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Reiter's syndrome (RS) is a clinical triad of non-septic arthritis, urethritis and conjunctivitis. Reactive arthritis (ReA) is another term frequently used, which is an acute arthritis that develops after an infection elsewhere in the body but the live microorganism is not present in the joint. As currently defined, reactive arthritis is restricted to the conditions frequently associated with HLA-B27and does not include rheumatic fever, Lymearthritis, arthritis associated with ulcerative colitis or regional enteritis and postviral arthritides ( 1 ). ReAor RS is induced by two important factors. One factor is the well-knownarthritis-causing microorganismswhichare Shigella, Salmonella, Yersinia and Chlamydia trachomatis. Another host-factor is HLA-B27.These are historically and statistically well-defined factors in this disease. However, some exceptions have been reported; infection with Vibrio parahaemolyticus (2) or C. pneumoniae also induce ReA. Moreover, from 20 to 30% of patients with ReA do not have HLA-B27, therefore, B27 is not included in the diagnostic criteria of ReA. Other than HLA-B27, which HLAis attributed to ReA?One possibility is a B27-cross-reacting HLA, that is B7, Bw22, B39, B40, B42 or B60 (3, 4). It is important to study HLA typing in Japanese patients with seronegative spondyloarthropathy (SNSA) since B27 is found in less than 1% in Japan. In addition to mucocutaneous manifestation in Behget's disease (BD), arthritis in BDhas been reported to have clinical features similar to those in SNSAthat is peripheral oligoarthritis, sacroiliitis or enthesitis (5). Recently, Matsumoto et al (6) proposed B5 1-related arthropathy (personal communication). Therefore, HLA-B51 might be implicated in the pathogenesis of RS which Shimamoto et al describe in this issue (7).

Reactive Arthritis or Reiter''s Syndrome and B51-associated Seronegative Spondyloarthropathy