Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0003864 (arthritis)
 69,039 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Medical records of 138 patients with psoriatic arthritis and 138 with rheumatoid arthritis were reviewed for the occurrence of an environmental factor triggering arthritis. Twelve (9%) of the patients with psoriatic arthritis had had an acute disorder immediately preceding onset of arthritis (an operation in four cases, articular trauma in three, abortion in two, myocardial infarction, thrombophlebitis, and phosphoric ester intoxication in one case each). Peripheral arthritis occurred in all these patients. Among the rheumatoid patients, an acute event immediately preceding the onset of the disease was recorded in two cases (1%) only (chi 2 = 7.52; p = 0.006). No significant association was found in the arthritic patients between the incidence of acute events preceding arthritis onset and positivity of the HLA-B27 phenotype.
 ...
PMID:Interplay between environmental factors, articular involvement, and HLA-B27 in patients with psoriatic arthritis. 154 42

Oligoarticular synovitis of undetermined origin can closely resemble an incomplete form of reactive arthritis/Reiter's syndrome. Eighty three patients with oligoarthritis of undetermined origin were studied prospectively to identify asymptomatic infections potentially triggering the inflammatory response in the synovial fluid. At the time of initial evaluation, 57 (69%) of the patients with oligoarthritis and 4/20 (20%) of the control subjects were carriers of clinically silent infections. Evidence for persistent or prior chlamydial infections was frequently and exclusively found in the study group (30/83 (36%) patients v no controls), whereas undetected urogenital infections with mycoplasma were present in nine (11%) patients and four (20%) controls. Eleven (13%) of the patients carried cellular and humoral responses to Borrelia burgdorferi. The HLA-B27 haplotype represented a major risk factor for the development of oligoarthritis but not for development of sacroiliitis. Re-evaluation after one year showed that the course and outcome of the oligoarticular disease did not correlate with a specific infectious organism and were not affected by antibiotic treatment sufficient to treat the carrier state.
 ...
PMID:Clinically silent infections in patients with oligoarthritis: results of a prospective study. 155 Apr 13

We describe an amino acid homology between a virulence plasmid encoded outer membrane protein of Yersinia, YadA (previously called Yop1) and HLA-B27. This tetrapeptide is also included in the hexapeptide, earlier found to be identical between Klebsiella nitrogenase and HLA-B27. The synthetic peptide based on the HLA-B27 homologous portion of the YadA does not stimulate lymphocytes obtained from HLA-B27+ patients with Yersinia-triggered reactive arthritis or from controls. One-third of the yersiniosis patients have antibodies against the synthetic peptide. Instead of recognizing the HLA-B27 homologous portion, the antibodies are directed against the left flanking sequence of the synthetic peptide. Similar results were obtained regarding antibody response to Klebsiella nitrogenase derived synthetic peptide included in the panel of controls; the response was not restricted to patients with reactive arthritis nor was it specifically directed against the sequence shared by HLA-B27 and Klebsiella pneumoniae nitrogenase. The present results do not support the role of molecular mimicry or cross-reactive antibodies in the pathogenesis of spondyloarthropathies.
 ...
PMID:Molecular mimicry in the pathogenesis of spondyloarthropathies. A critical appraisal of cross-reactivity between microbial antigens and HLA-B27. 155 37

A 40-year-old woman with Reiter's syndrome had low-grade fever, a psoriasislike eruption on feet and hands, and multiple esophageal ulcers. She had keratoderma blennorrhagica, aseptic vaginitis, and ileosacral arthritis, but no ocular lesions. The patient was HLA-B27 negative. Radiographic and endoscopic examinations of the upper gastrointestinal (GI) tract showed multiple round or irregularly shaped small ulcers in the middle and distal portion of the esophagus. One month later, all esophageal ulcers disappeared spontaneously. A case like this of Reiter's syndrome with esophageal involvement has not been reported before.
 ...
PMID:Esophageal ulcer complicated by Reiter's syndrome. A case report. 155 29

Ankylosing spondylitis and related spondyloarthropathies form a family of rheumatic diseases that are characterized by inflammatory peripheral and axial arthritis, with predilection for sacroiliitis, and a remarkably strong association with a genetic marker, HLA-B27. The association with B27 has provided a great impetus to the epidemiologic studies of spondyloarthropathies and also helped broaden the clinical spectrum of these diseases. There are at least six subtypes of B27, and the x-ray crystallographic structure of the common B27 subtype (B*2705) is now known. Endogenous peptides bound in the B27 antigen-binding cleft have been isolated and all seem to be nonamers (i.e., nine amino acids long).
 ...
PMID:An overview of clinical spectrum and heterogeneity of spondyloarthropathies. 156 95

Ankylosing spondylitis is a form of reactive arthritis following Klebsiella infection, usually occurring in an HLA-B27-positive individual. This conclusion is based on evidence obtained from several disciplines: immunogenetic studies show that there is molecular mimicry between HLA-B27 and Klebsiella; increased isolation of fecal Klebsiella has been reported in both Europe and North America; and finally, antibodies to Klebsiella have been demonstrated in ankylosing spondylitis patients in England and Finland. It is suggested that therapeutic trials should be set up with the aim of eliminating Klebsiella microbes, in an endeavor to test the validity of this theory.
 ...
PMID:Ankylosing spondylitis is caused by Klebsiella. Evidence from immunogenetic, microbiologic, and serologic studies. 156 97

We are beginning to understand the clinical nature of JAS, its relationship with other SSA, and factors involved in its pathogenesis. Clinical data may now allow early recognition of JAS through the identification of children with the SEA syndrome or chronic arthritis associated with the HLA-B27. Comparative clinical studies of the prevalence of the disease and the role of immunogenetic, racial and environmental factors are needed. It may be necessary to review current criteria for the diagnosis of JRA and to develop similar criteria for the diagnosis of AS in childhood and adolescence.
 ...
PMID:Juvenile ankylosing spondylitis. 156 99

We described the clinical symptoms and signs of 11 cases of polyenthesitis, confirmed by the presence of inflammation in biopsies and increased activity in scintigraphy. All cases are negative for HLA-B27, and there is no presence of systemic inflammatory reaction, radiographic sacroiliitis, or chronic arthritis. The enthesitis is not ossifying and follows a rather benign clinical course. In one case, herpes virus-like particles were detected in the fibroblast debris of the tissue removed from Achilles tendon insertion. This fact suggests that polyenthesitis may be a clinical manifestation due to a reaction to an infectious agent.
 ...
PMID:Polyenthesitis. 156 3

There are at least three common features among the microbes causing reactive arthritis: (1) they primarily cause infections on mucosal areas, (2) they are intracellularly living microorganisms, and (3) they have lipopolysaccharide as an essential structure of their outer membrane. It is obvious that during or after the acute infection microbial antigens are not properly eliminated, and they persist for long times in HLA-B27-positive persons developing ReA. Bacterial lipopolysaccharide has also been shown to enter the joints and is an important factor in the pathogenesis of ReA.
 ...
PMID:Do bacterial antigens cause reactive arthritis? 156 8

In this article, the mechanisms by which infection at a distant site could lead to ReA and whether they could explain the association of ReA with HLA-B27 have been discussed. We propose that ReA synovitis is primarily due to specific synovial T-cell proliferation to fragments of the triggering bacterial found in the joint. Nonspecific T cells amplify synovitis with antibodies playing only a secondary role. First, we have shown that the triggering bacterial antigen is present in a nonviable form in ReA synovium and that this, not cross-reactive joint autoantigen, stimulates the specific synovial immune response. Second, the studies of the humoral immune response in ReA have been reviewed. Further evidence of bacterial persistence in the joint comes from work demonstrating intrasynovial bacteria-specific antibody synthesis. Continuing maturation of the antibody response also points to persisting antigen. In enteric but not genitourinary ReA, the humoral response is mainly IgA, implying chronic stimulation of the gut mucosa. Analysis of the molecules against which the humoral response is directed has shown no difference between yersinia arthritis and yersiniosis, but in CTA, the response to the 57kD and 59kD antigens differs from CT urethritis suggesting they may be arthritogenic. Finally, the antibody response may be absent in ReA patients rendering antibody titres diagnostically less useful and confirming their secondary role in the pathogenesis of synovitis. Third, studies of cellular response in ReA have been analyzed. We show there is a specific synovial MNC proliferative response to fragments of the triggering bacteria found in the joint, which is potentially of diagnostic use. The proliferation is due to CD4+ and CD8+ T cells and restricted by MHC class I and II antigens. This antigen-specific T-cell response is accompanied by an antigen-independent recruitment of nonspecific T cells, which may contribute to the amplification of synovitis. The importance of the synovial APC in determining the synovial immune response is unarguable but the exact mechanisms are unclear. Further details on the possible role of HLA-B27 in the presentation of arthritogenic peptides and on the exact identity of the antigenic epitopes recognized in ReA must await analysis of a large panel of T-cell clones. Finally, it is hoped that advances in this field will lead to specific and effective immunologic therapies or vaccines for this currently untreatable disease.
 ...
PMID:Antigenic responses in reactive arthritis. 156 9


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>