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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.
7                                              Reactive arthritis affected 1.4% of children with C diff
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
12 een linked to the postinfectious sequelae of reactive arthritis and Guillain-Barre syndrome.
13                                          For reactive arthritis and undifferentiated spondylarthropat
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
16 rthropathies (including psoriatic arthritis, reactive arthritis, ankylosing spondylitis), and osteoar
17 ate deposition disease, psoriatic arthritis, reactive arthritis, ankylosing spondylitis, and osteoart
18                            Poststreptococcal reactive arthritis appears to be a heterogeneous clinica
19 tis is an underdiagnosed, potentially morbid reactive arthritis associated with C difficile infection
20  organisms are in the joints of persons with reactive arthritis at some point in the illness.
21  many enterobacterial infections can trigger reactive arthritis, but an infectious trigger for ankylo
22 upports the hypothesis that glycine prevents reactive arthritis by blunting cytokine release from mac
23 ysiology, and treatment of Chlamydia-induced reactive arthritis (CiReA).
24 e study of Mur levels in inflammation (e.g., reactive arthritis) could prove important in testing the
25  majority of patients with Chlamydia-induced reactive arthritis do not present with the classic triad
26 is, although long-term complications such as reactive arthritis (due to Salmonella, Yersinia, and Shi
27 ctious agents in the joints of patients with reactive arthritis has raised questions about whether ch
28  of TNFalpha antagonists in the treatment of reactive arthritis; however, the possibility that the tr
29 imated that C difficile infection-associated reactive arthritis incidence was 5.0 cases per million p
30             C difficile infection-associated reactive arthritis is an underdiagnosed, potentially mor
31 ctions, better recognition of its associated reactive arthritis is needed.
32 f pediatric C difficile infection-associated reactive arthritis is poorly understood.
33 , the role of HLA-B27 in the pathogenesis of reactive arthritis may lie downstream of the invasion an
34 t group, which consisted of one patient with reactive arthritis, one patient with pauciarticular juve
35 ved from patients with clinical diagnoses of reactive arthritis or Reiter's syndrome, and 1 was from
36 yloarthropathy, such as psoriatic arthritis, reactive arthritis, or ankylosing spondylitis.
37                            Poststreptococcal reactive arthritis (PSRA) refers to a poststreptococcal
38 ce of an entity designated poststreptococcal reactive arthritis (PSReA) has been highlighted in recen
39 (Chlamydia) pneumoniae are known triggers of reactive arthritis (ReA) and exist in a persistent metab
40 model of Yersinia enterocolitica O:3-induced reactive arthritis (ReA) in TNFRp55(-/-) mice.
41                                              Reactive arthritis (ReA) is an HLA-B27-associated spondy
42                                              Reactive arthritis (ReA) is postulated to be caused by a
43 expressed transcripts in RA and, as control, reactive arthritis (ReA) synovium.
44 s in varying disease phases, 8 patients with reactive arthritis (ReA), 10 patients with inflammatory
45 pecies in joint specimens from patients with reactive arthritis (ReA).
46 ought to be important in the pathogenesis of reactive arthritis (ReA).
47 ndylitis (AS), psoriatic arthritis (PsA), or reactive arthritis (ReA): presence of 1) > or =1 or 2) >
48 dylitis (AS), psoriatic arthritis (PsA), and reactive arthritis (ReA; Reiter's syndrome).
49 ed from 55 patients, including patients with reactive arthritis, Reiter's syndrome, and other arthrop
50                                              Reactive arthritis, sacroiliitis, and ankylosing spondyl
51 D8+ T cells from the joints of patients with reactive arthritis support the etiological link between
52 spondylitis (AS), psoriatic arthritis (PsA), reactive arthritis, the arthritis associated with inflam
53  with PsA supports the concept that PsA is a reactive arthritis to certain streptococci.
54  associated with inflammatory bowel disease, reactive arthritis, undifferentiated spondyloarthropathy
55 ankylosing spondylitis, psoriatic arthritis, reactive arthritis, undifferentiated spondyloarthropathy
56 kly) in 16 patients with undifferentiated or reactive arthritis was assessed in a 6-month open-label
57 ncidence of C difficile infection-associated reactive arthritis was calculated based on (1) pediatric
58 of cases of C difficile infection-associated reactive arthritis were correctly diagnosed by treating
59 s, cases of C difficile infection-associated reactive arthritis were less likely to have underlying c