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Reactive arthritis or post-infectious arthritis?

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The term ‘reactive arthritis’ was first used in 1969 to describe the development of sterile inflammatory arthritis as a sequel to remote infection, often in the gastrointestinal or urogenital tract. The demonstration of antigenic material (e.g. Salmonella and Yersinia lipopolysaccharide), DNA and RNA, and, in occasional cases, evidence of metabolically active Chlamydia spp. in the joints has blurred the boundary between reactive and post-infectious forms of arthritis.

No validated and generally agreed diagnostic criteria exist, but the diagnosis of reactive arthritis is mainly clinical based on acute oligoarticular arthritis of larger joints that develops within 2–4 weeks of the preceding infection. In about 25% of patients, the infection can be asymptomatic. Diagnosis of the triggering infection is very helpful for the diagnosis of reactive arthritis. This is mainly achieved by isolating the triggering infection (stools, urogenital tract) by cultures (stool cultures for enteric microbes) or ligase reaction (Chlamydia trachomatis). However, after the onset of arthritis, this is less likely to be possible. Therefore, the diagnosis must rely on various serological tests to demonstrate evidence of previous infection, but, these serological tests are unfortunately not standardized. Treatment with antibiotics to cure Chlamydia infection is important, but the use of either short or prolonged courses of antibiotics in established arthritis has not been found to be effective for the cure of arthritis. The long-term outcome of reactive arthritis is usually good; however, about 25–50% of patients, depending on the triggering infections and possible new infections, subsequently develop acute arthritis. About 25% of patients proceed to chronic spondyloarthritis of varying activity.

Section snippets

Clinical features

The typical clinical picture of reactive arthritis (ReA) is characterized by asymmetrical oligoarthritis, often in large joints of the lower extremities. Patients can also have arthritis in the upper limbs. Moreover, a mild polyarticular form has been described, particularly in the small joints.1, 2

In addition to arthritis, patients with ReA can have bursitis or enthesitis, which can also exist as the only musculoskeletal manifestation. Other extra-articular features include inflammatory low

When should antibiotic treatment be given in ReA?

It is important to discuss the role of antibiotic therapy both with respect to treatment of infection and treatment of arthritis. In practice, the issue is whether short-term or long-term treatment is warranted.

Outcome and prognosis of ReA

The duration of acute ReA usually varies between 3 and 5 months.64 The long-term prognosis of enteroarthritides is best known for Yersinia- and Shigella-triggered ReA. Mild peripheral arthralgia and low back pain are frequent in patients with previous ReA (Table 2). About 15% of patients develop AS and about 30% develop radiological sacroiliitis.65, 66 It is still not known whether ReA contributes to the development of sacroiliitis or AS, or whether sacroiliac changes would have occurred in a

Summary

ReA can be regarded as a form of post-infectious arthritis in which microbial structures have been detected in the inflamed joints. While ReA is a sequel of infection (usually in the gastrointestinal or the urogenital tract), the role of antibiotic therapy to prevent the triggering of arthritis or to prevent the development of chronic sequels has not been determined. In the case of established ReA, prolonged treatment of Chlamydia-induced ReA may be of benefit, but in other forms of ReA, there

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      There is an unresolved issue regarding the precise role played by the triggering bacteria in the development of ReA. By definition, no viable bacteria can be cultivated from the inflamed joint, and the triggering enterobacteria have generally been eliminated from the gut at the time of disease outburst [6]. However, in the case of Chlamydia-induced ReA, there is evidence for the persistence of bacteria within monocytic cells in the synovium [8].

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