Abstract

The term reactive arthritis was first introduced in 1969 as to describe a sequel to an old infection, usually being genitourinary or GI infection. This condition has a diverse clinical manifestations. Initially it was know as Reiter's disease or Fiessinger Leroy disease. It is a member of spondyloarthritis family. HLA-B27 is a known predisposing genetic factor and is triggered by systemic infection. CREG-B7 group of antigens are found in B27 negative patients and these antigens are cross reactive to B27. Long term follow up is needed in children to determine if more number of children develop recurrent arthritis or any other disease like psoriatic arthritis, ankylosing spondylitis etc. cytokines like TNF alpha and interferon secrete T helper cells which help in eliminating the bacteria. NSAIDs, corticosteroids and antibiotics play a role in mainstay treatment. Reactive arthritis is characterized by both articular and extraarticular symptoms. Extra-articular manifestations include genitourinary symptoms, ocular symptoms, skin manifestations and cardiac manifestations. The diagnosis of this conditions is mostly clinical. Eliminating the infectious agent is the mainstay of the treatment followed by NSAIDs, corticosteroids and DMARDs in severe cases not responding to primary treatment is important.

• 1.   Kvien T, Glennas A, Melby K, et al: Reactive arthritis: Incidence, triggering agents and clinical presentation. JRheumatol1994;21:115.
• 2.   Keat A. Reiter’s syndrome and reactive arthritis in perspective. N Eng J Med 1983; 309: 1606-15.
• 3.   Wu IB, Schwartz RA. Reiter's syndrome: the classic triad and more. J Am AcadDermatol. Jul 2008;59(1):113-21.
• 4.   Barth WF, Segal K. Reactive arthritis (Reiter's syndrome). Am Fam Physician. Aug 1999; 60(2):499-503, 507.
• 5.   Colmegna I, Cuchacovic R, Espinoza LR. HLAB27 Assosiated Reac tive Arthritis: Pathogenetic and Clinical Considerations. ClinMicrobiol Rev. 2004; 17: 348 369.
• 6.   Ramesh BN, Mahalakshmi AM, Mallappa HS, Biradar BS and MdImad U, World J Pharm PharmSci, 2013, 2(5):2526-2538.
• 7.   Ajene AN, Fischer Walker CL, Black RE. Enteric pathogens and reactive arthritis: a systematic review of Campylobacter, Salmonella and Shigella-associated reactive arthritis. J Health PopulNutr 2013; 31: 299–307.
• 8.   Inman R.D. and Chiu B. Nafamostatmesylate, a serine protease inhibitor, demonstrates novel antimicrobial properties and effectiveness in Chlamydia-induced arthritis. Arthritis Res. Ther. 2012;14, R150.
• 9.   Leirisalo-Repo M, Sieper J. Reactive arthritis: epidemiology, clinical features, and treatment. In: Weisman M, van der Heijde D, Reveille J (eds). Ankylosing Spondylitis and the Spondyloarthropathies. Philadelphia: Mosby Elsevier; 2006. p.53–64.
• 10.   Kim PS, Klausmeier TL, Orr DP. Reactive arthritis: a review. J Adolesc Health 2009; 44: 309–15.
• 11.   Hamdulay SS, Glynne SJ, Keat A. When is arthritis reactive? Postgrad Med J 2006; 82: 446–53.
• 12.   Sieper J. Disease mechanisms in reactive arthritis. CurrRheumatol Rep 2004; 6: 110–6.
• 13.   Kohm AP, Fuller KG, Miller SD. Mimicking the way to autoimmunity: an evolving theory of sequence and structural homology. Trends in Microbiology 2003; 11: 101–105.
• 14.   Bas S, Kvien TK, Buchs N et al. Lower level of synovial fluid interferon-gamma in HLA-B27- positive than in HLA-B27- negative patients with Chlamydia trachomatis reactive arthritis. Rheumatology (Oxford) 2003; 42: 461–7.
• 15.   Meyer A., Chatelus E., Wendling D., Berthelot J.M., Dernis E., Houvenagel E. et al. Safety and efficacy of anti-tumor necrosis factor α therapy in ten patients with recent onset refractory reactive arthritis. Arthritis Rheum.2011; 63, 1274–1280.
• 16.   Sieper J. and Poddubnyy D. (2016) New evidence on the management of spondyloarthritis. Nat. Rev. Rheumatol. 2016;12, 282–295.

Data Sharing Statement

Funding