SEARCH · PubMed Health

Results for “Arthritis, Reactive”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 181 records · Page 10Linked to original sources

PubMed1997

Is undifferentiated seronegative spondyloarthropathy a forme fruste of reactive arthritis?

Undifferentiated spondyloarthropathy (USpa) may either represent a forme fruste of other spondyloarthropathies like reactive arthritis or be a different disease entity. To study the link between USpa and reactive arthritis, we studied the presence of IgA antibodies to Yersinia enterocolitica, Salmonella typhimurium, Shigella flexneri, Campylobacter jejuni and Chlamydia trachomatis in sera from 14 patients with USpa (European Spondyloarthropathy Study Group criteria) using ELISA. Escherichia coli was used as a control antigen. An OD value of more than the mean +/- 2 S.D. of 51 blood donors was considered positive. Five patients had elevated IgA antibodies to S. flexneri, while two patients each had elevated antibody levels to S. typhimurium and Chlamydia. No patient had elevated antibodies to Y. enterocolitica, C. jejuni and E. coli. Among 51 normals, 1, 4, 3, 2 and 3 had elevated antibodies to S. flexneri, S. typhimurium, Y. enterocolitica, C. jejuni and E. coli, respectively. Nine of 14 patients with USpa had antibodies to one of the bacteria implicated in reactive arthritis: of these, antibodies to Shigella were the most frequent. Thus, a proportion of patients with USpa may in fact have reactive arthritis.

Adolescent↗

PubMed1989

Yersinia antigens in synovial-fluid cells from patients with reactive arthritis.

We examined synovial-fluid cells from 15 patients with reactive arthritis after yersinia infection for the presence of yersinia antigens. Extensive bacterial cultures of the synovial fluid were negative. All the samples were studied by immunofluorescence with use of a rabbit antiserum to Yersinia enterocolitica O:3 and a monoclonal antibody to Y. enterocolitica O:3 lipopolysaccharide. Synovial-fluid cells from 41 patients with other rheumatic diseases served as controls. Synovial-fluid cells from 10 patients with reactive arthritis after yersinia infection stained positively on immunofluorescence; rabbit antiserum and the monoclonal antibody yielded similar results. In most patients the percentage of positive cells ranged from 1 to 10 percent, but in one patient nearly all the cells in the sample stained strongly. Most of the positively stained cells were polymorphonuclear leukocytes, but yersinia antigens were also found in mononuclear phagocytes. All the control samples were negative. Synovial-fluid cell deposits from nine patients were also studied by Western blotting with use of the same antibodies. The results were positive in six of the nine cell deposits from patients with reactive arthritis and in none of the 10 cell deposits from control patients with rheumatoid arthritis. We conclude that in patients with reactive arthritis after yersinia infection, microbial antigens can be found in synovial-fluid cells from the affected joints.

Adult↗

PubMed1981

Reactive arthritis associated with Yersinia enterocolitica gastroenteritis.

Reactive arthritis associated with Yersinia enterocolitis in adults has not been reported in this country. We are reporting a 26-year old female with a polyarticular arthritis, primarily of the large joints following an episode of diarrhea. She was also observed to have erythema nodosum and erythema multiforme. Yersinia enterocolitica grew in abundance in stool culture. The clinical picture is consistent with the reactive arthritis associated with Yersinia enterocolitis.

Adult↗

PubMed1999

Different humoral immune response to Chlamydia trachomatis major outer membrane protein variable domains I and IV in Chlamydia-infected patients with or without reactive arthritis.

OBJECTIVE: The possibility that some bacterial-specific factor(s) may play a role in triggering Chlamydia trachomatis reactive arthritis was investigated. METHODS: Since the variable domains of the major outer membrane protein (MOMP) contain the serovar-determining epitopes of C. trachomatis, the ability of serum IgG to recognize peptides mimicking these epitopes was determined in 2 groups of infected patients, one with and the other without reactive arthritis. Because asymptomatic C. trachomatis infections are frequent, and nonspecific reactions due to inflammation could be observed, this study was also performed with samples from healthy blood donors and from patients with inflammatory arthritis unrelated to C. trachomatis infection. RESULTS: A predominant reactivity against peptides duplicating the J serovar-specific epitopes was only observed in the group of patients with reactive arthritis. For positive samples, differences between the two groups of C. trachomatis-infected patients were clearly observed. The mean numbers of positive responses obtained for each of the 7 peptides of the MOMP domain I or each of the 8 peptides of the MOMP domain IV were significantly higher for samples from patients with reactive arthritis (4.7 and 6) than for those from patients with only C. trachomatis urogenital infection (1.3 and 2.9). CONCLUSION: Patients with reactive arthritis had a pattern of reactivities that was compatible with infection by several serotypes of bacteria. Repeated exposures to C. trachomatis might therefore be involved in the development of the disease.

Adolescent↗

PubMed1987

Chlamydia trachomatis and reactive arthritis: the missing link.

Reactive inflammatory arthritis is a common sequel to sexually acquired non-gonococcal genital-tract infection. Approximately 50% of cases are associated with Chlamydia trachomatis infection in the genital tract, although conventional cultures of joint material are sterile. Synovium, synovial-fluid cells, or both, from eight patients with sexually acquired reactive arthritis (SARA) and eight with knee effusions associated with other rheumatic diseases were examined by means of a fluorescein-labelled monoclonal antibody to C trachomatis ('Micro Trak'; Syva). Typical chlamydial elementary bodies were seen in joint material from five patients with SARA but in none of the controls. An inclusion-like cluster of elementary bodies was seen in one synovial biopsy sample. All five patients had high titres of serum chlamydial antibody. It is likely that the synovitis of SARA results directly from the presence of chlamydial elementary bodies in the joint.

Adult↗

PubMed1992

Yersinia enterocolitica activates a T helper type 1-like T cell subset in reactive arthritis.

The profile of lymphokines secreted by 14 T cell clones and 24 T cell lines reactive with Yersinia Ag isolated from the synovial fluid cells of two HLA-B27+ patients with Yersinia-triggered reactive arthritis was characterized. In response to Ag-specific or -nonspecific stimulation, all of the Yersinia-reactive T cell clones and lines had a pattern of lymphokine secretion resembling that of murine (Th1) cells. A total of 50% of T cell lines and clones randomly isolated from a reactive arthritis patient, without prior in vitro stimulation with Yersinia Ag, also exhibited a Th1-like profile of cytokine secretion upon nonspecific activation. This indicates that the selective expansion of this subset of T cells had already occurred in vivo. The possibility that the predominance of Th1-like T cells was an artefact generated by the T cell cloning procedure was excluded; 50% of the randomly isolated T cell clones and lines produced IL-4, IL-5, or both cytokines upon nonspecific activation. These results indicate that Yersinia Ag selectively activate a Th1-like subset of T cells in patients with Yersinia-triggered reactive arthritis. Accumulation of such cells in the synovial tissue of patients with reactive arthritis may play a key role in the pathogenesis of this disease.

Antigens, Bacterial↗

PubMed1992

AB0 and Lewis blood groups in reactive arthritis.

In this study we evaluated secretor status in patients with reactive arthritis. Previous evidence indicates that non-secretion of AB0 and Lewis blood group antigens to saliva and other secretions is associated with susceptibility to certain bacterial infections and certain diseases with suspected autoimmune etiology. Secretor status can be determined based on the Lewis phenotype. We studied AB0, Lewis and Rhesus blood groups of 54 patients with previous reactive arthritis, 26 of whom had uroarthritis and 28 of whom had arthritis after enteric infection. Furthermore, 25 patients with uncomplicated yersiniosis and 57 healthy controls were studied. We did not find any correlation between secretor status and reactive arthritis or gastroenteritis due to Yersinia. AB0 blood group antigen B appeared to be protective against uroarthritis.

ABO Blood-Group System↗

PubMed2001

Indirect evidence of intra-articular immunoglobulin G synthesis in patients with Chlamydia trachomatis reactive arthritis.

OBJECTIVES: To investigate whether B-cell stimulation occurs in joints of Chlamydia trachomatis reactive arthritis patients by comparing the immunoglobulin G (IgG) anti-C. trachomatis antibody responses in serum and synovial fluid (SF). METHODS: The number and spectrum of C. trachomatis antigens recognized by paired serum and SF samples from 16 patients with C. trachomatis reactive arthritis and 20 patients with other inflammatory arthropathies independent of this bacteria, were studied by immunoblotting. The responses to five different Chlamydia antigens were also determined in enzyme-linked immunosorbent assays. RESULTS: In C. trachomatis reactive arthritis patients, a higher number of C. trachomatis antigens was recognized by SF (17.6+/-5.1) than by serum (11.1+/-6.3) IgG and a higher intensity of SF IgG binding to the outer membrane protein 2 (OMP2) was observed. CONCLUSIONS: These results suggest an intra-articular IgG production and a possible role of some Chlamydia antigens like OMP2 in the pathogenesis of C. trachomatis reactive arthritis.

Antigens, Bacterial↗

PubMed1995

[Diagnostic evaluation of suspected reactive arthritis].

On the basis of an epidemiological study on recently onset, possible reactive arthritides in Oslo we propose a programme for diagnostic evaluation. Disease symptoms and signs provided little help for an ethiological diagnosis. Therefore a variety of diagnostic tests and examinations are recommended in order to obtain a correct diagnosis; such as clinical examination, chemical and serological blood tests, bacteriological examinations from throat, of stools and of specimens from urethra-cervix, examination of synovial fluid and synovial tissue and X-ray examination of affected joints, sacroiliacal joints and lungs. About one third of the recently onset arthritides in the Oslo study were diagnosed as reactive arthritis, one third as possible reactive arthritis and another third as inflammatory arthritides.

Arthritis, Reactive↗

PubMed1997

Reactive arthritis with a severe lesion of the cervical spine.

Reactive arthritis, or Reiter's disease, characteristically affects the joints of the lower limbs in an asymmetrical pattern. Usually it does not affect the cervical spine, and atlantoaxial subluxations are the exception. This paper describes the case of an HLA-B27-positive female patient with a sexually acquired reactive arthritis where a non-reducible atlantoaxial subluxation was present. The patient was followed from age 27 to 41. By the age of 38, an anterior decompression of the cervico-medullary junction was performed by a transoral approach; in a second stage, the patient underwent an occipito-cervical posterior fusion. The pathological study revealed a non-specific and chronic inflammatory infiltrate.

Adult↗

PubMed1994

The humoral immune response to Chlamydia trachomatis in patients with acute reactive arthritis.

Sera from 25 patients with clinical signs of reactive arthritis were analysed for antibodies against Chlamydia trachomatis by immunoblotting. Purified elementary bodies, purified Chlamydia outer membrane complexes, and purified recombinant subcomponents were used as antigens. Antibodies against C. trachomatis cysteine rich outer membrane protein 2 (Omp2) and lipopolysaccharide (LPS) were detected in 10 patients. Thus 40% of the patients presented antibodies specific for C. trachomatis. There was no correlation between acute reactive arthritis and antibodies to heat-shock proteins GroEL, GroES and DnaK.

Acute Disease↗

PubMedDate not supplied

Poststreptococcal reactive arthritis mimicking acute septic arthritis: a hospital-based study.

Poststreptococcal reactive arthritis (PSRA) is an inflammatory arthritis that follows group A streptococcal pharyngitis. The clinical presentation of PSRA can mimic acute septic arthritis. We present 12 children with PSRA seen between December 1991 and September 1993. Most children had only mild pharyngitis by history. The pattern of arthritis was variable and included migratory polyarthritis, additive polyarthritis, and monoarthritis, and was accompanied by fever in seven children. In four patients, the presentation of fever and acute onset of painful monoarthritis mimicked septic arthritis, and synovial fluid cultures were negative in all four cases. All 12 patients demonstrated an immune response to group A streptococcus. PSRA should be in the differential diagnosis of any child presenting with acute onset of painful arthritis, including those cases of presumed septic arthritis with negative synovial fluid cultures.

Acute Disease↗

PubMed2005

[Effectiveness of ronkoleukin in children with reactive arthritis of chlamydial etiology].

14 children with reactive arthritis (ReA) were treated by antibiotics of macrolid group--vilprafen and anti-inflammatory medicines. Immunocorrective mean ronkoleukin (recombinant interleukin-2) was used as an additional therapy for activation of lymphocytes and NK cells. Five patients from 14 were treated by intravenous injections of ronkoleukin followed by oral administration of this drug. 9 children were treated by oral administration of ronkoleukin. All 14 children were treated by ronkoleukin along with the basic therapy. All children got repeated course of ronkoleukin one year later. From 14 children 12 reached remission of the disease.

Administration, Oral↗

PubMed1987

[Reactive arthritis in enteral infections].

Certain gastrointestinal tract infections can trigger reactive arthritis. The best known triggering agents are yersinia, salmonella, shigella, campylobacter jejuni, and possibly clostridium difficile. The clinical findings show a subacute onset of mono- or oligoarthritis, less often of asymmetric polyarthritis with predominance of the lower limbs. The clinical picture is somewhat modified by the genetic constitution (HLA type) of the patient. HLA-B27-positive patients appear to have more severe symptoms, extraarticular features and incomplete or complete Reiter's syndrome than HLA-B27-negative patients. Diagnosis of postenteritic reactive arthritis is based on bacteriological stool analysis and/or examination of serumantibodies to the corresponding agents. Reactive arthritis is usually self-limiting and therefore treatment of the disease has to be mainly symptomatic. Only more severe chronic or destroying arthritis is thought to be treated locally (i.e. by synoviorthesis) or by immunoregulatory drugs.

Arthritis, Infectious↗

PubMed1992

Aetiological role of bacteria associated with reactive arthritis in pauciarticular juvenile chronic arthritis.

BACKGROUND: The cause of juvenile chronic arthritis (JCA) is unknown. Pauciarticular JCA is the most common subtype and can be subdivided into early (type I) and late onset (type II) forms, the latter clinically resembling reactive arthritis. METHODS: The cellular immune responses to bacteria associated with reactive arthritis in blood and synovial fluid from 39 children with pauciarticular JCA, three children with classical reactive arthritis, and two children with psoriatic arthritis were examined. Specific titres of antibodies to bacteria in serum samples were measured in all patients. RESULTS: A bacteria specific synovial cellular immune response was found in two of three (67%) patients with reactive arthritis and 14 of 28 (50%) patients with pauciarticular JCA type II but only in one of 11 (9%) patients with pauciarticular JCA type I and none in patients with psoriatic arthritis. Six patients responded specifically to Chlamydia trachomatis and 11 to Yersinia enterocolitica. Antigen specific lymphocyte proliferation correlated poorly with the specific antibody response. CONCLUSIONS: These findings suggest that bacteria with associated reactive arthritis may have a causative role in pauciarticular JCA type II but not in JCA type I.

Adolescent↗

PubMed2005

Aberrant TNF secretion by whole blood in healthy subjects with a history of reactive arthritis: time course in adherent and non-adherent cultures.

BACKGROUND: The pathogenesis of reactive arthritis (ReA) apparently involves aberrations in innate immune functions such as monocyte tumour necrosis factor (TNF) generation. OBJECTIVE: To investigate TNF production in healthy subjects with previous yersinia triggered reactive arthritis. METHODS: The study comprised HLA-B27 positive subjects with previous reactive arthritis (B27+ReA+), and B27+ReA- and B27-ReA- subjects (n = 15 each). Whole blood TNF production was induced by lipopolysaccharide (LPS), which binds to CD14/TLR4 on the monocyte surface, or by a combination of phorbol 12-myristate 13-acetate (PMA) and Ca(2+) ionophore A23187, which activates monocytes independently of cell surface receptors. To further evaluate the possible role of adhesion mediated signalling on TNF production, blood samples were incubated in adherent or non-adherent conditions. TNF levels in culture supernatants were measured using an automated immunoassay analyser. The CD14(-159)C/T genotype was determined by a cycle minisequencing method. RESULTS: B27+ReA+ supernatants had higher TNF levels than B27+ReA- supernatants in PMA/A23187 wells in two hour (p = 0.004) and four hour cultures (p = 0.001). Rapid initial TNF release took place in adherent but not in non-adherent conditions. This adhesion associated difference was greater in the B27+ReA+ group than in the B27+ReA- or B27-ReA- group in response to PMA/A23187 (p values <0.001), and greater in the B27+ReA+ group than in the B27-ReA- group in response to LPS (p = 0.021). CD14(-159)T was associated allele dose dependently with an increase in the LPS induced TNF secretion allele (p = 0.030). CONCLUSIONS SUBJECTS: who have recovered from yersinia arthritis show enhanced TNF production, which may be regulated at the level of monocyte adhesion.

Adult↗

PubMed1988

Factors associated with the development of reactive arthritis.

The role of the causative microorganism in the generation of reactive arthritis is decisive, but host factors are also of major importance. Patients who develop reactive arthritis after Yersinia enteritis show several interesting features in the immunological defence against Yersinia when compared to those who recover uneventfully. When all these peculiarities are taken together, they strongly indicate that in the patients developing reactive arthritis the causative microorganism enters host tissues to persist within the body for prolonged periods of time.

Antibody Formation↗

PubMed1985

Pathogenesis of Yersinia-triggered reactive arthritis: immunological, microbiological and clinical aspects.

When a patient develops reactive arthritis after Yersinia enteritis, the following conditions are often fulfilled: the patient is HLA-B27-positive; however, some B27-negative individuals develop severe arthritis and some positives do not, in the initial phase, the diarrhea is milder, the anti-Yersinia antibody response of IgG class is more vigorous and persists longer, the anti-Yersinia antibody response of IgA class is more vigorous and persists much longer, the anti-Yersinia antibodies of IgA1 and IgA2 subclass, those with J-chain and, especially, those with secretory piece are produced more vigorously, indicating local immunostimulation close to the intestinal epithelium, in the early phase, Yersinia-IgM immune complexes are found in the circulation, and the lymphocyte transformation response against not only Yersinia but also against other gram-negative enteric bacteria is weaker. When all these aspects are considered together a strong suspicion arises that the patients who are destined to develop reactive arthritis fail in their first line of defense against the invading organism when contracting a Yersinia enteritis. This may lead to persistence of the microorganism within the body, e.g., in the intestinal epithelium or in the mesenteric lymphoid tissues, maintaining a stimulus for a prolonged--apparently futile and perhaps harmful--antibody production. Finally, the initiating and decisive factor should not be forgotten: the Yersinia. Why and how it triggers the process is at present one of the enigmas of the pathogenesis of reactive arthritis.

Antibodies, Bacterial↗