Ankylosing spondylitis pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
AS is a systemic rheumatic disease, and is one of the seronegative spondyloarthropathies. About 90% of the patients express the HLA-B27 genotype. Tumor necrosis factor-alpha (TNF α) and IL-1 are also implicated in ankylosing spondylitis. Although specific autoantibodies cannot be detected, its response to immunosuppresive medication has prompted its classification as an autoimmune disease.
Pathophysiology
Hypotheses on its pathogenesis include a cross-reaction with antigens of the Klebsiella bacterial strain (Tiwana et al. 2001).[1] Particular authorities argue that elimination of the prime nutrients of Klebsiella (starches) would decrease antigenemia and improve the musculoskeletal symptoms. On the other hand, Khan (2002) argues that the evidence for a correlation between Klebsiella and AS is circumstantial so far, and that the efficacy of low-starch diets has not yet been scientifically evaluated.[2] Similarly, Toivanen (1999) found no support for the role of klebsiella in the etiology of primary AS.[3]
Associated Conditions
References
- ↑ Tiwana H, Natt R, Benitez-Brito R, Shah S, Wilson C, Bridger S, Harbord M, Sarner M, Ebringer A (2001). "Correlation between the immune responses to collagens type I, III, IV and V and Klebsiella pneumoniae in patients with Crohn's disease and ankylosing spondylitis". Rheumatology (Oxford). 40 (1): 15–23. PMID 11157137.
- ↑ Khan MA. (2002). Ankylosing spondylitis: The facts. Oxford University Press. ISBN 0-19-263282-5.
- ↑ Toivanen P, Hansen D, Mestre F, Lehtonen L, Vaahtovuo J, Vehma M, Möttönen T, Saario R, Luukkainen R, Nissilä M (1999). "Somatic serogroups, capsular types, and species of fecal Klebsiella in patients with ankylosing spondylitis". J Clin Microbiol. 37 (9): 2808–12. PMID 10449457.