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Reactive Arthritis

  • Robert D. Inman
  • Andrew Keat

Abstract

In reactive arthritis (ReA), exposure to an infectious agent leads to the development of an inflammatory arthritis and other characteristic clinical findings. However, this syndrome occurs in the absence of an ongoing infectious process. About 50% of ReA and undifferentiated oligoarthritis cases can be attributed to a specific pathogen by a combination of culture and serology. The predominant organisms are Chlamydia, Salmonella, Shigella, Yersinia, and Campylobacter species. The frequency of ReA following exposure to potential etiologic agents is between 3% and 10%. ReA characteristically involves the joints of the lower extremities in an asymmetric, oligoarticular pattern. The presence of HLAB27 increases disease susceptibility, but is neither sufficient nor necessary for ReA to occur. Individuals who are HLA-B27 positive tend to have more severe and longer episodes of ReA. A dactylitis (“sausage digit”) pattern of arthritis in the feet is typical of ReA, as it is of psoriatic arthritis. ReA has a predilection for joints of the lower extremities, usually in an asymmetric, oligoarticular pattern. Enthesopathy and anterior uveitis often occur in ReA.

Keywords

Psoriatic Arthritis Septic Arthritis Anterior Uveitis Reactive Arthritis Acute Rheumatic Fever 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

References

  1. Ahvonen P, Sievers K, Aho K. Arthritis associated with Yersinia entero-colitica infection. Acta Rheumatol Scand 1969; 15(3):232–253PubMedGoogle Scholar
  2. Barash J, Mashiach E, Navon-Elkan P, et al Differentiation of post-strep-tococcal reactive arthritis from acute rheumatic fever. J Pediatrics 2008; 153:696CrossRefGoogle Scholar
  3. Colmegna I, Cuchacovich R, Espinosa LR. HLA-associated reactive arthritis: Pathogenic and clinical considerations. Clin Microbiol Rev 2004; 17:348–369PubMedCrossRefGoogle Scholar
  4. Hamdulay SS, Glynne SJ, Keat A. When is arthritis reactive? Postgrad Med J 2006; 82(969):446–453PubMedCrossRefGoogle Scholar
  5. Hannu T, Inman R, Granfors K, Leirisalo-Repo M. Reactive arthritis or post-infectious arthritis? Best Pract Res Clin Rheumatol 2006; 20 (3):419–433PubMedCrossRefGoogle Scholar
  6. Keat A. Reiter's syndrome and reactive arthritis in perspective. N Engl J Med 1983; 29;309(26):1606–1615PubMedCrossRefGoogle Scholar
  7. Kempsell KE, Cox CJ, Hurle M, et al Reverse transcriptase-PCR analysis of bacterial rRNA for detection and characterization of bacterial species in arthritis synovial tissue. Infect Immun 2000; 68(10): 6012–6026PubMedCrossRefGoogle Scholar
  8. Leirisalo-Repo M. Prognosis, course of diseases and treatment of the spondyloarthropathies. Rheum Dis Clin N Amer 1998; 24:737–751CrossRefGoogle Scholar

Copyright information

© Springer Science+Business Media B.V. 2009

Authors and Affiliations

  • Robert D. Inman
    • 1
  • Andrew Keat
    • 2
  1. 1.RheumatologyUniversity of Toronto and Toronto Western HospitalTorontoCanada
  2. 2.Northwick Park HospitalHarrowEngland

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