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1                                              FCAS was previously mapped to a 10-cM region on chromoso
2                    To identify the genes for FCAS and MWS, we screened exons in the 1q44 region for m
3 h equal potency in LPS-stimulated cells from FCAS and control subjects.
4 we examined cytokine secretion in PBMCs from FCAS patients and found a marked hyperresponsiveness of
5    Cryopyrin, the protein that is altered in FCAS, is one of the adaptor proteins that activate caspa
6 s occurring after a general cold exposure in FCAS patients and to investigate the effects of pretreat
7 s, that have hitherto been described only in FCAS and NOMID, respectively.
8 ory syndrome (FCAS), and 3 probands with MWS/FCAS.
9 ated with autoinflammatory diseases, but not FCAS, showed neither enhanced interaction with HSC70 nor
10 ion in patients with NOMID/CINCA syndrome or FCAS.
11     Familial cold autoinflammatory syndrome (FCAS) and the related autoinflammatory disorders, Muckle
12 ses familial cold autoinflammatory syndrome (FCAS) characterized by cold-induced hyperactivation of c
13     Familial cold autoinflammatory syndrome (FCAS) is an autosomal dominant disorder characterised by
14     Familial cold autoinflammatory syndrome (FCAS) is caused by mutations in the CIAS1 gene, leading
15 lial cold-induced autoinflammatory syndrome (FCAS), and 3 probands with MWS/FCAS.
16 S), familial cold autoinflammatory syndrome (FCAS), and neonatal-onset multisystem inflammatory disea
17 ing familial cold autoinflammatory syndrome (FCAS), Muckle-Wells syndrome (MWS), and neonatal onset m
18     Familial cold autoinflammatory syndrome (FCAS, MIM 120100), commonly known as familial cold urtic
19                               Patients whose FCAS was not completely controlled were allowed a dosage
20 ted with the disorder in three families with FCAS and one family with MWS.
21 fter cold challenge, untreated patients with FCAS developed rash, fever, and arthralgias within 1-4 h
22 cal and biochemical changes in patients with FCAS indicates a central role for interleukin 1beta in t
23                           Five patients with FCAS were studied in an open-label trial.
24 romising therapeutic option in patients with FCAS, and the data led to the design of a phase III stud
25 -1 receptor fusion protein, in patients with FCAS.
26 a on rilonacept treatment in 5 patients with FCAS.