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At least 19 recordsLinked to original sources
PubMed1995

Soluble receptors for tumor necrosis factor and interleukin-2 in serum and synovial fluid of patients with rheumatoid arthritis, reactive arthritis and osteoarthritis.

OBJECTIVE: To compare levels of soluble tumor necrosis factor receptor (TNF-R) and soluble interleukin 2 receptor (sIL-2R) in sera and synovial fluids (SF) of patients with rheumatoid arthritis (RA), reactive arthritis (ReA), and osteoarthritis (OA) in order to investigate the usefulness of soluble cytokine receptors for differentiation diagnosis and their involvement in the pathophysiology of rheumatic diseases. METHODS: Soluble TNF-R (55 kDa), sIL-2R, and TNF-alpha were measured by ELISA in sera and SF of patients with RA, ReA, and OA and correlated with serological and clinical disease activity variables. RESULTS: Serum TNF-R was significantly (p < 0.0001) elevated in RA (4.6 +/- 2.1 ng/ml, mean +/- SD) compared to ReA (2.5 +/- 0.6 ng/ml), OA (2.2 +/- 0.7 ng/ml), and healthy controls (2.0 +/- 0.4 ng/ml). In SF mean TNF-R levels were 21 +/- 9.3 ng/ml in RA, 12.5 +/- 5.1 ng/ml in ReA, and 8.7 +/- 3.7 ng/ml in OA (p < 0.0001 for RA vs ReA or OA; p < 0.02 for ReA vs OA). SF levels were significantly higher in rheumatoid factor (RF) positive than in RF negative patients with RA. In patients with RA, correlations were found between TNF-R and TNF-alpha in SF (r = 0.32, p < 0.01), and between TNF-R and early morning stiffness (r = 0.4, p < 0.003 in serum; r = 0.29, p < 0.05 in SF). However, there was no correlation with disease activity variables such as Ritchie index, erythrocyte sedimentation rate (ESR) or C-reactive protein. Serum levels of IL-2R were elevated in RA and ReA, but a significant difference was found only for RA versus OA and controls (p < 0.0005), whereas in SF significant differences existed between all 3 patient groups (RA/ReA: p < 0.004; RA/OA: p < 0.0001; ReA/OA: p < 0.0003); both in serum and SF, levels of RF positive patients with RA were higher than those of RF negative patients. In patients with RA, IL-2R correlated weakly with ESR (r = 0.24, p < 0.05), iron concentration (r = -0.35, p < 0.005), and CRP (r = 0.24, p < 0.05). CONCLUSION: In RA, in contrast to ReA and OA, TNF-R and IL-2R were not only elevated in the joint fluid but also in serum. This indicates general activation of the immune system in RA, but not in ReA and OA. Therefore the soluble receptors, especially TNF-R, might become useful diagnostic variables to distinguish RA from ReA and OA.

Adult↗
PubMed1999

Reactive arthritis.

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].

Anti-Bacterial Agents↗
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↗
PubMed2000

Reiter's syndrome and reactive arthritis.

Reactive arthritis is an infection-induced systemic illness characterized by an inflammatory synovitis from which no viable microorganisms can be cultured. The paradigm of reactive arthritis is an infectious trigger that occurs in a genetically susceptible individual in whom the immune system continues to be stimulated or "react" to an ongoing or cleared infection, resulting in intermittent exacerbations of a variety of immune-mediated signs and symptoms. Although the terms Reiter's syndrome and reactive arthritis are sometimes used interchangeably, Reiter's syndrome is actually the complete clinical triad of urethritis, conjunctivitis, and arthritis. Some patients will never fulfill all three components of Reiter's triad, however, and although the term incomplete Reiter's syndrome is often used in such cases, the authors believe that the term reactive arthritis should be used, as it is less confusing and is inclusive of any extra-articular manifestations.

Arthritis, Reactive↗
PubMedDate not supplied

A case of post-streptococcal reactive arthritis.

Reactive arthritis is a term used to describe a sterile inflammatory arthritis occurring after a documented infection elsewhere in the body. Group A streptococcus is known to cause such an arthropathy in the setting of acute rheumatic fever. Friedberg first postulated that a reactive arthritis might occur in response to a streptococcal pharyngeal infection as a separate entity from rheumatic fever in the 1950s. Then, in the 1980s, other investigators began describing cases of reactive arthritis that were not characteristic of acute rheumatic fever based on certain observations and application of criteria. We present a patient whose clinical features are more consistent with post-streptococcal reactive arthritis than acute rheumatic fever.

Anti-Inflammatory Agents↗
PubMed2004

[Reactive arthritis].

Reactive arthritis are definied as steriles arthropathies using classic bacteriological techniques. They are due to extra articular infection and are often associated with HLA B27. The outcome of these arthritis is characterised by the recurrence of flares with sometimes appearition of ankylosing spondylitis. The pathogenesis of reactive arthritis is modified when bacterial antigens or alive micro-organisms are discovered in involved joints. Several current works have underlined the interest of antibiotic therapy in the chlamydial reactive arthritis. Chronic forms can justify the use of anti-rheumatic drugs such as salazopyrine.

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↗
PubMed1998

Infectious agents as triggers of reactive arthritis.

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.

Animals↗
PubMed2001

From reactive arthritis to rheumatoid arthritis.

Reactive arthritis was initially described as a sterile synovitis, without microbial components present in the joint tissue. It has, however, become evident that bacterial degradation products, and even bacterial DNA, are present in the synovium of patients with this disease. Since intestinal pathogens are important causes of reactive arthritis, and since cellular homing allows transport of bacterial products from the gut to synovium, we have approached the etiology of rheumatoid arthritis from this point of view. A series of observations has led to a hypothesis that patients with rheumatoid arthritis might favour, for genetic reasons, intestinal bacteria which are capable of inducing arthritis. In the long-run, with continuous seeding of bacterial products from the gut, the synovial inflammation is followed by erosion, exposition of cartilage antigens, and autoimmunity.

Animals↗
PubMed2001

Sexually-acquired reactive arthritis.

Reactive arthritis is the most frequent cause of acute peripheral arthritis in young men. The aetiopathogenesis of reactive arthritis is reviewed, together with the varied clinical features. Finally the treatment and prognosis of this challenging condition are discussed.

Adolescent↗
PubMed1999

Pathogenesis of reactive arthritis.

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.

Animals↗
PubMed1998

Undifferentiated arthritis and reactive arthritis.

The terms undifferentiated arthritis and undifferentiated characterize arthritides that do not fit into well-known clinical disease categories (e.g., seronegative rheumatoid arthritis and reactive arthritis) and that are an early stage or forme fruste of a definite rheumatic disease, an overlap syndrome between such diseases, or an unknown, etiologically undefined disease that remains to be differentiated from other types of arthritis or spondylarthritis. Undifferentiated arthritis and undifferentiated spondylarthritis share some clinical features with reactive arthritides. Recent data suggest that, at least in Chlamydia-induced reactive arthritis, the triggering bacteria persist in affected joints for some time during the course of the disease in a viable but nonreplicative state, providing an antigenic stimulus for a bacteria-specific immune reaction in the joint. The clinical manifestations of reactive arthritis include not only Reiter's syndrome or clinically suspected postinfectious arthritis but also undifferentiated oligoarthritis and spondylarthritis. The optimal treatment remains to be defined, but there is increasing data that antibiotic therapy is not as effective in cases of well-established reactive arthritis as has been suggested.

Arthritis↗
PubMedDate not supplied

Three-colour flowcytometric examination of CD4/CD45 subsets reveals no differences in peripheral blood and synovial fluid between patients with reactive arthritis and rheumatoid arthritis.

Reactive arthritis (ReA) and rheumatoid arthritis (RA) are inflammatory joint diseases which differ in several clinical and immunological aspects. In both diseases locally activated T cells are considered important for pathogenesis. Subsets of T cells are demonstrated by staining with monoclonal antibodies recognizing isotypes of the common leukocyte antigen: CD45RA, which is considered to be a marker of native T cells, and CD45RO a marker of primed T cells; a third subset was also identified according to the staining intensity of CD45RB: CD45RBbright and CD45RBdim. The expression of these and the surface markers CD3, CD4, CD8, CD14 and CD56 was studied in synovial fluid (SF) and peripheral blood (PB) of patients with ReA (n = 11), RA (n = 10) and normal controls (n = 10) by three-colour immunocytometry. Significantly more CD45RBbright were found in the PB of patients with ReA (64.1%) and RA (63.5%) than in the SF of ReA (36.8%) and RA (40.6%) patients. However, when analyzed in relation to CD45RO, the CD45RO/CD45RBbright population was not significantly different between the SF and PB of patients with ReA (32.2% vs. 26.8%) and RA (30.6% vs. 28.1%), respectively. Among the three cellular subtypes of CD4+ lymphocytes demonstrated in this study (CD45RA/RBbright, CD45RO/CD45RBbright and CD45RO/CD45RBdim) none, in contrast to previous results of other groups, showed marked differences between ReA and RA in either of the compartments examined.

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↗