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1 ision diagnosis codes for psoriasis, PsA, or spondylarthritis.
2 velop in both degenerative joint disease and spondylarthritis.
3 showed many features characteristic of human spondylarthritis.
4 sfolding plays a role in the pathogenesis of spondylarthritis.
5 ut also affects patients with no evidence of spondylarthritis.
6 n other variants of NOD2 and either UC or CD spondylarthritis.
7 fore, B27-transgenic rats provide a model of spondylarthritis.
8 to, and clinical manifestations of, colitic spondylarthritis.
9 OR 0.55, 95% CI 0.37-0.82), but not with CD spondylarthritis.
10 in patients with MRI-determined early axial spondylarthritis.
11 , 13 with undifferentiated arthritis, 9 with spondylarthritis, 4 with inflammatory osteoarthritis, an
12 , and B and T lymphocytes from patients with spondylarthritis, and controls carried receptors for HLA
14 associated with IBD (referred to as colitic spondylarthritis; comprising 78 with CD and 119 with ulc
15 ook this study to ascertain if patients with spondylarthritis express beta(2)-microglobulin-free HLA-
18 though patients with CD had a younger age at spondylarthritis onset than did those with UC (22.4 year
21 Ser variant was inversely associated with UC spondylarthritis (P = 0.003, OR 0.55, 95% CI 0.37-0.82),
22 on was identified between Gly(908)Arg and UC spondylarthritis (P = 0.016, odds ratio [OR] 4.6, 95% co
25 illes tendon enthesis at different stages of spondylarthritis (SpA) with microanatomic studies of nor
26 increasingly used for the diagnosis of axial spondylarthritis (SpA), but it is unknown whether charac
27 HLA-B27 is implicated in the pathogenesis of spondylarthritis (SpA), yet the molecular mechanisms are
30 cular JIA, 18 with systemic JIA, and 19 with spondylarthritis [SpA]) and 830 healthy control subjects
31 examine the effects of a lack of CD8 on the spondylarthritis that develops in B27/human beta(2)-micr
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