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1 trachomatis in its role in Chlamydia-induced reactive arthritis.
2 in bacteria, possibly implicated directly in reactive arthritis.
3 mmation, indicating therapeutic potential in reactive arthritis.
4 Salmonella spp., are also known triggers of reactive arthritis.
5 th a history of Salmonella infection develop reactive arthritis.
6 stics of the spondyloarthropathies including reactive arthritis.
8 g genetic predisposition to development of a reactive arthritis after infection by bacteria such as S
9 iatric health care networks, we screened for reactive arthritis among 148 children between ages 2 and
10 his bacterium can trigger the development of reactive arthritis, an acute inflammation that is associ
11 um causes epididymo-orchitis, proctitis, and reactive arthritis and facilitates human immunodeficienc
14 long-term sequelae (Guillain-Barre syndrome, reactive arthritis, and postinfectious irritable bowel s
15 at primarily include ankylosing spondylitis, reactive arthritis, and the arthritis associated with ps
17 tis is an underdiagnosed, potentially morbid reactive arthritis associated with C difficile infection
19 many enterobacterial infections can trigger reactive arthritis, but an infectious trigger for ankylo
20 upports the hypothesis that glycine prevents reactive arthritis by blunting cytokine release from mac
22 e study of Mur levels in inflammation (e.g., reactive arthritis) could prove important in testing the
23 majority of patients with Chlamydia-induced reactive arthritis do not present with the classic triad
24 is, although long-term complications such as reactive arthritis (due to Salmonella, Yersinia, and Shi
25 ctious agents in the joints of patients with reactive arthritis has raised questions about whether ch
26 of TNFalpha antagonists in the treatment of reactive arthritis; however, the possibility that the tr
27 imated that C difficile infection-associated reactive arthritis incidence was 5.0 cases per million p
31 , the role of HLA-B27 in the pathogenesis of reactive arthritis may lie downstream of the invasion an
32 t group, which consisted of one patient with reactive arthritis, one patient with pauciarticular juve
33 ved from patients with clinical diagnoses of reactive arthritis or Reiter's syndrome, and 1 was from
36 ce of an entity designated poststreptococcal reactive arthritis (PSReA) has been highlighted in recen
37 (Chlamydia) pneumoniae are known triggers of reactive arthritis (ReA) and exist in a persistent metab
41 s in varying disease phases, 8 patients with reactive arthritis (ReA), 10 patients with inflammatory
44 ndylitis (AS), psoriatic arthritis (PsA), or reactive arthritis (ReA): presence of 1) > or =1 or 2) >
46 ed from 55 patients, including patients with reactive arthritis, Reiter's syndrome, and other arthrop
48 D8+ T cells from the joints of patients with reactive arthritis support the etiological link between
50 associated with inflammatory bowel disease, reactive arthritis, undifferentiated spondyloarthropathy
51 ankylosing spondylitis, psoriatic arthritis, reactive arthritis, undifferentiated spondyloarthropathy
52 kly) in 16 patients with undifferentiated or reactive arthritis was assessed in a 6-month open-label
53 ncidence of C difficile infection-associated reactive arthritis was calculated based on (1) pediatric
54 of cases of C difficile infection-associated reactive arthritis were correctly diagnosed by treating
55 s, cases of C difficile infection-associated reactive arthritis were less likely to have underlying c
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