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Results for “Arthritis, Reactive”

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PubMed1990

Salmonella lipopolysaccharide in synovial cells from patients with reactive arthritis.

Synovial cells from nine patients with reactive arthritis following Salmonella enteritidis or Salmonella typhimurium infection were examined for salmonella antigens. Extensive bacterial cultures of the synovial fluid were negative. Eight synovial-fluid cell samples stained positively on immunofluorescence with rabbit antisera against heat-killed S enteritidis or S typhimurium or with monoclonal antibodies specific for the causative salmonella lipopolysaccharide (LPS). Synovial tissue from the ninth patient stained positively in the avidin-biotin-peroxidase complex method with the monoclonal antibody. Control samples (synovial-fluid cells from thirteen patients with other rheumatic diseases and synovial tissue from two) were negative. Synovial cells from eight patients and five controls were studied by western blotting with the same monoclonal antibodies. Four of the eight patients but no controls had blots indicating salmonella LPS in the synovial cells. The presence of bacterial LPS in the joint is a common and pathogenetically important feature of reactive arthritis.

Acute Disease↗

PubMedDate not supplied

Poststreptococcal reactive arthritis.

Acute rheumatic fever is a delayed inflammatory disease that follows streptococcal infection of the throat. Poststreptococcal reactive arthritis is a sterile arthritis associated with antecedent streptococcal infection in patients not fulfilling the Jones criteria for acute rheumatic fever. Poststreptococcal reactive arthritis has been reported to have lower-extremity predominance and, therefore, should be included in the differential diagnosis of patients with lower-extremity arthritis. A review of the literature, distinguishing poststreptococcal reactive arthritis from acute rheumatic fever, and treatment options are discussed here. A case report is also presented.

Acute Disease↗

PubMed1987

Yersinia specific immune complexes in the synovial fluid of patients with yersinia triggered reactive arthritis.

Yersinia specific immune complexes were demonstrated in the synovial fluid of three patients out of 12 with yersinia triggered reactive arthritis. They were not detectable in the synovial fluid of any of the 16 control patients, including nine with reactive arthritis triggered by factors other than yersiniae. Platelet reactive IgG was detectable in the synovial fluid of eight out of the 12 patients with yersinia triggered reactive arthritis and in three of the 16 control patients, all three having rheumatoid arthritis. An enzyme linked immunosorbent assay and a platelet 125I labelled staphylococcal protein A test were used to measure yersinia specific immune complexes and platelet reactive IgG respectively. The results obtained show for the first time the occurrence of bacterial antigens, derived from the causative strain, in the synovial fluid in yersinia triggered reactive arthritis.

Adolescent↗

PubMed2001

Male sex predominance in Chlamydia trachomatis sexually acquired reactive arthritis: are women more protected by anti-chlamydia antibodies?

OBJECTIVE: To determine whether the humoral anti-chlamydia antibody response might be related to the ineffective bacterial elimination seen in patients with Chlamydia trachomatis reactive arthritis, particularly in men, who have a higher prevalence of the disease than women. METHODS: The number and specificity of the antibody responses to 27 different C trachomatis antigens were determined by western blots in serum samples from patients with C trachomatis urogenital infection, with and without reactive arthritis, with a special regard to the sex of the patients. RESULTS: Patients with reactive arthritis had antibodies to significantly fewer chlamydia antigens than those with urethritis only. Antibodies from men recognised significantly fewer antigens than antibodies from women. The IgA class antibodies were slightly more relevant than those of the IgG class for differentiation of patients with reactive arthritis from those with uncomplicated genitourinary infection. CONCLUSIONS: In patients with acute C trachomatis infection the development of reactive arthritis may be related, particularly in men, to a deficient humoral response, to antigens which perhaps play a part in the clearance of the bacteria. Men who cannot generate antibodies to a large number of antigens may be less able to contain the local infection, allowing a wide systemic dissemination of the organisms to the joints.

Adolescent↗

PubMedDate not supplied

Reactive arthritis associated with Campylobacter enteritis.

Campylobacter jejuni has recently become recognized as a leading cause of diarrhea. To date reactive arthritis has rarely been diagnosed in association with Campylobacter enteritis. Clinical manifestations, diagnostic studies and management of 21 patients with Campylobacter-reactive arthritis are reviewed. The symptom-free interval between diarrhea and arthritis lasts from a few days to several weeks. In two-thirds of the patients sterile joint involvement is multiple, is migratory and includes large joints. Fever and leukocytosis are usually absent, whereas the erythrocyte sedimentation rate is elevated. Positive association with HLA-B27 is found in approximately 60% of cases. Arthritic course is self-limiting and ranges from one week to several months, and prognosis is excellent. These features of Campylobacter-reactive arthritis are consistent with those of reactive arthritis associated with Salmonella, Shigella or Yersinia intestinal infection.

Adolescent↗

PubMed1996

Reactive arthritis induced by tonsillitis.

We describe 13 adult patients with reactive arthritis induced by tonsillitis. Arthritis occurred 710 days after tonsillitis and involved the wrists, knees, feet and sternoclavicular joints. Some cases had pain in the Achilles tendon areas. Synovial fluid examined in 4 patients was sterile. All patients except 3 showed unequivocal elevation of serum ASO and/or ASK. Streptococcus was isolated from tonsillar swabs in 7 patients. One had maculopapular erythema and 2 had abdominal pain of unknown origin, but none had cardiac involvement, chorea and subcutaneous nodule. HLA examination revealed that 4 had B39 (p <0.005). Eight cases were treated with antibiotics. Five cases underwent tonsillectomy. All tonsils had cryptic abscess. No exacerbation was seen thereafter. These cases probably represent reactive arthritis induced by tonsillitis and should be distinguished from other rheumatic diseases.

Adult↗

PubMed1991

Analysis of function-associated receptor molecules on peripheral blood and synovial fluid granulocytes from patients with rheumatoid and reactive arthritis.

In this study we report the expression pattern of 13 different function-associated surface molecules on synovial fluid and peripheral blood granulocytes from rheumatoid and reactive arthritis patients. We found increased expression of the complement receptors 1 (CD35) and 3 (CD11b) and of the activation-associated antigens CD67, CD24, and M5 on synovial fluid granulocytes from rheumatoid and/or reactive arthritis patients compared to autologous peripheral blood granulocytes. In addition, synovial fluid granulocytes expressed IgG Fc receptor 1 (CD64) and complement receptor 4 (CD11c), neither of which can be found on peripheral blood granulocytes. Peripheral blood granulocytes from rheumatoid and reactive arthritis patients expressed higher levels of leucocyte function-associated antigen 1 (CD11a) and of the membrane proteins CD31, CD24, M5, and M6 compared to peripheral blood granulocytes from healthy controls and patients with degenerative joint disease. No significant differences in the expression of any of the molecules studied could be observed between cells from rheumatoid and cells from reactive arthritis patients, suggesting a similar activation process for granulocytes in these two diseases.

Antigens, CD↗

PubMed1987

HLA antigens in seronegative spondylarthropathies. Reactive arthritis and arthritis in ankylosing spondylitis: relation to gut inflammation.

The prevalence of HLA-A, B, C and DR antigens was determined and compared in 94 patients with reactive arthritis, 54 patients with ankylosing spondylitis (AS), 37 patients with inflammatory bowel disease (IBD) and in 1,010 apparently normal blood donors. The 185 patients all underwent ileocolonoscopy with biopsy of ileum, ileocecal valve and cecum. HLA-B27 was found elevated in the groups with reactive arthritis (48%, chi 2 = 82, p less than 0.0005) and the AS groups (78%, chi 2 = 157, p less than 0.0005), compared to healthy controls. HLA-Bw62 was significantly raised in the patients with reactive arthritis (34%, chi 2 = 73, p less than 0.0005) (particularly the HLA-B27 negatives (48%, chi 2 = 90, p less than 0.0005) and in the HLA-B27 negative patients with AS (25%, chi 2 = 5.5, p less than 0.02). This did not apply to the other patients with AS (4.7% NS). HLA-Bw62 could be associated with a specific clinical picture of asymmetrical pauciarticular arthritis, accompanied by enthesopathies and sacroiliitis classified as idiopathic reactive arthritis, especially when the disease is of enterogenic origin. The frequency of HLA-Bw62 was very high in patients with reactive arthritis and in patients with AS with active chronic (n = 39, 23%, chi 2 = 13, p less than 0.0005) and Crohn-like lesions (n = 14, 50%, chi 2 = 35, p less than 0.0005) on gut biopsy, normal in patients with acute lesions (n = 35, 11%, NS).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1997

A single nonamer from the Yersinia 60-kDa heat shock protein is the target of HLA-B27-restricted CTL response in Yersinia-induced reactive arthritis.

The reason for the high association of HLA-B27 with diseases such as ankylosing spondylitis and reactive arthritis is not clear. In reactive arthritis, the triggering bacteria are known, thus allowing investigation of their interaction with HLA-B27. CTL lines derived from five patients with Yersinia-induced reactive arthritis were raised by repeated stimulation in vitro with either Yersinia-infected autologous macrophages (four patients) or pooled peptides (three patients) having the HLA-B27-binding motif. The peptides were derived from five Yersinia proteins and from the chlamydial 57-kDa heat shock protein (hsp). Cytotoxicity of T cell lines was then tested against these peptides. Lytic activity was obtained with T cells stimulated with viable Yersinia or pooled peptides. Targets successfully used for lysis were cells pulsed with peptides from the Yersinia 60-kDa hsp, but not cells pulsed with peptides from other Yersinia proteins or the chlamydial hsp. T cell lines raised with 60-kDa peptides also lysed targets infected with Yersinia. Most interestingly, all three CTL lines tested (one raised with Yersinia; two with pool of peptides) recognized only one single peptide (321-329) of seven tested from the Yersinia hsp60. Cytotoxicity occurred only when target cells were matched for HLA-B27. This identification of an immunogenic peptide derived from an arthritogenic bacterium and presented by HLA-B27 opens the way for future investigation of the role of T cells specific for this peptide or cross-reacting peptides, in the immunopathology of HLA-B27-associated diseases.

Arthritis, Infectious↗

PubMedDate not supplied

Reactive arthritis. A clinical approach.

What do conjunctivitis, urethritis/cervicitis, and arthritis have in common? These are all clues to the diagnosis of reactive arthritis. It takes a keen eye, a thorough history, a good physical examination, and a broad differential diagnosis to pull together the picture when sorting through seemingly unrelated clinical symptoms. Often a team approach is used when caring for patients with reactive arthritis. This article presents the diagnosis and treatment of reactive arthritis.

Algorithms↗

PubMed1998

Bacterial antigens in reactive arthritis and spondarthritis. Rational use of laboratory testing in diagnosis and follow-up.

An aetiological diagnosis of reactive arthritis is based on the demonstration of recent or ongoing infection with the causative bacterium. This may be done by serological demonstration of antibacterial antibodies, demonstration of the causative microorganism at an extra-articular site or by identification of bacterial nucleic acids or antigens in joint material from patients with aseptic arthritis. The finding of elevated titres of bacteria-specific IgG- and IgA-class antibodies may indicate recent or persistent infection, but has some limitations due to the prevalence of such antibodies among apparently healthy individuals and the persistence of such antibodies after the infection. While Chlamydia can be demonstrated in urogenital specimens in at least one-third of patients with Chlamydia-induced arthritis, the triggering microorganisms are usually no longer detectable in post-dysenteric reactive arthritides. Assays involving molecular amplifications have been successfully used to demonstrate bacterial nucleic acids in joint specimens from patients with reactive arthritis. In addition, bacterial antigens have been detected by immunofluorescence tests. Even though examination of synovial fluid and synovial membrane specimens for bacterial DNA by the polymerase chain reaction is increasingly used to diagnose reactive arthritis, such assays have not been standardized and are not generally available. While some problems remain, these techniques will facilitate the exact diagnosis of reactive arthritides in the near future.

Antigens, Bacterial↗

PubMed1983

Yersinia reactive arthritis.

A review of Yersinia reactive arthritis is presented with a description of clinical manifestations and immunological features. The pathogenesis of the reactive lesion has so far not been resolved since no conclusive data on the existence or nonexistence of Yersinia antigens in the inflamed joints have been reported. It does not appear that Yersinia is involved in rheumatoid arthritis.

Adult↗

PubMed1997

Reactive arthritis.

The complex interactions between the triggering microbe and the defense mechanisms of the host in reactive arthritis have been studied in several laboratories around the world, and interesting observations have been made. Research has also focused on the mediators in the inflammatory process in joints, and these results are helping to slowly build a comprehensive picture about the pathogenetic process in reactive arthritis. For the practicing clinician, some important new findings have emerged. It is known that asymptomatic urogenital infections are quite common as a trigger of reactive arthritis. More aggressive treatment, including disease-modifying drugs as used in the therapy of rheumatoid arthritis, is becoming accepted. The value of antibiotic treatment is being studied, but final conclusions will not be made for perhaps a few years.

Animals↗

PubMed2000

Poststreptococcal reactive arthritis.

The occurrence of an entity designated poststreptococcal reactive arthritis (PSReA) has been highlighted in recent reports. The syndrome was considered part of the spectrum of acute rheumatic fever by some, whereas others stressed the differences between the two diseases. As distinct from acute rheumatic fever, PSReA is characterized by a shorter latency period between the inciting streptococcal infection and the onset of arthritis, a higher frequency of involvement of the small joints and axial skeleton, poor response to aspirin and other nonsteroidal anti-inflammatory drugs, a protracted course of arthritis, a low incidence of carditis, and absence of other major manifestations of acute rheumatic fever. Recent studies have demonstrated an increased frequency of DRB1*01 in patients with PSReA, which contrasts with the increased frequency of DRB1*16 in rheumatic fever. Because 6% of patients with PSReA have been reported to have late onset carditis, it is judicious to recommend that patients with PSReA receive prophylactic antimicrobials for a minimum period of 5 years or until the age of 21 years, whichever is longer.

Adolescent↗

PubMed1982

Reactive arthritis associated with Clostridium difficile.

A case of reactive arthritis in a patient with a previously documented history of Reiter's syndrome is described. The precipitating agent appears to have been Clostridium difficile. High levels of toxin were demonstrable in the faeces and neutralising antitoxin was detected in the patient's serum but not synovial fluid. Resolution of the polyarthropathy was slow despite successful eradication of the C. difficile with a course of vancomycin.

Adult↗

PubMed1991

[The clinical and immunogenetic characteristics of reactive arthritis in children].

Altogether 52 children suffering from reactive arthritis were placed under observation. In 45 patients arthritis developed after nasopharyngeal infection and was marked by a favourable course with a rapid positive dynamics. 7 children with a history of intestinal infection manifested Reiter's syndrome; in these children arthritis was characterized by a grave and prolonged course and by a high laboratory activity. HLA A10 (RR = 2.7), B27 (RR = 2.5) and DR2 (RR = 2.19) antigen were detected significantly more frequently in ReA patients who suffered nasopharyngeal infection. In children with Reiter's syndrome, the genetic markers of predisposition to the disease were HLA A10 (RR = 5.93) and B27 (RR = 149.1) antigens.

Adolescent↗

PubMed1998

In situ hybridisation and direct fluorescence antibodies for the detection of Chlamydia trachomatis in synovial tissue from patients with reactive arthritis.

BACKGROUND: Chlamydia trachomatis is associated with Reiter's syndrome and reactive arthritis but the form in which the organism survives in synovial cells is unclear. AIM: To compare in situ hybridisation with direct fluorescence in the detection of inapparent chlamydial infection in synovial tissue. METHODS: Synovial tissue from four patients with reactive arthritis patients was examined using biotin labelled probes for chlamydial DNA and fluorescein isothiocyanate (FITC) labelled monoclonal antibodies against the major outer membrane protein. RESULTS: In two of the four patients, evidence of chlamydial infections was detected by in situ hybridisation in parallel sections but not with FITC labelled monoclonal antibodies. CONCLUSIONS: Detection of chlamydial DNA by in situ DNA hybridisation may be a better way to identify chlamydial infection in synovial tissue than phenotype targeting with FITC conjugated antibodies, which is used as a standard procedure for screening clinical specimens for chlamydia.

Adult↗

PubMed1992

Clostridium difficile toxin-induced reactive arthritis in a patient with chronic Reiter's syndrome.

The first case of Clostridium difficile toxin-induced reactive arthritis in a patient with chronic Reiter's syndrome is described and compared with previous cases of reactive arthritis associated with this organism. This case demonstrates how distinct clinical manifestations may develop at different times in Reiter's syndrome, according to the infecting organism. Diagnostic terminology is discussed in this context. Clostridium difficile should now be considered a firmly established cause of reactive arthritis.

Adult↗