Abstract
The objective of the study was to investigate potential triggering events for the onset of ankylosing spondylitis (AS). A large retrospective population survey of 1,080 AS patients was carried out by multi-faceted questionnaire. A nested case–control study compared the cohort to 102 patients with lumbar disc prolapse. Participants with AS had a mean age of 49.8 years, mean age of disease onset was 25.2 years and 63% of the cohort were male. Seventy-nine per cent knew they were human leucocyte antigen (HLA)-B27-positive, and a further 12.5% were unaware of their HLA-B27 status. Infections were relatively common in the 3 months leading to the first symptoms, 4.6% reporting gastrointestinal infection, 2.5% reporting urinary tract infection and 2.6% respiratory infection. Five per cent reported heavy physical activity in the 3 months prior to the onset of symptoms, 4.2% emotional stressors and 3.1% work stressors. Injury and surgery were less commonly reported (1.7 and 0.7%, respectively). Pregnancy was reported by 7.4% of the female participants. When the 12 months leading up to the first symptoms was compared to the 12 months previous to that, work stressors (OR 1.5), and pregnancy (OR 2.5) infection (OR 1.5 to 1.8) were significantly more common closer to disease onset. Infection and work stressors are potential triggers for the onset of AS; however, low rates suggest they are only a small part of the environmental milieu that combines with a genetic predisposition to cause the development of this chronic inflammatory disease.
This is a preview of subscription content, log in via an institution to check access.
Similar content being viewed by others
References
Sims AM, Wordsworth BP, Brown MA (2004) Genetic susceptibility to ankylosing spondylitis. Curr Mol Med 4(1):13–20
Lee JH, Jun JB, Jung S, Bae SC, Yoo DH, Kim TY, Kim SY, Kim TH (2002) Higher prevalence of peripheral arthritis among ankylosing spondylitis patients. J Korean Med Sci 17(5):669–673
Weiss G, Shemer A, Trau H (2002) The Koebner phenomenon: review of the literature. J Eur Acad Dermatol Venereol 16(3):241–248
Sieper J (2004) Disease mechanisms in reactive arthritis. Curr Rheumatol Rep 6(2):110–116
Vaile JH, Meddings JB, Yacyshyn BR, Russell AS, Maksymowych WP (1999) Bowel permeability and CD45RO expression on circulating CD20+ B cells in patients with ankylosing spondylitis and their relatives. J Rheumatol 26(1):128–135
Tani Y, Tiwana H, Hukuda S, Nishioka J, Fielder M, Wilson C, Bansal S, Ebringer A (1997) Antibodies to Klebsiella, Proteus, and HLA-B27 peptides in Japanese patients with ankylosing spondylitis and rheumatoid arthritis. J Rheumatol 24(1):109–114
Hermann E, Sucké B, Droste U, Meyer zum Büschenfelde KH (1995) Klebsiella pneumoniae-reactive T cells in blood and synovial fluid of patients with ankylosing spondylitis. Comparison with HLA-B27+ healthy control subjects in a limiting dilution study and determination of the specificity of synovial fluid T cell clones. Arthritis Rheum 38(9):1277–1282
Braun J, Bollow M, Remlinger G, Eggens U, Rudwaleit M, Distler A, Sieper, J (1998) Prevalence of spondylarthropathies in HLA-B27 positive and negative blood donors. Arthritis Rheum 41(1):58–67
Rudwaleit M, Andermann B, Alten R, Sorensen H, Listing J, Zink A, Sieper J, Braun J (2002) Atopic disorders in ankylosing spondylitis and rheumatoid arthritis. Ann Rheum Dis 61(11):968–974
Feldtkeller E, Khan MA, van der Heijde D, van der Linden S, Braun J (2003) Age at disease onset and diagnosis delay in HLA-B27 negative vs. positive patients with ankylosing spondylitis. Rheumatol Int 23(2):61–66
Zochling J, Bohl-Bühler MHJ, Baraliakos X, Feldtkeller E, Braun J (2005) The high prevalence of infections and allergic symptoms in patients with ankylosing spondylitis is associated with clinical symptoms. Clin Rheumatol DOI 10.1007/s10067-005-0130-0
Feldtkeller E (1999) Erkrankungsalter und Diagnoseverzögerung bei Spondylarthropathien. Z Rheumatol 58:21–30
Feldtkeller E, Lemmel EM (1999) Zur Situation von Spondyloarthritis-Patienten. Ergebnisse einer Repräsentativbefragung der Deutschen Vereinigung Murbus Bechterew. Novartis Pharma, Nuremberg
Feldtkeller E, Bruckel J, Khan MA (2000) Scientific contributions of ankylosing spondylitis patient advocacy groups. Curr Opin Rheumatol 12:239–247
Olivieri I, Gemignani G, Christou C, Semeria R, Giustarini S, Pasero G (1991) The triggering role of physical injury in the onset of peripheral arthritis in seronegative spondyloarthropathy. Rheumatol Int 10(6):251–253
Olivieri I, Gherardi S, Bini C, Trippi D, Ciompi ML, Pasero G (1988) Trauma and seronegative spondyloarthropathy: rapid joint destruction in peripheral arthritis triggered by physical injury. Ann Rheum Dis 47(1):73–76
Jun JB, Kim TH, Jung SS, Yoo DH, Kim TY, Kim SY (2000) Seronegative spondyloarthropathy initiated by physical trauma. Clin Rheumatol 19(5):348–351
Jacoby RK, Newell RL, Hickling P (1985) Ankylosing spondylitis and trauma: the medicolegal implications. A comparative study of patients with non-specific back pain. Ann Rheum Dis 44(5):307–311
Alcalay M, Debiais F, Prieur AM, Azais I, Masson G, Thomas P, Bontoux D (1987) Retrospective study of the possible role of injuries in the genesis of ankylosing spondylitis, Fiessinger–Leroy–Reiter syndrome and other reactive arthritis, unclassified B27 rheumatism in adults and chronic B27 arthritis in children. (French) Rev Rhum Mal Osteo-Artic 54(3):235–241
Colombini D, Riva F, Lue D, Nava C, Petri A, Basilico S, Linzalata M, Morselli G, Cotroneo L, Ricci MG, Menoni O, Battevi N (1999) Initial epidemiological data on the clinical effects in health workers employed in the manual lifting of patients in wards. Med Lav 90(2):201–228
Maksymowych WP (2003) Etiology and pathogenesis of ankylosing spondylitis. In: Hochberg MC, Silman AJ, Smolen JS, Weinblatt ME, Weisman MH (eds) Rheumatology, 3rd edn. Elsevier, London, pp 1183–1192
Taurog JD, Richardson JA, Croft JT, Simmons WA, Zhou M, Fernandez-Sueiro JL, Balish E, Hammer RE (1994) The germfree state prevents development of gut and joint inflammatory disease in HLA-B27 transgenic rats. J Exp Med 180(6):2359–2364
Tani Y, Sato H, Tanaka N, Hukuda S (1997) Antibodies against bacterial lipopolysaccharides in Japanese patients with ankylosing spondylitis. Rheumatology 36(4):491–493
Hermann E, Yu DT, Meyer zum Büschenfelde KH, Fleischer B (1993) HLA-B27 restricted CD8+ T cells derived from synovial fluids of patients with reactive arthritis and ankylosing spondylitis. Lancet 342(8872):646–650
Höhler T, Schaper T, Schneider PM, Meyer zum Büschenfelde KH, Märker-Hermann E (1998) Association of different tumor necrosis factor alpha promoter allele frequencies with ankylosing spondylitis in HLA-B27 positive individuals. Arthritis Rheum 41(8):1489–1492
Braun J, Tuszewski M, Ehlers S, Haberle J, Bollow M, Eggens U, Distler A, Sieper J (1997) Nested polymerase chain reaction strategy simultaneously targeting DNA sequences of multiple bacterial species in inflammatory joint diseases. II. Examination of sacroiliac and knee joint biopsies of patients with spondyloarthropathies and other arthritides. J Rheumatol 24(6):1101–1105
Hannu T, Kauppi M, Tuomala M, Laaksonen I, Klemets P, Kuusi M (2004) Reactive arthritis following an outbreak of Campylobacter jejuni infection. J Rheumatol 31(3):528–530
Dworkin MS, Shoemaker PC, Goldoft MJ, Kobayashi JM (2001) Reactive arthritis and Reiter’s syndrome following an outbreak of gastroenteritis caused by salmonella enteritidis. Clin Infect Dis 33(7):1010–1014
Rose GA, Blackburn H (1968) Cardiovascular survey methods. World Health Organization, Geneva
Author information
Authors and Affiliations
Corresponding author
Rights and permissions
About this article
Cite this article
Zochling, J., Bohl-Bühler, M.H.J., Baraliakos, X. et al. Infection and work stress are potential triggers of ankylosing spondylitis. Clin Rheumatol 25, 660–666 (2006). https://doi.org/10.1007/s10067-005-0131-z
Received:
Revised:
Accepted:
Published:
Issue Date:
DOI: https://doi.org/10.1007/s10067-005-0131-z