Reactive arthritis (ReA) refers to acute nonpurulent arthritis complicating an infection elsewhere in the body.
Reiter's syndrome (post-infectious arthritis, urethritis, conjunctivitis) can be said to represent one part of the spectrum of the clinical manifestations of reactive arthritis, particularly that induced by Shigella or Chlamydia. The term Reiter's syndrome is now largely of historic interest only. Since most patients with spondyloarthropathy do not have the classic features of Reiter's syndrome, it has become customary to employ the term reactive arthritis, regardless of whether or not there is evidence for a triggering infection.
The most common bacterial infections known to cause reactive arthritis are Salmonella, Y. enterocolitica, C. jejuni, and C. trachomatis.
The majority of patients will present with a history of previous infection (1-4 weeks earlier). Urinary tract symptoms (urethritis) as well as occular symptoms (conjunctivitis) may occur later in the course of the disease.
Lab tests show an increase in acute phase reactants in the blood. In early or mild disease, radiographic changes may be absent or confined to juxtaarticular osteoporosis. With long-standing persistent disease, marginal erosions and loss of joint space can be seen in affected joints. Periostitis with reactive new bone formation is characteristic of the disease, as it is with all the spondyloarthropathies. Spurs at the insertion of the plantar fascia are common.
Reactive arthritis is a clinical diagnosis and should be entertained with any case of asymmetric inflammatory arthritis or tendinitis.
NSAID (Non steroidal anti-inflammatory drugs) may benefit some patients (e.g. indomethicin). It is unclear if antibiotics have a role at all reactive arthritis.
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