias. CONCLUSION: Enteric bacteria may have a role in exacerbation of disease in patients with ERA. The immune response in patients with ERA is Th1-dominant.

Adolescent↗
PubMed1989

Immune responses to Borrelia burgdorferi in patients with reactive arthritis.

In reactive arthritis (ReA), including Reiter's syndrome, a close relationship between chronic enteric and genitourinary infections and the clinical features of enthesitis has been described. In contrast, in Lyme arthritis, a distinct clinical entity, chronic infection with the tick-transmitted spirochete Borrelia burgdorferi has been associated with the disease. In a prospective study, 51 patients with ReA were tested for evidence of chlamydial and spirochetal infection. The presence of Chlamydia was determined by culture in 8 patients, and 7 additional patients had markedly elevated antibody titers. In 9 patients, antibodies specific to B burgdorferi were found. Purified peripheral blood T lymphocytes of all 9 patients proliferated specifically to stimulation with macrophages pre-pulsed with B burgdorferi antigens. Compared with other protein antigens, higher numbers of antigen-pulsed macrophages were necessary to activate B burgdorferi-specific T cells. Although antibody titers decreased in response to antibiotic treatment in 8 of 9 patients, second-line therapy with sulfasalazine or methotrexate was required to obtain clinical remission. These data suggest that chronic infection with B burgdorferi can cause ReA. In predisposed individuals, the arthritogenic immune response might be triggered by persisting infectious agents independent of their antigenic specificities.

Antibodies, Bacterial↗
PubMed1999

Reactive arthritis (Reiter's syndrome).

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.

Anti-Infective Agents↗
PubMed1984

[Reactive arthritis in children].

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)

Antigen-Antibody Complex↗
PubMed1998

Reactive arthritis.

Concepts about reactive arthritis are changing and must embrace consideration of the fact that bacteria or their products are present in the joint, not just at the portal of entry in the gastrointestinal (GI) or genitourinary (GU) tracts. With chlamydia-associated disease, atypical elementary bodies can be seen in synovium by electron microscopy, and nucleic acids, including RNA, can be found. It is not yet clear if bacterial nucleic acids are present in postenteric reactive arthritis and whether disease courses are predictably different after GI or GU infection. How bacteria are disseminated to joints and local factors, including cytokines that influence their persistence, are under study. Treatment with antibiotics may help some chlamydia-associated reactive arthritis but is not invariably effective.

Antigens, Bacterial↗
PubMed1997

B-cell activation and development within chronically inflamed synovium in rheumatoid and reactive arthritis.

In autoimmune diseases, B cells often accumulate in the affected tissue. In patients with rheumatoid arthritis or reactive arthritis, germinal center-like structures may develop in the inflamed synovial tissue. B cells from these structures were isolated and their V-gene repertoire determined. The majority of synovial B cells are long-term memory cells and thus are part of the chronic inflammatory reaction. In the synovium a micro-environment is built up which allows the activation of naive and memory B cells and the diversification of their V-gene repertoire. The analysis of plasma cells suggests that these cells are long lived and hence accumulate in the synovial tissue under chronic activation.

Arthritis, Reactive↗