Reactive Arthritis: From Clinical Features to Pathogenesis


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.

Share and Cite:

E. Cargnelutti and M. Di Genaro, "Reactive Arthritis: From Clinical Features to Pathogenesis," International Journal of Clinical Medicine, Vol. 4 No. 12B, 2013, pp. 20-30. doi: 10.4236/ijcm.2013.412A2004.

Conflicts of Interest

The authors declare no conflicts of interest.


[1] M. Dougados and D. Baeten, “Spondyloarthritis,” Lancet, Vol. 377, No. 9783, 2011, pp. 2127-2137.
[2] D. Baeten, M. Breban, R. Lories, G. Schett and J. Sieper, “Are Spondylarthritides Related but Distinct Conditions or a Single Disease with a Heterogeneous Phenotype?” Arthritis & Rheumatism, Vol. 65, No. 1, 2013, pp. 12-20.
[3] A. Van Tubergen and U. Weber, “Diagnosis and Classification in Spondyloarthritis: Identifying a Chameleon,” Nature Reviews Rheumatology, Vol. 8, No. 5, 2012, pp. 253-261.
[4] P. Ahvonen, K. Sievers and K. Aho, “Arthritis Associated with Yersinia enterocolitica Infection,” Acta Rheumatologica Scandinavica, Vol. 15, No. 3, 1969, pp. 232-253.
[5] O. Laitenen, J. Tuuhea and P. Ahvonen, “Polyarthritis Associated with Yersinia enterocolitica Infection. Clinical Features and Laboratory Findings in Nine Cases with Severe Joint Symptoms,” Annals of the Rheumatic Diseases, Vol. 31, No. 1, 1972, pp. 34-39.
[6] K. Aho, P. Ahvonen, T. Juvakoski, M. Kousa, M. Leirisalo and O. Laitinen, “Immune Responses in Yersinia-Associated Reactive Arthritis,” Annals of the Rheumatic Diseases, Vol. 38, Suppl. 1, 1979, pp. 123-126.
[7] C. J. Cox, K. E. Kempsell and J. S. Gaston, “Investigation of Infectious Agents Associated with Arthritis by Reverse Transcription PCR of Bacterial rRNA,” Arthritis Research & Therapy, Vol. 5, No. 1, 2003, pp. R1-R8.
[8] K. Granfors, S. Jalkanen, A. A. Lindberg, O. Maki-Ikola, R. Von Essen, R. Lahesmaa-Rantala, H. Isomaki, R. Saario, W. J. Arnold and A. Toivanen, “Salmonella Lipopolysaccharide in Synovial Cells from Patients with Reactive Arthritis,” Lancet, Vol. 335, No. 8691, 1990, pp. 685-688.
[9] J. S. Hill Gaston, C. Cox and K. Granfors, “Clinical and Experimental Evidence for Persistent Yersinia Infection in Reactive Arthritis,” Arthritis & Rheumatism, Vol. 42, No. 10, 1999, pp. 2239-2242.<2239::AID-ANR29>3.0.CO;2-L
[10] R. Merilahti-Palo, K. O. Soderstrom, R. Lahesmaa-Rantala, K. Granfors and A. Toivanen, “Bacterial Antigens in Synovial Biopsy Specimens in Yersinia Triggered Reactive Arthritis,” Annals of the Rheumatic Diseases, Vol. 50, No. 2, 1991, pp. 87-90.
[11] A. M. Beutler, J. A. Whittum-Hudson, R. Nanagara, H. R. Schumacher and A. P. Hudson, “Intracellular Location of Inapparently Infecting Chlamydia in Synovial Tissue from Patients with Reiter’s Syndrome,” Immunologic Research, Vol. 13, No. 2-3, 1994, pp. 163-171.
[12] H. C. Gerard, P. J. Branigan, H. R. Schumacher Jr. and A. P. Hudson, “Synovial Chlamydia trachomatis in Patients with Reactive Arthritis/Reiter’s Syndrome Are Viable but Show Aberrant Gene Expression,” The Journal of Rheumatology, Vol. 25, No. 4, 1998, pp. 734-742.
[13] J. M. Townes, “Reactive Arthritis after Enteric Infections in the United States: The Problem of Definition,” Clinical Infectious Diseases, Vol. 50, No. 2, 2010, pp. 247-254.
[14] J. Braun, G. Kingsley, D. Van Der Heijde and J. Sieper, “On the Difficulties of Establishing a Consensus on the Definition of and Diagnostic Investigations for Reactive Arthritis. Results and Discussion of a Questionnaire Prepared for the 4th International Workshop on Reactive Arthritis, Berlin, Germany, July 3-6, 1999,” The Journal of Rheumatology, Vol. 27, No. 9, 2000, pp. 2185-2192.
[15] T. Hannu, “Reactive Arthritis,” Best Practice & Research Clinical Rheumatology, Vol. 25, No. 3, 2011, pp. 347-357.
[16] T. K. Kvien, A. Glennas, K. Melby, K. Granfors, O. Andrup, B. Karstensen and J. E. Thoen, “Reactive Arthritis: Incidence, Triggering Agents and Clinical Presentation,” The Journal of Rheumatology, Vol. 21, No. 1, 1994, pp. 115-122.
[17] J. M. Townes, A. A. Deodhar, E. S. Laine, K. Smith, H. E. Krug, A. Barkhuizen, M. E. Thompson, P. R. Cieslak and J. Sobel, “Reactive Arthritis Following Culture-Confirmed Infections with Bacterial Enteric Pathogens in Minnesota and Oregon: A Population-Based Study,” Annals of the Rheumatic Diseases, Vol. 67, No. 12, 2008, pp. 1689-1696.
[18] E. Collantes, P. Zarco, E. Munoz, X. Juanola, J. Mulero, J. L. Fernandez-Sueiro, J. C. Torre-Alonso, J. Gratacos, C. Gonzalez, E. Batlle, P. Fernandez, L. F. Linares, E. Brito and L. Carmona, “Disease Pattern of Spondyloarthropathies in Spain: Description of the First National Registry (REGISPONSER) Extended Report,” Rheumatology (Oxford), Vol. 46, No. 8, 2007, pp. 1309-1315.
[19] E. Buschiazzo, J. A. Maldonado-Cocco, P. Arturi, G. Citera, A. Berman, A. Nitsche and O. L. Rillo, “Epidemiology of Spondyloarthritis in Argentina,” The American Journal of the Medical Sciences, Vol. 341, No. 4, 2011, pp. 289-292.
[20] M. Vasala, S. Hallanvuo, P. Ruuska, R. Suokas, A. Siitonen and M. Hakala, “High Frequency of Reactive Arthritis in Adults after Yersinia pseudotuberculosis O:1 Outbreak Caused by Contaminated Grated Carrots,” Annals of the Rheumatic Diseases, 2013.
[21] A. Mcmichael and P. Bowness, “HLA-B27: Natural Function and Pathogenic Role in Spondyloarthritis,” Arthritis Research, Vol. 4, Suppl. 3, 2002, pp. S153-158.
[22] A. Toivanen and P. Toivanen, “Reactive Arthritis,” Best Practice & Research Clinical Rheumatology, Vol. 18, No. 5, 2004, pp. 689-703.
[23] A. Chatzikyriakidou, P. V. Voulgari and A. A. Drosos, “What Is the Role of HLA-B27 in Spondyloarthropathies?” Autoimmunity Reviews, Vol. 10, No. 8, 2011, pp. 464-468.
[24] G. P. Thomas and M. A. Brown, “Genetics and Genomics of Ankylosing Spondylitis,” Immunological Reviews, Vol. 233, No. 1, 2010, pp. 162-180.
[25] R. Bonfiglioli, R. A. Conde, P. D. Sampaio-Barros, P. Louzada-Junior, E. A. Donadi and M. B. Bertolo, “Frequency of HLA-B27 Alleles in Brazilian Patients with Psoriatic Arthritis,” Clinical Rheumatology, Vol. 27, No. 6, 2008, pp. 709-712.
[26] A. Cipriani, S. Rivera, M. Hassanhi, G. Marquez, R. Hernandez, C. Villalobos and M. Montiel, “HLA-B27 Subtypes Determination in Patients with Ankylosing Spondylitis from Zulia, Venezuela,” Human Immunology, Vol. 64, No. 7, 2003, pp. 745-749.
[27] B. Martinez, L. Caraballo, M. Hernandez, R. Valle, M. Avila and A. Iglesias Gamarra, “HLA-B27 Subtypes in Patients with Ankylosing Spondylitis (as) in Colombia,” Revista de Investigación Clínica, Vol. 51, No. 4, 1999, pp. 221-226.
[28] J. S. Hill Gaston and M. S. Lillicrap, “Arthritis Associated with Enteric Infection,” Best Practice & Research Clinical Rheumatology, Vol. 17, No. 2, 2003, pp. 219-239.
[29] V. Bellomio, A. Berman, R. Sueldo, M. J. Molina, A. Spindler, E. Lucero, H. Berman, A. Nitsche, C. Asnal, J. A. Maldonado Cocco, G. Citera, S. Paira, C. Sandoval, R. Wong, R. Gallo, O. Rillo, R. Chaparro, A. Alvarellos, J. A. Albiero, C. Graf, A. Zunino, C. G. Casado, C. B. Romeo, J. C. Barreira and E. Aroca Briones, “Respondia. Iberoamerican Spondyloarthritis Registry: Argentina,” Reumatología Clínica, Vol. 4, Suppl. 4, 2008, pp. S23-29.
[30] S. Kobayashi and I. Kida, “Reactive Arthritis: Recent Advances and Clinical Manifestations,” Annals of Internal Medicine, Vol. 44, No. 5, 2005, pp. 408-12.
[31] M. Leirisalo-Repo, “Reactive Arthritis,” Scandinavian Journal of Rheumatology, Vol. 34, No. 4, 2005, pp. 251-259.
[32] W. F. Barth and K. Segal, “Reactive Arthritis (Reiter’s Syndrome),” American Family Physician, Vol. 60, No. 2, 1999, pp. 499-503, 507.
[33] B. Kwiatkowska and A. Filipowicz-Sosnowska, “Reactive Arthritis,” Polskie Archiwum Medycyny Wewnetrznej, Vol. 119, No. 1-2, 2009, pp. 60-65.
[34] T. Hannu, L. Mattila, H. Rautelin, P. Pelkonen, P. Lahdenne, A. Siitonen and M. Leirisalo-Repo, “Campylobacter-Triggered Reactive Arthritis: A Population-Based Study,” Rheumatology (Oxford), Vol. 41, No. 3, 2002, pp. 312-318.
[35] T. Rathod, A. Chandanwale, S. Chavan and M. Shah, “Polyarthritic, Symmetric Arthropathy in Reactive Arthritis,” Journal of Natural Science, Biology and Medicine, Vol. 2, No. 2, 2011, pp. 216-218.
[36] M. Rudwaleit, D. Van Der Heijde, R. Landewe, J. Listing, N. Akkoc, J. Brandt, J. Braun, C. T. Chou, E. Collantes-Estevez, M. Dougados, F. Huang, J. Gu, M. A. Khan, Y. Kirazli, W. P. Maksymowych, H. Mielants, I. J. Sorensen, S. Ozgocmen, E. Roussou, R. Valle-Onate, U. Weber, J. Wei and J. Sieper, “The Development of Assessment of Spondyloarthritis International Society Classification Criteria for Axial Spondyloarthritis (Part II): Validation and Final Selection,” Annals of the Rheumatic Diseases, Vol. 68, No. 6, 2009, pp. 777-783.
[37] W. Taylor, D. Gladman, P. Helliwell, A. Marchesoni, P. Mease and H. Mielants, “Classification Criteria for Psoriatic Arthritis: Development of New Criteria from a Large International Study,” Arthritis & Rheumatism, Vol. 54, No. 8, 2006, pp. 2665-2673.
[38] J. D. Carter and A. P. Hudson, “Reactive Arthritis: Clinical Aspects and Medical Management,” Rheumatic Disease Clinics of North America, Vol. 35, No. 1, 2009, pp. 21-44.
[39] I. B. Wu and R. A. Schwartz, “Reiter’s Syndrome: The Classic Triad and More,” Journal of the American Academy of Dermatology, Vol. 59, No. 1, 2008, pp. 113-121.
[40] B. M. Rosner, D. Werber, M. Hohle and K. Stark, “Clinical Aspects and Self-Reported Symptoms of Sequelae of Yersinia enterocolitica Infections in a Population-Based Study, Germany 2009-2010,” BMC Infectious Diseases, Vol. 13, 2013, p. 236.
[41] I. Colmegna, R. Cuchacovich and L. R. Espinoza, “HLAB27-Associated Reactive Arthritis: Pathogenetic and Clinical Considerations,” Clinical Microbiology Reviews, Vol. 17, No. 2, 2004, pp. 348-369.
[42] T. E. Feltkamp and J. H. Ringrose, “Acute Anterior Uveitis and Spondyloarthropathies,” Current Opinion in Rheumatology, Vol. 10, No. 4, 1998, pp. 314-318.
[43] M. Huhtinen, K. Laasila, K. Granfors, M. Puolakkainen, I. Seppala, L. Laasonen, H. Repo, A. Karma and M. Leirisalo-Repo, “Infectious Background of Patients with a History of Acute Anterior Uveitis,” Annals of the Rheumatic Diseases, Vol. 61, No. 11, 2002, pp. 1012-1016.
[44] D. Monnet, M. Breban, C. Hudry, M. Dougados and A. P. Brezin, “Ophthalmic Findings and Frequency of Extraocular Manifestations in Patients with HLA-B27 Uveitis: A Study of 175 Cases,” Ophthalmology, Vol. 111, No. 4, 2004, pp. 802-809.
[45] N. Kozeis, M. Trachana and S. Tyradellis, “Keratitis in Reactive Arthritis (Reiter Syndrome) in Childhood,” Cornea, Vol. 30, No. 8, 2011, pp. 924-925.
[46] S. Kiss, E. Letko, S. Qamruddin, S. Baltatzis and C. S. Foster, “Long-Term Progression, Prognosis, and Treatment of Patients with Recurrent Ocular Manifestations of Reiter’s Syndrome,” Ophthalmology, Vol. 110, No. 9, 2003, pp. 1764-1769.
[47] L. Bergfeldt, “HLA B27-Associated Rheumatic Diseases with Severe Cardiac Bradyarrhythmias. Clinical Features and Prevalence in 223 Men with Permanent Pacemakers,” American Journal of Medicine, Vol. 75, No. 2, 1983, pp. 210-215.
[48] H. Nielsen, “Complete Heart Block in Reiter’s Syndrome,” Acta Cardiologica, Vol. 41, No. 6, 1986, pp. 451-455.
[49] L. E. Brown, P. Forfia and J. A. Flynn, “Aortic Insufficiency in a Patient with Reactive Arthritis: Case Report and Review of the Literature,” HSS Journal, Vol. 7, No. 2, 2011, pp. 187-189.
[50] C. Fendler, S. Laitko, H. Sorensen, C. Gripenberg-Lerche, A. Groh, J. Uksila, K. Granfors, J. Braun and J. Sieper, “Frequency of Triggering Bacteria in Patients with Reactive Arthritis and Undifferentiated Oligoarthritis and the Relative Importance of the Tests Used for Diagnosis,” Annals of the Rheumatic Diseases, Vol. 60, No. 4, 2001, pp. 337-343.
[51] M. K. Söderlin, H. Kautiainen, M. Puolakkainen, K. Hedman, M. Söderlund-Venermo, T. Skogh and M. Leirisalo-Repo, “Infections Preceding Early Arthritis in Southern Sweden: A Prospective Population-Based Study,” Journal of Rheumatology, Vol. 30, No. 3, 2003, pp. 459-464.
[52] M. G. Lacoste, H. Tamashiro, S. G. Correa, A. M. de Guzmán and M. S. Di Genaro, “Correlation between Yersinia enterocolitica and Type I Collagen Reactivity in Patients with Arthropathies,” Rheumatology International, Vol. 27, No. 7, 2007, pp. 613-620.
[53] J. Birnbaum, J. G. Bartlett and A. C. Gelber, “Clostridium difficile: An under-Recognized Cause of Reactive Arthritis?” Clinical Rheumatology, Vol. 27, No. 2, 2008, pp. 253-255.
[54] P. Schiellerup, K. A. Krogfelt and H. Locht, “A Comparison of Self-Reported Joint Symptoms Following Infection with Different Enteric Pathogens: Effect of HLAB27,” Journal of Rheumatology, Vol. 35, No. 3, 2008, pp. 480-487.
[55] T. Hannu, M. Puolakkainen and M. Leirisalo-Repo, “Chlamydia pneumoniae as a Triggering Infection in Reactive Arthritis,” Rheumatology, Vol. 38, No. 5, 1999, pp. 411-414.
[56] A. Rizzo, M. D. Domenico, C. R. Carratelli and R. Paolillo, “The Role of Chlamydia and Chlamydophila Infections in Reactive Arthritis,” Internal Medicine, Vol. 51, No. 1, 2012, pp. 113-117.
[57] I. Galadari and H. Galadari, “Nonspecific Urethritis and Reactive Arthritis,” Clinics in Dermatology, Vol. 22, No. 6, 2004, pp. 469-475.
[58] M. K. Soderlin, E. Alasaarela and M. Hakala, “Reactive Arthritis Induced by Clostridium difficile Enteritis as a Complication of Helicobacter pylori Eradication,” Clinical Rheumatology, Vol. 18, No. 4, 1999, pp. 337-338.
[59] D. W. Carlson and D. R. Finger, “Beaver Fever Arthritis,” Journal of Clinical Rheumatology, Vol. 10, No. 2, 2004, pp. 86-88.
[60] A. Sing, S. Bechtold, J. Heesemann, B. H. Belohradsky and H. Schmidt, “Reactive Arthritis Associated with Prolonged Cryptosporidial Infection,” Journal of Infection, Vol. 47, No. 2, 2003, pp. 181-184.
[61] B. Tejera, D. Grados, M. Martinez-Morillo and S. Roure, “Reactive Arthritis Caused by Blastocystis hominis,” Reumatología Clinica, Vol. 8, No. 1, 2012, pp. 50-51.
[62] K. Granfors, R. Merilahti-Palo, R. Luukkainen, T. Mottonen, R. Lahesmaa, P. Probst, E. Marker-Hermann and P. Toivanen, “Persistence of Yersinia Antigens in Peripheral Blood Cells from Patients with Yersinia enterocolitica O:3 Infection with or without Reactive Arthritis,” Arthritis & Rheumatism, Vol. 41, No. 5, 1998, pp. 855-862.<855::AID-ART12>3.0.CO;2-J
[63] J. A. Curfs, J. G. Meis, H. L. Van Der Lee, J. Mulder, W. G. Kraak and J. A. Hoogkamp-Korstanje, “Persistent Yersinia enterocolitica Infection in Three Rat Strains,” Microbial Pathogenesis, Vol. 19, No. 1, 1995, pp. 57-63.
[64] M. Saarinen, L. J. Pelliniemi and K. Granfors, “Survival and Degradation of Salmonella enterica Serotype Enteritidis in Intestinal Epithelial Cells in Vitro,” Journal of Medical Microbiology, Vol. 45, No. 6, 1996, pp. 463-471.
[65] J. Braun, Z. Yin, I. Spiller, S. Siegert, M. Rudwaleit, L. Liu, A. Radbruch and J. Sieper, “Low Secretion of Tumor Necrosis Factor Alpha, but No Other Th1 or Th2 Cytokines, by Peripheral Blood Mononuclear Cells Correlates with Chronicity in Reactive Arthritis,” Arthritis & Rheumatism, Vol. 42, No. 10, 1999, pp. 2039-2044.<2039::AID-ANR3>3.0.CO;2-6
[66] I. Butrimiene, S. Jarmalaite, J. Ranceva, A. Venalis, L. Jasiuleviciute and A. Zvirbliene, “Different Cytokine Profiles in Patients with Chronic and Acute Reactive Arthritis,” Rheumatology, Vol. 43, No. 10, 2004, pp. 1300-1304.
[67] H. Shen, J. C. Goodall and J. S. Gaston, “Frequency and Phenotype of T Helper 17 Cells in Peripheral Blood and Synovial Fluid of Patients with Reactive Arthritis,” Journal of Rheumatology, Vol. 37, No. 10, 2010, pp. 2096-2099.
[68] R. J. Eliçabe, E. Cargnelutti, M. I. Serer, P. W. Stege, S. R. Valdez, M. A. Toscano, G. A. Rabinovich and M. S. Di Genaro, “Lack of TNFR p55 Results in Heightened Expression of IFN-γ and Il-17 During the Development of Reactive Arthritis,” Journal of Immunology, Vol. 185, No. 7, 2010, pp. 4485-4495.
[69] E. Cargnelutti, J. L. Arias, S. R. Valdez, G. A. Rabinovich and M. S. Di Genaro, “TNFR p55 Controls Regulatory T Cell Responses in Yersinia-Induced Reactive Arthritis,” Immunology and Cell Biology, Vol. 91, No. 2, 2013, pp. 159-166.
[70] J. Sieper, J. Braun, P. Wu and G. Kingsley, “T Cells Are Responsible for the Enhanced Synovial Cellular Immune Response to Triggering Antigen in Reactive Arthritis,” Clinical & Experimental Immunology, Vol. 91, No. 1, 1993, pp. 96-102.
[71] C. Alvarez-Navarro, J. J. Cragnolini, H. G. Dos Santos, E. Barnea, A. Admon, A. Morreale and J. A. López De Castro, “Novel HLA-B27-Restricted Epitopes from Chlamydia trachomatis Generated Upon Endogenous Processing of Bacterial Proteins Suggest a Role of Molecular Mimicry in Reactive Arthritis,” Journal of Biological Chemistry, Vol. 288, No. 36, 2013, pp. 25810-25825.
[72] R. Benjamin and P. Parham, “Guilt by Association: HLA-B27 and Ankylosing Spondylitis,” Immunology Today, Vol. 11, No. 4, 1990, pp. 137-142.
[73] W. Kuon, H. G. Holzhutter, H. Appel, M. Grolms, S. Kollnberger, A. Traeder, P. Henklein, E. Weiss, A. Thiel, R. Lauster, P. Bowness, A. Radbruch, P. M. Kloetzel and J. Sieper, “Identification of HLA-B27-Restricted Peptides from the Chlamydia trachomatis Proteome with Possible Relevance to HLA-B27-Associated Diseases,” Journal of Immunology, Vol. 167, No. 8, 2001, pp. 4738-4746.
[74] E. May, M. L. Dorris, N. Satumtira, I. Iqbal, M. I. Rehman, E. Lightfoot and J. D. Taurog, “CD8 Alpha Beta T Cells Are Not Essential to the Pathogenesis of Arthritis or Colitis in HLA-B27 Transgenic Rats,” Journal of Immunology, Vol. 170, No. 2, 2003, pp. 1099-1105.
[75] J. D. Taurog, M. L. Dorris, N. Satumtira, T. M. Tran, R. Sharma, R. Dressel, J. Van Den Brandt and H. M. Reichardt, “Spondylarthritis in HLA-B27/Human Beta2-Microglobulin-Transgenic Rats Is Not Prevented by Lack of CD8,” Arthritis & Rheumatism, Vol. 60, No. 7, 2009, pp. 1977-1984.
[76] M. A. Whelan and J. R. Archer, “Chemical Reactivity of an HLA-B27 Thiol Group,” European Journal of Immunology, Vol. 23, No. 12, 1993, pp. 3278-3285.
[77] R. A. Colbert, T. M. Tran and G. Layh-Schmitt, “HLAB27 Misfolding and Ankylosing Spondylitis,” Molecular Immunology, Vol. 57, No. 1, 2014, pp. 44-51.
[78] L. H. Boyle, J. C. Goodall, S. S. Opat and J. S. Gaston, “The Recognition of HLA-B27 by Human CD4(+) T Lymphocytes,” Journal of Immunology, Vol. 167, No. 5, 2001, pp. 2619-2624.
[79] J. D. Reveille, “Genetics of Spondyloarthritis-Beyond the MHC,” Nature Reviews Rheumatology, Vol. 8, No. 5, 2012, pp. 296-304.
[80] J. D. Carter, H. C. Gerard, J. A. Whittum-Hudson and A. P. Hudson, “Combination Antibiotics for the Treatment of Chlamydia-Induced Reactive Arthritis: Is a Cure in Sight?” International Journal of Clinical Rheumatology, Vol. 6, No. 3, 2011, pp. 333-345.
[81] J. Sieper, “Developments in Therapies for Spondyloarthritis,” Nature Reviews Rheumatology, Vol. 8, No. 5, 2012, pp. 280-287.
[82] A. Toivanen, “Managing Reactive Arthritis,” Rheumatology, Vol. 39, No. 2, 2000, pp. 117-119.
[83] M. Dougados, “Current Therapy for Seronegative Arthritides (Spondyloarthritis),” Bulletin of the NYU Hospital for Joint Diseases, Vol. 69, No. 3, 2011, pp. 250-252.
[84] D. Flores, J. Marquez, M. Garza and L. R. Espinoza, “Reactive Arthritis: Newer Developments,” Rheumatic Disease Clinics of North America, Vol. 29, No. 1, 2003, pp. 37-59.
[85] D. O. Clegg, D. J. Reda, M. H. Weisman, J. J. Cush, F. B. Vasey, H. R. Schumacher Jr., E. Budiman-Mak, D. J. Balestra, W. D. Blackburn, G. W. Cannon, R. D. Inman, F. P. Alepa, E. Mejias, M. R. Cohen, R. Makkena, M. L. Mahowald, J. Higashida, S. L. Silverman, N. Parhami, J. Buxbaum, C. M. Haakenson, R. H. Ward, B. J. Manaster, R. J. Anderson, W. G. Henderson, et al., “Comparison of Sulfasalazine and Placebo in the Treatment of Reactive Arthritis (Reiter’s Syndrome). A Department of Veterans Affairs Cooperative Study,” Arthritis & Rheumatism, Vol. 39, No. 12, 1996, pp. 2021-2027.
[86] L. Goh and A. Samanta, “Update on Biologic Therapies in Ankylosing Spondylitis: A Literature Review,” International Journal of Rheumatic Diseases, Vol. 15, No. 5, 2012, pp. 445-454.
[87] S. D. Flagg, R. Meador, E. Hsia, T. Kitumnuaypong and H. R. Schumacher, “Decreased Pain and Synovial Inflammation after Etanercept Therapy in Patients with Reactive and Undifferentiated Arthritis: An Open-Label Trial,” Arthritis Care & Research, Vol. 53, No. 4, 2005, pp. 613-617.
[88] R. Meador, E. Hsia, T. Kitumnuaypong and H. R. Schumacher, “TNF Involvement and Anti-TNF Therapy of Reactive and Unclassified Arthritis,” Clinical and Experimental Rheumatology, Vol. 20, No. 6, 2002, pp. S130-S134.
[89] A. Meyer, E. Chatelus, D. Wendling, J. M. Berthelot, E. Dernis, E. Houvenagel, J. Morel, O. Richer, T. Schaeverbeke, J. E. Gottenberg and J. Sibilia, “Safety and Efficacy of Anti-Tumor Necrosis Factor Alpha Therapy in Ten Patients with Recent-Onset Refractory Reactive Arthritis,” Arthritis & Rheumatism, Vol. 63, No. 5, 2011, pp. 1274-1280.
[90] K. S. Oili, H. Niinisalo, T. Korpilahde and J. Virolainen, “Treatment of Reactive Arthritis with Infliximab,” Scandinavian Journal of Rheumatology, Vol. 32, No. 2, 2003, pp. 122-124.
[91] M. Rihl, A. Klos, L. Kohler and J. G. Kuipers, “Infection and Musculoskeletal Conditions: Reactive Arthritis,” Best Practice & Research Clinical Rheumatology, Vol. 20, No. 6, 2006, pp. 1119-1137.
[92] M. D. Schafranski, “Infliximab for Reactive Arthritis Secondary to Chlamydia trachomatis Infection,” Rheumatology International, Vol. 30, No. 5, 2010, pp. 679-680.
[93] R. J. Eliçabe, J. L. Arias, G. A. Rabinovich and M. S. Di Genaro, “TNFRp55 Modulates IL-6 and Nitric Oxide Responses Following Yersinia Lipopolysaccharide Stimulation in Peritoneal Macrophages,” Immunobiology, Vol. 216, No. 12, 2011, pp. 1322-1330.
[94] A. Gottlieb, A. Menter, A. Mendelsohn, Y. K. Shen, S. Li, C. Guzzo, S. Fretzin, R. Kunynetz and A. Kavanaugh, “Ustekinumab, a Human Interleukin 12/23 Monoclonal Antibody, for Psoriatic Arthritis: Randomised, Double-Blind, Placebo-Controlled, Crossover Trial,” Lancet, Vol. 373, No. 9664, 2009, pp. 633-640.
[95] I. B. Mcinnes, J. Sieper, J. Braun, P. Emery, D. Van Der Heijde, J. D. Isaacs, G. Dahmen, J. Wollenhaupt, H. Schulze-Koops, J. Kogan, S. Ma, M. M. Schumacher, A. P. Bertolino, W. Hueber and P. P. Tak, “Efficacy and Safety of Secukinumab, a Fully Human Anti-Interleukin17A Monoclonal Antibody, in Patients with Moderateto-Severe Psoriatic Arthritis: A 24-Week, Randomised, Double-Blind, Placebo-Controlled, Phase II Proof-of-Concept Trial,” Annals of the Rheumatic Diseases, 2013.
[96] M. Leirisalo-Repo, P. Helenius, T. Hannu, A. Lehtinen, J. Kreula, M. Taavitsainen and S. Koskimies, “Long-Term Prognosis of Reactive Salmonella Arthritis,” Annals of the Rheumatic Diseases, Vol. 56, No. 9, 1997, pp. 516-520.
[97] M. Leirisalo-Repo and H. Suoranta, “Ten-Year Follow-up Study of Patients with Yersinia Arthritis,” Arthritis & Rheumatism, Vol. 31, No. 4, 1988, pp. 533-537.
[98] E. Sairanen, I. Paronen and H. Mähönen, “Reiter’s Syndrome: A Follow-up Study,” Acta Medica Scandinavica, Vol. 185, No. 1-6, 1969, pp. 57-63.

Copyright © 2024 by authors and Scientific Research Publishing Inc.

Creative Commons License

This work and the related PDF file are licensed under a Creative Commons Attribution 4.0 International License.