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At least 19 recordsLinked to original sources
PubMed1992

Synovial fluid leukocytosis in bacterial arthritis vs. reactive arthritis and rheumatoid arthritis in the adult knee.

In this comparative analysis of laboratory data, we examined the characteristics of synovial fluid leukocytosis in eighty adult patients with bacterial arthritis, reactive arthritis or rheumatoid arthritis of the knee joint. Synovial fluid leukocyte count and the percentage of polymorphonuclear cells seemed to perform well as a discriminator between bacterial infection and acute flare of the underlying disease in patients with rheumatoid arthritis. In contrast, there were no definite difference in the intensity of synovial fluid leukocytosis between patients with bacterial arthritis caused by living bacteria and patients with reactive arthritis probably caused by bacterial antigens.

Adolescent↗
PubMed1989

[Reactive arthritis].

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.

Arthritis, Reactive↗
PubMed1992

[Poststreptococcal reactive arthritis].

Reactive arthritis is defined as arthritis of 1 or more joints, in association with infection at a distant site, but without the infective agent being found in the synovial fluid. Patients with Group A beta-hemolytic streptococcal infection and articular disease, who do not fulfill the modified Jones criteria for diagnosis of acute rheumatic fever, have been classified as having poststreptococcal reactive arthritis. We describe 6 patients seen during the winter of 1991 who had various clinical presentations of poststreptococcal reactive arthritis. This condition is considered by some as a distinct disease, but by others as part of the spectrum of acute rheumatic fever.

Adolescent↗
PubMedDate not supplied

[Value of microbiologic studies for diagnosis of post-enteritis reactive arthritis].

Reactive arthritis may develop within a period of some days until upto 3 weeks after infections with Yersinia enterocolitica, Yersinia pseudotuberculosis, Campylobacter jejuni/coli, Shigella and Salmonella. Intestinal infections with Klebsiella pneumoniae, Clostridium perfringens, Clostridium difficile, Cryptosporidium, Strongyloides stercoralis, Taenia saginata and Schistosoma mansoni are, in some cases, considered to be responsible for reactive arthritis. Detection of pathogenic bacteria in feces is generally most successful in the early stage of the infection. A large spectrum of special tests is required in order to detect all the causative agents and to ensure reliable results. It is therefore necessary that the laboratory is provided with information about the diagnostic object and the tentative diagnosis. The detection of serum antibodies to Y. enterocolitica, Y. pseudotuberculosis, C. jejuni/coli, and Schistosoma may suggest connections between infection and reactive arthritis.

Arthritis, Infectious↗
PubMed1988

The aminoterminal-type-III procollagen peptide and proteoglycans in serum and synovial fluid of patients with rheumatoid arthritis or reactive arthritis.

The concentrations of aminoterminal-type-III procollagen (procollagen N-) peptide, and of proteoglycans were measured in knee-joint synovial fluid and serum from patients with rheumatoid arthritis or reactive arthritis. All synovial fluids contained large amounts of intact propeptide. The synovial fluid: serum propeptide ratios were high, suggesting local propeptide liberation. A correlation was demonstrated between the propeptide concentration in synovial fluid and in serum. In rheumatoid arthritis, the propeptide concentration in synovial fluid was related to local inflammatory activity, and the serum concentration was correlated with the presence of nonspecific markers of inflammation. The presence of smaller propeptide fragments in synovial fluid indicated that some degradation occurred locally. The local metabolic changes were most prominent in patients with joint erosions. Patients with nonerosive rheumatoid arthritis and reactive arthritis had similar synovial fluid propeptide concentrations. The proteoglycan content of synovial fluid was inversely related to the degree of joint destruction, and was highest in patients with reactive arthritis. No correlation was observed between the concentrations of propeptide and proteoglycan in synovial fluid. Intraarticular glucocorticoid injection reduced the levels of propeptide and proteoglycan in synovial fluid.

Adult↗
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↗
PubMed1990

[Nosologic concept and new developments in the etiopathogenesis of reactive arthritis].

Reactive inflammatory arthritis is caused by extraarticular infection with different arthritogenic microorganisms. The causative bacteria can not be cultured from synovial specimens, but bacterial antigens have been demonstrated in cells of synovial fluid and synovial membrane, respectively. Thus, latent intraarticular infection may be the cause of reactive arthritis. A model of the etiopathogenesis of reactive arthritis is described on the basis of recent immunological and microbiological findings.

Antibodies, Bacterial↗
PubMed1989

Synovial T lymphocyte recognition of organisms that trigger reactive arthritis.

Reactive arthritis (ReA) is believed to be "triggered' by infection with certain bacteria. When the proliferative responses of mononuclear cells (MC) obtained from the synovial fluid (SF) of ReA patients were examined, it was found that they responded maximally to the specific organism responsible for the preceding infection. The response was shown to be due to Class II MHC-restricted T cells by inhibition experiments using cyclosporin A and monoclonal antibodies. Significant SFMC responses to additional organisms associated with ReA were also recorded; since there was no serological evidence of preceding infection by these organisms, this finding suggests that these bacteria share common T cell-recognized antigenic epitopes. The corresponding responses by peripheral blood mononuclear cells (PBMC) were much lower and often barely detectable, whereas their responses to PHA were consistently higher than those of SFMC. These results, combined with evidence that bacterial antigens localize in the joint, indicate that a bacteria-specific, T-cell-mediated response may play a central role in the pathogenesis of ReA.

Antigens, Bacterial↗
PubMed1989

[The state of humoral immunity to enterobacterial antigens in juvenile rheumatoid arthritis and reactive arthritis in children].

Investigation findings are generalized based on quantitation of antibodies against the antigens of intestinal microorganisms of Enterobacteriaceae family conducted in 66 children with various joint disease using the enzyme-linked immunoassay (ELISA) methodology. High antibody titres were revealed in 77.1% juvenile rheumatoid arthritis cases and in 80% cases with chronic juvenile arthritis which was not defined nosologically. All the patients with reactive arthritis associated with intestinal infection showed high tension of immunity to all tested enterobacteriaceae antigens with cross reactions to them. Patients with reactive arthritis associated with oral infection, with Reiter's disease and other disorders exhibited high antibody titres at the same rate as in the control.

Antibody Formation↗
PubMed1985

Difference in cartilage proteoglycan level in synovial fluid in early rheumatoid arthritis and reactive arthritis.

Cartilage proteoglycans were measured, by the use of an enzyme-linked immunosorbent assay, in synovial fluids obtained from 109 unselected patients attending an outpatient rheumatology clinic because of inflammation of the knee. The content of proteoglycans in synovial fluid was inversely related to the degree of joint destruction shown on X-ray. The proteoglycan concentrations in knee-joint exudates were higher in patients with reactive arthritis than in patients with rheumatoid arthritis having synovitis of corresponding duration and lacking radiological evidence of cartilage destruction. The measurement of proteoglycan levels may therefore be useful in differentiating between the two conditions.

Arthritis↗
PubMed1988

Serum and synovial fluid adenosine deaminase activity in patients with rheumatoid arthritis, osteoarthritis, and reactive arthritis.

Adenosine deaminase activity was determined in paired samples of serum and synovial fluid taken from patients with rheumatoid arthritis (n = 12), reactive arthritis (n = 13), and osteoarthritis (n = 7), and the value of this investigation in the diagnosis of synovial swellings was assessed. Increased activity was found in the synovial fluid taken from patients with rheumatoid disease and reactive arthritis, though values were less raised in the latter. Synovial fluid taken from patients with osteoarthritis did not show significantly raised adenosine deaminase activity as compared with that of normal controls (n = 3).

Adenosine Deaminase↗
PubMed1989

Bowel infection predisposing to reactive arthritis.

Postenteric reactive arthritis is one of several syndromes in which arthritis appears to be secondary to gastrointestinal tract pathology. A wide range of microbes may trigger this type of arthritis. On the other hand, there are differences between strains in their arthritogenic potential. Two possible mechanisms, not mutually exclusive, can be forwarded to explain these findings: first, particular characteristics of the infective organisms are necessary to initiate events leading to reactive arthritis and, second, particular anatomical locations and a certain degree of mucosal involvement are needed to initiate the process. Studies on humoral and cellular immune responses have not revealed any unifying feature that could explain the pathogenesis of reactive arthritis. The HLA allele B27 plays some kind of key role. Yet the elucidation of the fine structure of B27 specificity has not led to any immediate breakthrough in the understanding of the pathogenetic pathways. Experience of reactive arthritis associated with acquired immunodeficiency syndrome suggests that helper T cells are not involved. Antigen persistence may be connected with continuation of the inflammation. Recent developments in the serology of enteric bacterial infections will provide additional tools for uncovering the triggering agents in reactive arthritis. 'Idiopathic reactive arthritis' associated with clinically silent terminal ileitis is an interesting disease entity requiring further characterization.

Arthritis↗
PubMed1988

Synovial lymphocyte responses to microbial antigens differentiate the arthritis of enteric reactive arthritis from the arthritis of inflammatory bowel disease.

Synovial lymphocyte responses to microbial antigens were measured by the 3H-thymidine uptake method in 5 patients with bacteriologically defined enteric reactive arthritis and 7 patients with arthritis associated with inflammatory bowel disease. All the patients with enteric reactive arthritis had maximal synovial lymphocyte responses to the relevant enteric antigen; in contrast, the synovial lymphocytes of the patients with inflammatory bowel disease all responded maximally to nonenteric antigens.

Antigens, Bacterial↗
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↗
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↗
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↗