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1 101/*0401 may be of particular importance to rheumatoid vasculitis.
2 tion of SE presence, dose, and genotype with rheumatoid vasculitis.
3 evention, treatment or even as a trigger for rheumatoid vasculitis.
4 des for CD158j, is a genetic risk factor for rheumatoid vasculitis.
5 pact of biologic agents used to treat RA, on rheumatoid vasculitis.
9 f cyclophosphamide in patients with systemic rheumatoid vasculitis, and methotrexate in the case of o
10 ere was a clear decline in the prevalence of rheumatoid vasculitis, and this decline remained evident
11 he genetic determinants that confer risk for rheumatoid vasculitis are not known, but patients with v
12 respectively, to determine the prevalence of rheumatoid vasculitis, as defined by the International C
13 itis nodosa, microscopic polyangiitis (MPA), rheumatoid vasculitis, Churg-Strauss syndrome (CSS), and
14 s significantly enriched among patients with rheumatoid vasculitis compared with normal individuals (
16 was significantly different in patients with rheumatoid vasculitis in comparison with the control pop
18 patients with RA who were hospitalized with rheumatoid vasculitis or to undergo splenectomy for Felt
20 results demonstrate a significant decline in rheumatoid vasculitis prevalence after 2000 in this nati
21 eakpoints representing a significant drop in rheumatoid vasculitis prevalence between the years 2000
24 (i.e., 1 or 2 alleles versus 0 alleles) and rheumatoid vasculitis (summary OR 1.4, 95% CI 0.7-2.7).
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