Skin inflammation associated with arthritis, synovitis and enthesitis. Part 2: rheumatoid arthritis, reactive arthritis, Reiter's syndrome, Lyme borreliosis, dermatomyositis and lupus erythematosus

2019 ◽  
Vol 17 (2) ◽  
pp. 167-181
Author(s):  
Christoph M. Schempp ◽  
Franziska Schauer ◽  
Christian K. Huhn ◽  
Nils Venhoff ◽  
Stephanie Finzel
Keyword(s):  
Rheumatoid Arthritis ◽  
Lyme Borreliosis ◽  
Lupus Erythematosus ◽  
Reactive Arthritis ◽  
Skin Inflammation ◽  
Reiter's Syndrome ◽  
Reiter’S Syndrome

Arthritis and Foodborne Bacteria

1994 ◽  
Vol 57 (10) ◽  
pp. 935-941 ◽  
Author(s):  
JAMES L. SMITH
Keyword(s):  
T Cells ◽  
Ankylosing Spondylitis ◽  
Reactive Arthritis ◽  
Molecular Mimicry ◽  
Food Poisoning ◽  
Cell Subset ◽  
Bacterial Cells ◽  
Hla B27 ◽  
Reiter's Syndrome ◽  
Reiter’S Syndrome

Diarrheic episodes caused by the foodborne pathogens Campylobacter, Salmonella, Shigella or Yersinia may lead to a sterile arthritis such as reactive arthritis, Reiter's syndrome or ankylosing spondylitis. Reiter's syndrome and reactive arthritis have been shown to be sequelae in a few well-studied bacterial food poisoning outbreaks. Reactive arthritis, Reiter's syndrome and ankylosing spondylitis show strong familial association related to the gene for HLA-B27 (HLA = human leucocyte antigen) antigen. Why HLA-B27-positive individuals are more susceptible to arthritis is not known, but molecular mimicry between the HLA-B27 antigen and antigens of triggering bacteria has been demonstrated and this mimicry has been proposed as a mechanism involved in etiology of the arthritides. Antigens from bacteria that triggered the arthritis are present in arthritic joints but bacterial cells are not found. Antibodies and T-cells specific for the triggering bacteria have been demonstrated in arthritic patients. T-cells present in synovial joints respond specifically to the particular arthritic triggering pathogen. The cells that respond to bacterial antigens belong to the T-cell subset TH1 that secrete a limited number of cytokines but it is not known if cytokines are involved in arthritis. A few studies have demonstrated that T-cells from the joints of arthritic patients respond to both bacterial and human heat shock proteins indicating that autoimmunity may be involved in causation of arthritis. While only about 2% of a population exposed to a triggering infection will acquire arthritis, these individuals undergo pain and suffering as well as economic hardships as a result of their disease.

Cyclic Nucleotides in Joint Fluid in Rheumatoid Arthritis and in Reiter's Syndrome

1979 ◽  
Vol 8 (2) ◽  
pp. 91-96 ◽  
Author(s):  
L. E. Trang ◽  
O. Lovgren ◽  
A. E. Roch-norlund ◽  
R. S. Horn ◽  
O. Walaas
Keyword(s):  
Rheumatoid Arthritis ◽  
Cyclic Nucleotides ◽  
Joint Fluid ◽  
Reiter's Syndrome ◽  
Reiter’S Syndrome

Bacteriological Findings in 25 Patients with Reiter's Syndrome (Reactive Arthritis)

1983 ◽  
Vol 12 (2) ◽  
pp. 157-160 ◽  
Author(s):  
Ann Bengtsson ◽  
Christer Ahlstrand ◽  
Folke D. Lindstrom ◽  
Erik Kihlstrom
Keyword(s):  
Reactive Arthritis ◽  
Reiter's Syndrome ◽  
Reiter’S Syndrome

Reiter's Syndrome in Children: Case Report and Review of Literature

1962 ◽  
Vol 1 (3) ◽  
pp. 148-151
Author(s):  
Andrew M. Margileth
Keyword(s):  
Rheumatoid Arthritis ◽  
Case Report ◽  
Juvenile Rheumatoid Arthritis ◽  
No Value ◽  
Recent Literature ◽  
Classical Case ◽  
Review Of Literature ◽  
Reiter's Syndrome ◽  
The Past ◽  
Reiter’S Syndrome

1. Our experience with a six-year-old boy who had diarrhea, urethritis, conjunctivitis and arthritis is presented as a classical case of Reiter's syndrome. The patient recovered fully in a period of five months and has remained well during the past five years. 2. The cause of Reiter's syndrome remains unknown but in children may be related to Flexner bacillus dysentery. 3. The disease in children is usually less severe than in adults and all 11 children reported have recovered. The recent literature is reviewed. 4. Treatment with antibiotics is of no value and steroid therapy has not prevented exacerbations nor shortened the course of the disease. 5. The nongonococcal triad of urethritis, conjunctivitis, and arthritis is a distinct clinicopathologic entity which differs from known infections and juvenile rheumatoid arthritis.

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