Patients may give a history of an antecedent genitourinary or dysenteric infection 1 to 4 weeks before the onset of arthritis.
Presenting features include systemic symptoms such as fever, peripheral and axial arthritis, enthesitis (inflammation where tendons insert into bone), dactylitis (swelling of an entire finger or toe), conjunctivitis and iritis, and skin lesions including circinate balanitis and keratoderma blennorrhagicum.
The peripheral arthritis in reactive arthritis (ReA) is usually an asymmetric oligoarticular arthritis affecting the large joints of the lower limb, although monoarticular and polyarticular arthritis can also occur.
There is no specific test for diagnosing ReA. Rather, a group of tests is used to confirm the suspicion in someone who has clinical symptoms suggestive of an inflammatory arthritis in the postvenereal or postdysentery period.
Treatment is aimed at symptomatic relief and preventing or halting further joint damage. Typical agents include nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, and disease-modifying antirheumatic drugs (DMARDs).
Approximately 30% to 50% of patients will go on to develop some form of chronic ReA.
An inflammatory arthritis that occurs after exposure to certain gastrointestinal and genitourinary infections. The classical triad of postinfectious arthritis, nongonococcal urethritis, and conjunctivitis is frequently described but found only in a minority of cases and not required for diagnosis. This triad of symptoms was described by Hans Reiter in 1916. However, the term "Reiter syndrome" has fallen out of favor because of his ties to the Nazi Party and medical experiments on concentration camp prisoners. ReA belongs to the family of spondyloarthropathies, which share similar clinical, radiographic, and laboratory features that include spinal inflammation and an association with HLA-B27. They include psoriatic arthritis, ankylosing spondylitis, arthritis related to inflammatory bowel disease, and undifferentiated spondyloarthropathy.
Professor of Medicine
Division of Rheumatology
University of South Florida College of Medicine
JDC is a co-author of several references cited in this monograph.
Dr John D. Carter would like to gratefully acknowledge Dr Jason P. Guthrie, a previous contributor to this monograph. JPG declares that he has no competing interests.
Professor of Rheumatology
University of Cambridge
JSHG declares that he has no competing interests.
Professor and Chief
Section of Rheumatology
Department of Internal Medicine
LSU Health Sciences Center
LRE is a co-author of several references cited in this monograph.
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