Polyautoimmunity is one of the major clinical characteristics of autoimmune diseases (ADs). The aim of this study was to investigate the prevalence of ADs in spondyloarthropathies (SpAs) and vice versa. This was a two-phase cross-sectional study. First, we examined the presence of ADs in a cohort of patients with SpAs ( ). Second, we searched for the presence of SpAs in a well-defined group of patients with ADs ( ) including rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), and Sj?gren’s syndrome (SS). Among patients with SpAs, ankylosing spondylitis was observed in the majority of them (55.6%). There were two patients presenting with SS in the SpA group (1.4%) and 5 patients with autoimmune thyroiditis (3.5%). The global prevalence of ADs in SpAs was 4.86%. In the ADs group, there were 5 patients with SpAs (0.46%). Our results suggest a lack of association between SpAs and ADs. Accordingly, SpAs might correspond more to autoinflammatory diseases rather than to ADs. 1. Introduction Spondyloarthropathies (SpAs) are a group of interrelated diseases with joint inflammatory involvement such as arthritis (axial and peripheral) and extraarticular involvement such as uveitis, enthesitis, psoriasis, and inflammatory bowel disease (IBD). This group of diseases is characterized by familial aggregation, absence of rheumatoid factor, and association with human leukocyte antigen (HLA)-B27 [1]. Classically, SpAs have been classified as ankylosing spondylitis (AS), Reiter syndrome (RS), reactive arthritis (ReA), psoriatic arthritis (PsA), IBD-associated SpA, and forms called undifferentiated SpA (uSpA) that do not meet the criteria for previous categories [2]. However, currently, there is a new classification for SpAs. This new classification includes two types of SpAs: axial and peripheral SpA depending on the predominant spinal or peripheral involvement [3, 4] and extraarticular involvement such as anterior uveitis or IBD, which are also considered part of the SpA group [5]. Autoimmune diseases (ADs), in turn, are a clinical syndrome caused by the loss of immune tolerance and characterized by T- or B-cell activation leading to tissue damage in the absence of any other evident cause [6]. Criteria for AD definition have been described and revisited [7]. These criteria, which include direct and indirect proof as well as circumstantial evidence [6], are described in Table 1. However, in many diseases labeled as autoimmune, there are several limitations to fulfill the concept of autoimmunity, which are mainly related to the lack of direct proof
References
[1]
J. D. Reveille and F. C. Arnett, “Spondyloarthritis: update on pathogenesis and management,” American Journal of Medicine, vol. 118, no. 6, pp. 592–603, 2005.
[2]
I. Olivieri, A. van Tubergen, C. Salvarani, and S. van der Linden, “Seronegative spondyloarthritides,” Best Practice and Research, vol. 16, no. 5, pp. 723–739, 2002.
[3]
M. Rudwaleit, D. van der Heijde, R. Landewé et al., “The Assessment of SpondyloArthritis international Society classification criteria for peripheral spondyloarthritis and for spondyloarthritis in general,” Annals of the Rheumatic Diseases, vol. 70, no. 1, pp. 25–31, 2011.
[4]
M. Rudwaleit, D. van der Heijde, R. Landewé et al., “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, pp. 777–783, 2009.
[5]
H. Zeidler and B. Amor, “The Assessment in Spondyloarthritis International Society (ASAS) classification criteria for peripheral spondyloarthritis and for spondyloarthritis in general: the spondyloarthritis concept in progress,” Annals of the Rheumatic Diseases, vol. 70, no. 1, pp. 1–3, 2011.
[6]
J.-M. Anaya, Y. Shoenfeld, P. Correa, M García-Carrasco, and R. Cervera, “Autoinmunidad y enfermedad autoinmune: el mosaico de la autoinmunidad,” in Autoinmunidad y Enfermedad Autoinmune, CIB, Ed., pp. 183–201, Medellín, Colombia, 2005.
[7]
N. R. Rose and C. Bona, “Defining criteria for autoimmune diseases (Witebsky's postulates revisited),” Immunology Today, vol. 14, no. 9, pp. 426–430, 1993.
[8]
D. McGonagle and M. F. McDermott, “A proposed classification of the immunological diseases,” PLoS Medicine, vol. 3, no. 8, pp. 1242–1248, 2006.
[9]
M. C. Hochberg, “Updating the American College of Rheumatology revised criteria for the classification of systemic lupus erythematosus,” Arthritis and rheumatism, vol. 40, no. 9, article 1725, 1997.
[10]
F. C. Arnett, S. M. Edworthy, D. A. Bloch et al., “The American Rheumatism Association 1987 revised criteria for the classification of rheumatoid arthritis,” Arthritis and Rheumatism, vol. 31, no. 3, pp. 315–324, 1988.
[11]
C. Vitali, S. Bombardieri, R. Jonsson et al., “Classification criteria for Sj?gren's syndrome: a revised version of the European criteria proposed by the American-European Consensus Group,” Annals of the Rheumatic Diseases, vol. 61, no. 6, pp. 554–558, 2002.
[12]
S. van der Linden, H. A. Valkenburg, and A. Cats, “Evaluation of diagnostic criteria for ankylosing spondylitis. A proposal for modification of the New York criteria,” Arthritis and Rheumatism, vol. 27, no. 4, pp. 361–368, 1984.
[13]
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 and Rheumatism, vol. 54, no. 8, pp. 2665–2673, 2006.
[14]
J. Satsangi, M. S. Silverberg, S. Vermeire, and J. F. Colombel, “The Montreal classification of inflammatory bowel disease: controversies, consensus, and implications,” Gut, vol. 55, no. 6, pp. 749–753, 2006.
[15]
M. Dougados, S. van der Linden, R. Juhlin et al., “The European Spondylarthropathy Study Group preliminary criteria for the classification of spondylarthropathy,” Arthritis and Rheumatism, vol. 34, no. 10, pp. 1218–1227, 1991.
[16]
G. S. Cooper and B. C. Stroehla, “The epidemiology of autoimmune diseases,” Autoimmunity Reviews, vol. 2, no. 3, pp. 119–125, 2003.
[17]
J. D. Reveille, “Epidemiology of spondyloarthritis in North America,” American Journal of the Medical Sciences, vol. 341, no. 4, pp. 284–286, 2011.
[18]
E. Haglund, A. B. Bremander, I. F. Petersson et al., “Prevalence of spondyloarthritis and its subtypes in southern Sweden,” Annals of the Rheumatic Diseases, vol. 70, no. 6, pp. 943–948, 2011.
[19]
M. J. Cross, E. U. R. Smith, J. Zochling, and L. M. March, “Differences and similarities between ankylosing spondylitis and rheumatoid arthritis: epidemiology,” Clinical and Experimental Rheumatology, vol. 27, no. 4, pp. S36–S42, 2009.
[20]
J. Zochling and E. U. R. Smith, “Seronegative spondyloarthritis,” Best Practice and Research, vol. 24, no. 6, pp. 747–756, 2010.
[21]
K. Sundquist, J. C. Martineus, X. Li, K. Hemminki, and J. Sundquist, “Concordant and discordant associations between rheumatoid arthritis, systemic lupus erythematosus and ankylosing spondylitis based on all hospitalizations in Sweden between 1973 and 2004,” Rheumatology, vol. 47, no. 8, pp. 1199–1202, 2008.
[22]
P. Borman, F. Ayhan, and M. Okumu?, “Coexistence of rheumatoid arthritis and ankylosing spondylitis,” Clinical Rheumatology, vol. 30, no. 11, pp. 1517–1518, 2011.
[23]
B. Baksay, A. Dér, Z. Szekanecz, S. Szántó, and A. Kovács, “Coexistence of ankylosing spondylitis and rheumatoid arthritis in a female patient,” Clinical Rheumatology, vol. 30, no. 8, pp. 1119–1122, 2011.
[24]
E. Toussirot and P. C. Acquaviva, “Coexisting rheumatoid arthritis and ankylosing spondylitis. Discussion of 3 cases with review of the literature,” Clinical Rheumatology, vol. 14, no. 5, pp. 554–560, 1995.
[25]
E. L. Alexander, W. B. Bias, and F. C. Arnett, “The coexistence of rheumatoid arthritis with Reiter's syndrome and/or ankylosing spondylitis: a model of dual HLA-associated disease susceptibility and expression,” Journal of Rheumatology, vol. 8, no. 3, pp. 398–404, 1981.
[26]
E. Toussirot and D. Wendling, “Crohn's disease associated with seropositive rheumatoid arthritis,” Clinical and Experimental Rheumatology, vol. 15, no. 3, pp. 307–311, 1997.
[27]
D. A. Johnson, A. M. Diehl, F. D. Finkelman, and E. L. Cattau Jr., “Crohn's disease and systemic lupus erythematosus,” American Journal of Gastroenterology, vol. 80, no. 11, pp. 869–870, 1985.
[28]
R. Cohen, D. Robinson, C. Paramore, K. Fraeman, K. Renahan, and M. Bala, “Autoimmune disease concomitance among inflammatory bowel disease patients in the United States, 2001-2002,” Inflammatory Bowel Diseases, vol. 14, no. 6, pp. 738–743, 2008.
[29]
I. E. Koutroubakis, K. Karmiris, L. Bourikas, E. A. Kouroumalis, I. Drygiannakis, and D. Drygiannakis, “Antibodies against cyclic citrullinated peptide (CCP) in inflammatory bowel disease patients with or without arthritic manifestations,” Inflammatory Bowel Diseases, vol. 13, no. 4, pp. 504–505, 2007.
[30]
D. Mrabet, S. Rekik, H. Sahli et al., “Ankylosing spondylitis in female systemic lupus erythematosus: a rare combination,” Lupus, vol. 20, no. 7, pp. 777–778, 2011.
[31]
C. Pérez-García, J. Maymo, M. P. Lisbona Pérez, M. Almirall Bernabé, and J. Carbonell Abelló, “Drug-induced systemic lupus erythematosus in ankylosing spondylitis associated with infliximab,” Rheumatology, vol. 45, no. 1, pp. 114–116, 2006.
[32]
H. Bodur, F. Eser, S. Konca, and S. ArIkan, “Infliximab-induced lupus-like syndrome in a patient with ankylosing spondylitis,” Rheumatology International, vol. 29, no. 4, pp. 451–454, 2009.
[33]
A. Mounach, M. Ghazi, A. Nouijai et al., “Drug-induced lupus-like syndrome in ankylosing spondylitis treated with infliximab,” Clinical and Experimental Rheumatology, vol. 26, no. 6, pp. 1116–1118, 2008.
[34]
S. Kobak, A. Celebi Kobak, Y. Kabasakal, and E. Doganavsargil, “Sj?gren's syndrome in patients with ankylosing spondylitis,” Clinical Rheumatology, vol. 26, no. 2, pp. 173–175, 2007.
[35]
J. Brandt, M. Rudwaleit, U. Eggens et al., “Increased frequency of Sjogren's syndrome in patients with spondyloarthropathy,” Journal of Rheumatology, vol. 25, no. 4, pp. 718–724, 1998.
[36]
M. P. J. Vanderpump and W. M. G. Tunbridge, “Epidemiology and prevention of clinical and subclinical hypothyroidism,” Thyroid, vol. 12, no. 10, pp. 839–847, 2002.
[37]
A. Antonelli, A. Delle Sedie, P. Fallahi et al., “High prevalence of thyroid autoimmunity and hypothyroidism in patients with psoriatic arthritis,” Journal of Rheumatology, vol. 33, no. 10, pp. 2026–2028, 2006.
[38]
N. Kale, M. Icen, J. Agaoglu, I. Yazici, and O. Tanik, “Clustering of organ-specific autoimmunity: a case presentation of multiple sclerosis and connective tissue disorders,” Neurological Sciences, vol. 29, no. 6, pp. 471–475, 2008.
[39]
P. J. D. Londo?o, L. A. González, L. A. Ramirez, et al., “Caracterización de las espondiloartropatías y determinación de factores de mal pronóstico en una población de pacientes colombianos,” Revista Colombiana de Reumatología, vol. 12, pp. 195–207, 2005.
[40]
J. Marquez, L. Pinto, D. L. Candia, et al., “Espondiloartritis en el Hospital Pablo Tobón Uribe. Descripción de una cohorte,” Revista Colombiana de Reumatología, vol. 17, pp. 80–85, 2010.
[41]
B. Martínez, L. Caraballo, M. Hernández, R. Valle, M. ávila, and A. I. Gamarra, “HLA-B27 subtypes in patients with ankylosing spondylitis (As) in Colombia,” Revista de Investigacion Clinica, vol. 51, no. 4, pp. 221–226, 1999.