Abstract
Reactive arthritis (ReA) is a sterile synovitis which occurs after a gastrointestinal or urogenital infection. ReA belongs to Spondyloarthritis (SpA), a group of diseases that share several clinical and radiological features including familiar clustering, absence of rheumatoid factor and association with HLA-B27. Clinically, ReA is characterized by an asymmetric arthritis predominantly affecting the lower limbs, often associated with urethritis, conjunctivitis and other extraarticular symptoms. The ReA prevalence depends on the incidence of causative pathogens. The ReA diagnosis is based on clinical features and serological tests to evidence previous infection. Different treatment including antibiotics, disease modifying antirheumatic drugs (DMARs) and biologic agents has been recommended. Even though knowing that infections trigger the joint inflammation, the ReA pathogenesis remains to be poorly understood. Several animal models and in vitro studies have been used to elucidate the mechanisms involved in ReA development. In this sense, HLA-B27 transgenic rat or mice have been used to explain the role of this molecule in SpA aetiopathogenesis. Moreover, the infectious model of Yersinia-induced ReA in rodents has shed some lights on the relationship between host genetic susceptibility to infection and abnormal immune response in ReA development. Understanding the immune mediators triggering ReA will contribute to find a specific treatment for this arthritis. In this review, we focus on clinical features, epidemiology, treatment, and the different attempts to understand the pathogenesis of ReA.
Highlights
Reactive arthritis (ReA) is arthritis that arises following a gastrointestinal or urogenital infection
In addition to ReA, SpA includes ankylosing spondylitis (AS), psoriatic arthritis (PsA), arthritis related to inflammatory bowel disease (IBD-SpA) and undifferentiated SpA (U-SpA) [1]
According to the 4th International Workshop on Reactive Arthritis (Berlin, 1999), the term ReA must apply to a patient with typical clinical features of this disease and in those whose preceding infection was caused by the classic microorganisms involved in their development
Summary
Reactive arthritis (ReA) is arthritis that arises following a gastrointestinal or urogenital infection. In addition to ReA, SpA includes ankylosing spondylitis (AS), psoriatic arthritis (PsA), arthritis related to inflammatory bowel disease (IBD-SpA) and undifferentiated SpA (U-SpA) [1] At present it exist a discussion whether this classification represent alternative presentations of one entity with heterogeneous phenotype [2]. According to the 4th International Workshop on Reactive Arthritis (Berlin, 1999), the term ReA must apply to a patient with typical clinical features of this disease and in those whose preceding infection was caused by the classic microorganisms involved in their development. The minimum time interval between the gastrointestinal/genitourinary infection symptoms and arthritis should be of 1 - 7 days, maximum 4 weeks It is advisable for the investigation of microorganisms inducers of ReA by culturing urine/feces or through serological methods [14]. The investigations performed to ReA diagnosis, and to make a differential diagnosis are based on hematologic, microbiologic, serologic and radiologic findings, and on synovial fluid studies (Table 1)
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
