Characteristics | Reactive arthritis | ||
---|---|---|---|
HLA-B27 associated3-150 | HLA-B27 non-associated3-151 | ||
Triggers | Campylobacter, Chlamydia, Clostridium difficile, Salmonella, Shigella, Yersinia | A variety of other microbes | |
Cultivable microbes present in joint | No | No | |
Microbial structures demonstrated in joint | Yes | So far only rarely | |
Differential diagnosis to bacterial arthritis | Mostly clear | Often unclear | |
Oligo-or polyarthritis | Usually oligoarthritis, most commonly in knee | Polyarthritis more common than in the B27 associated form; other joints than knee affected as well | |
Reiter's syndrome | Occurs | Not usual, but found after genitourinary infections3-153 | |
Tendency for chronicity | Yes | Not clear | |
Evolution to ankylosing spondylitis | Possible | Not observed | |
Part of spondyloarthropathy group | Yes | No | |
Pathogenetic mechanisms | Similar to experimental antigen induced arthritis; in addition, an HLA-B27 associated mechanism | Similar to experimental antigen induced arthritis |
↵3-150 Sixty to ninety per cent of patients with this form of reactive arthritis are HLA-B27 positive.
↵3-151 In patients with this form, HLA-B27 occurs in the same frequency as in the normal population.
↵3-153 It is unclear if reactive arthritis developing afterUreaplasma and gonococcal infections is accompanied by other signs of Reiter's syndrome predominantly in HLA-B27 positive patients.