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1 n disease, multiple sclerosis, and relapsing polychondritis.
2 the aortitis of Cogan syndrome and relapsing polychondritis.
3 similar to those symptoms in human relapsing polychondritis.
4 important in susceptibility to experimental polychondritis.
5 maging assessment in patients with relapsing polychondritis.
8 is also a frequent target organ in relapsing polychondritis, and proptosis is a well-recognized manif
9 nd histologic manifestations of experimental polychondritis are similar to those symptoms in human re
10 anisms of pathogenesis involved in relapsing polychondritis as well as the influence of the expressio
11 of NOD.DQ8 mice develop severe experimental polychondritis, auricular chondritis, and polyarthritis,
13 habeta tg mice developed severe experimental polychondritis, exhibiting both polyarthritis and auricu
15 om malignant transformation of the relapsing polychondritis-induced inflammatory pseudotumor and emph
20 ognition and accurate diagnosis of relapsing polychondritis is crucial for appropriate management and
24 a man who was diagnosed as having relapsing polychondritis (RP) when he was 18 years of age and was
25 as other conditions, particularly relapsing polychondritis (RP), with which it shares several clinic
27 eria for an inflammatory syndrome (relapsing polychondritis, Sweet's syndrome, polyarteritis nodosa,
29 ' experience with 36 patients with relapsing polychondritis who were followed from 1980 to 1997, 30 p
30 t in the majority of patients with relapsing polychondritis who were referred for airway imaging, yet
31 nically diagnosed or biopsy-proved relapsing polychondritis who were referred for CT airway imaging d