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1 nflammatory myopathy (i.e., polymyositis and dermatomyositis).
2 human autoimmune settings including juvenile dermatomyositis.
3 tissue of adult dermatomyositis and juvenile dermatomyositis.
4 ontributions to the pathogenesis of juvenile dermatomyositis.
5 e type 1 interferon pathway for treatment of dermatomyositis.
6 rse effects in patients with polymyositis or dermatomyositis.
7 ts, 54 with inflammatory myopathies, 14 with dermatomyositis.
8 juvenile idiopathic arthritis, and juvenile dermatomyositis.
9 losporin in children with new-onset juvenile dermatomyositis.
10 inent data from adults with polymyositis and dermatomyositis.
11 c control of the immune response in juvenile dermatomyositis.
12 perimysial blood vessels in 10 patients with dermatomyositis.
13 small vessel occlusion in untreated juvenile dermatomyositis.
14 ear cells from children with active juvenile dermatomyositis.
15 d genetics play in the evolution of juvenile dermatomyositis.
16 derstanding the etiopathogenesis of juvenile dermatomyositis.
17 disability for adults with polymyositis and dermatomyositis.
18 imately 25% of patients with polymyositis or dermatomyositis.
19 enes are very strongly associated with adult dermatomyositis.
20 h juvenile idiopathic arthritis and juvenile dermatomyositis.
21 the 198 developed cancer after diagnosis of dermatomyositis.
22 d in serum of patients with polymyositis and dermatomyositis.
23 is of perifascicular muscle fibre atrophy in dermatomyositis.
24 atory myopathy, and the typical skin rash of dermatomyositis.
25 ammatory myopathies such as polymyositis and dermatomyositis.
26 flammatory demyelinating polyneuropathy, and dermatomyositis.
27 er inclusion body myositis, polymyositis, or dermatomyositis.
28 wide association study has been performed in dermatomyositis.
29 a differentiation-associated gene 5-positive dermatomyositis.
30 the diagnostic utility of autoantibodies in dermatomyositis.
31 ties between muscle and skin inflammation in dermatomyositis.
32 an important role in systemic sclerosis and dermatomyositis.
33 s a disease activity marker specifically for dermatomyositis.
34 e all manifestations of skin inflammation in dermatomyositis.
35 ifestations, and therapy for skin disease in dermatomyositis.
36 ad in regions of muscle fiber abnormality in dermatomyositis.
37 ans independently scored 10 children (9 with dermatomyositis, 1 with polymyositis; ages 4-15 years) t
38 d 3 pairs of monozygotic twins with juvenile dermatomyositis, 11 families with other siblings or rela
40 erythematosus (SLE); 17 had polymyositis or dermatomyositis; 16 had scleroderma; eight had ankylosin
41 erythematosus (3.06 [95% CI 1.78-4.90]) and dermatomyositis (2.64 [95% CI 0.86-6.17]) but not for sy
43 was characterized by a higher proportion of dermatomyositis (69% of adult Mestizos versus 35% of adu
45 ells contribute to the pathogenesis of adult dermatomyositis, a photoinduced autoimmune skin disease.
46 association of this polymorphism with adult dermatomyositis, a photosensitive disease that exhibits
48 be organized under two headings--amyopathic dermatomyositis (ADM) and classic dermatomyositis (CDM).
49 who developed classic cutaneous findings of dermatomyositis along with proximal muscle weakness and
52 ion may influence the relative prevalence of dermatomyositis and anti-Mi-2 autoantibodies in the US.
54 ment-induced microangiopathy is important in dermatomyositis and in the rare disorder, necrotizing my
58 alpha, are present in substantial numbers in dermatomyositis and may account for most of the cells pr
59 ime of onset with the relative prevalence of dermatomyositis and myositis autoantibodies in 380 patie
63 ratios (SIR) for individual cancer sites for dermatomyositis and polymyositis separately, using natio
64 syndromes of chronic inflammatory myopathy (dermatomyositis and polymyositis) may have in certain in
66 re is increasing evidence of autoimmunity in dermatomyositis and polymyositis, with strong correlatio
69 tissues in patients with SS from those with dermatomyositis and provide a relative weighting of the
71 fundamental mechanistic differences between dermatomyositis and subacute cutaneous lupus erythematos
73 tibodies found in the serum of patients with dermatomyositis and systemic lupus erythematosus, is rap
74 nous cyclophosphamide in refractory juvenile dermatomyositis and tacrolimus ointment for the dermatol
75 erstanding of autoantibodies associated with dermatomyositis and the autoimmune necrotizing myopathie
76 r with autoantibodies found in patients with dermatomyositis and the autoimmune necrotizing myopathie
77 genetics of children affected with juvenile dermatomyositis and the impact these genes have on disea
79 rproducing TNFalpha-308 A variant with adult dermatomyositis and with subacute cutaneous lupus erythe
80 tities, but is primarily made up of juvenile dermatomyositis and, to a lesser degree, juvenile polymy
81 ith systemic illnesses (lupus erythematosus, dermatomyositis), and the skin changes of potentially fa
82 r siblings or relatives with polymyositis or dermatomyositis, and 2 families with inclusion body myos
83 ents with systemic sclerosis, 1 patient with dermatomyositis, and a healthy volunteer were scanned us
84 ific information from children with juvenile dermatomyositis, and includes pertinent data from adults
85 mes (the most common forms are polymyositis, dermatomyositis, and inclusion body myositis) are system
91 with inclusion-body myositis, polymyositis, dermatomyositis, and neurogenic muscle atrophy, but it i
92 ce of systemic lupus erythematosus, juvenile dermatomyositis, and other primary systemic vasculitides
94 sitis (anti-SAE autoantibodies) and juvenile dermatomyositis (anti-p155/140 autoantibodies) (anti-MJ
95 ntibodies have been described in adult-onset dermatomyositis (anti-SAE autoantibodies) and juvenile d
96 or treatment of dermatomyositis and juvenile dermatomyositis are from anecdotal, non-randomised case
98 phil cytoplasmic antibodies+ vasculitis, and dermatomyositis are noteworthy but must be interpreted w
100 Inclusion body myositis, polymyositis, and dermatomyositis are three distinct categories of inflamm
101 articularly systemic lupus erythematosus and dermatomyositis, are also characterized by an up-regulat
102 be an important part of the pathogenesis of dermatomyositis, as it appears to be in systemic lupus e
103 erythematosus (SLE), diabetes mellitus, and dermatomyositis, as well as monogenic type I interferono
104 verse effects related to ipilimumab therapy, dermatomyositis associated with this agent has not previ
105 sequenced peptides eluted from the juvenile dermatomyositis-associated class II allele HLA-DQalpha1*
106 effective for the cutaneous complications of dermatomyositis but has been helpful in other extramuscu
107 available for evaluating the skin disease of dermatomyositis, but there is a need for new effective t
108 the reversibility of microvascular damage in dermatomyositis by intravenous immune globulin which app
111 5) dermatopulmonary syndrome is a subset of dermatomyositis defined by specific clinical features an
112 are certainly effective in polymyositis and dermatomyositis despite the lack of randomized controlle
113 ing patients with polymyositis (PM) (n=114), dermatomyositis (DM) (n=102), myositis associated with a
114 l muscle metabolism in vivo in patients with dermatomyositis (DM) and polymyositis (PM) in order to e
115 c acidosis and stroke-like episodes (MELAS), dermatomyositis (DM) and polymyositis (PM) using pairwis
116 non-inflammatory or dystrophic controls, two dermatomyositis (DM) and two polymyositis (PM) patients
117 ts have confirmed that polymyositis (PM) and dermatomyositis (DM) are not genetically identical disea
118 have estimated that up to 20% of adults with dermatomyositis (DM) have calcinosis, which can lead to
125 fication of novel autoantibodies in juvenile dermatomyositis (DM) may have etiologic and clinical imp
129 before and after therapy from patients with dermatomyositis (DM) who improved and patients with incl
131 -like modifier, and its enzymatic pathway in dermatomyositis (DM), an autoimmune disease primarily in
132 f the diverse entities of polymyositis (PM), dermatomyositis (DM), and inclusion body myositis (IBM),
133 ), sporadic inclusion body myositis (s-IBM), dermatomyositis (DM), and normal or disease controls.
134 symptom onset and the prevalence of juvenile dermatomyositis (DM), compared to juvenile polymyositis
135 ysed in biopsies of sIBM, polymyositis (PM), dermatomyositis (DM), dystrophic and non-myopathic muscl
136 rs of disease activity in juvenile and adult dermatomyositis (DM), especially during the active treat
137 To properly evaluate therapies for cutaneous dermatomyositis (DM), it is essential to administer an o
138 and 15 muscle samples from 44 patients with dermatomyositis (DM), polymyositis (PM), inclusion body
139 immune inflammatory muscle disorders include Dermatomyositis (DM), Polymyositis (PM), Necrotizing Myo
141 atients at the time of diagnosis of juvenile dermatomyositis (DM), to compare the RANKL:osteoproteger
153 y technology may also be used to distinguish dermatomyositis from the other inflammatory myopathies,
155 ls: alopecia areata, ankylosing spondylitis, dermatomyositis, Graves' disease, Hashimoto thyroiditis,
156 y of the -308A allele was 0.27 in the entire dermatomyositis group, versus 0.14 in the controls (p =
157 tion of the heterogeneity of skin disease in dermatomyositis has already provided evidence that clini
158 e conceptual model of the pathophysiology of dermatomyositis has been based on work extending back ov
162 lesions of patients with cutaneous lupus and dermatomyositis has provided valuable information about
164 classification criteria for polymyositis and dermatomyositis have been suggested by a number of inves
165 evidence that patients with polymyositis and dermatomyositis have specific clinico-serological profil
166 dies; myovasculopathies, including childhood dermatomyositis; immune polymyopathies, active myopathie
167 Studies in adults with polymyositis and dermatomyositis implicate interleukin-1alpha, transformi
168 MBL variants were over-represented in adult dermatomyositis in a dose-responsive fashion (p=0.0002).
169 allele was positively associated with adult dermatomyositis in a dose-responsive fashion (p=0.0004),
170 adverse events and consider drug-associated dermatomyositis in the differential diagnosis in patient
171 utoantibodies preferentially associated with dermatomyositis include those recognizing Mi-2, MDA5, TI
172 new insights into the disease mechanisms of dermatomyositis, inclusion body myositis, and polymyosit
173 specific response in muscle in patients with dermatomyositis, inclusion body myositis, and polymyosit
180 We conclude that: perifascicular atrophy in dermatomyositis is consistently associated with focal mi
181 e weakness in patients with polymyositis and dermatomyositis is due to autoimmune and inflammatory pr
182 rization of the type 1 interferon pathway in dermatomyositis is leading down a path of genomic medici
187 nective-tissue diseases, especially juvenile dermatomyositis (JDM) and systemic sclerosis; however, l
190 radiation exposure 1 month prior to juvenile dermatomyositis (JDM) may trigger the onset of disease.
192 d have been found in high levels in juvenile dermatomyositis (JDM), which may account the frequency o
194 develop in 20-40% of children with juvenile dermatomyositis (juvenile DM), contributing to disease m
195 ematosis, Wegener's granulomatosis, juvenile dermatomyositis, juvenile scleroderma and autoinflammato
196 a, mixed connective tissue disease, juvenile dermatomyositis, juvenile spondyloarthropathy and system
198 fferent pathways of complement activation in dermatomyositis, lupus nephritis, and necrotic muscle fi
199 iption and classification of skin disease in dermatomyositis may allow the clinician to predict more
200 se, immunotherapies to better treat juvenile dermatomyositis may become available in the future.
204 e that ISG15, which is highly upregulated in dermatomyositis muscle, does not appear to play a key ro
207 econd-line therapy in stiff-person syndrome, dermatomyositis, myasthenia gravis, and Lambert-Eaton my
208 lt patients with polymyositis (PM; n = 134), dermatomyositis (n = 129), or other CTDs (predominantly
209 jogren's syndrome (n = 30), polymyositis and dermatomyositis (n = 30), and progressive systemic scler
210 yositis and of an IFN-alpha/beta response in dermatomyositis, neither of which was previously describ
211 ith the relative proportion of patients with dermatomyositis (odds ratio [OR] 2.3, 95% confidence int
215 muscle function in patients with established dermatomyositis or polymyositis receiving chronic medica
216 or rheumatoid arthritis, Sjogren's syndrome, dermatomyositis or polymyositis, or scleroderma were of
218 l haplotype; however, African Americans with dermatomyositis or with anti-Jo-1 autoantibodies shared
219 temic disease such as lupus erythematosus or dermatomyositis, or be an early symptom of a rare group
220 scular complement deposition is a feature of dermatomyositis pathology but the trigger for complement
223 antigenic target on the endothelial cell in dermatomyositis patients and the pathogenic role of the
227 tor-alpha synthesis is increased in juvenile dermatomyositis patients with the tumor necrosis factor-
228 ications for systemic and malignancy risk in dermatomyositis patients, and that there may be several
229 in the same 10, as well as in 40 additional dermatomyositis patients, we searched for vascular depos
233 with a subset of patients with polymyositis/dermatomyositis (PM/DM) complicated by interstitial lung
234 whether sera from patients with polymyositis/dermatomyositis (PM/DM) with or without interstitial lun
235 -55-kd bands, all patients with polymyositis/dermatomyositis (PM/DM), and a random selection of SSc,
236 , 121 with scleroderma, 86 with polymyositis/dermatomyositis [PM/DM]) and 248 Italian patients with a
237 sus, Wegener's granulomatosis, polymyositis, dermatomyositis, polyarteritis nodosa, or scleroderma wh
239 ell into the typical IIM subclassifications: dermatomyositis, polymyositis and inclusion body myositi
240 pathies (IIMs) are typically subdivided into dermatomyositis, polymyositis and inclusion body myositi
241 esoangioblasts isolated from samples of IBM, dermatomyositis, polymyositis, and control muscles were
242 the results of recent therapeutic trials in dermatomyositis, polymyositis, and inclusion body myosit
243 muscle cells in the inflammatory myopathies (dermatomyositis, polymyositis, and inclusion body myosit
244 iopathic inflammatory myopathies, comprising dermatomyositis, polymyositis, and inclusion body myosit
245 iated into three major and distinct subsets: dermatomyositis, polymyositis, and inclusion-body myosit
246 BM patient sera, whereas their prevalence in dermatomyositis, polymyositis, and other neuromuscular d
248 arison, 2/15 (14%) age-matched patients with dermatomyositis, polymyositis, or necrotizing myopathy,
249 ritis; lupus; scleroderma; Sjogren Syndrome; dermatomyositis/polymyositis; unspecified/mixed CTD; oth
251 proportion of patients achieving a juvenile dermatomyositis PRINTO 20 level of improvement (20% impr
253 d Musculoskeletal and Skin Diseases Juvenile Dermatomyositis Research Registry and the National Pedia
254 py is essential, since both polymyositis and dermatomyositis respond to immunotherapeutic agents.
255 vascular membrane attack complex deposits in dermatomyositis result from activation of the classical
256 d unusual manifestations of cutaneous lupus, dermatomyositis, scleroderma, and rheumatoid arthritis.
258 ow the possibility that, for the first time, dermatomyositis skin disease can serve as a valid outcom
259 lases HDAC1/2, histone-binding proteins, the dermatomyositis-specific autoantigen Mi2beta, a polypept
261 , and the LX promoter polymorphism) in adult dermatomyositis, subacute cutaneous lupus erythematosus,
262 liminary gene expression studies in juvenile dermatomyositis, systemic lupus erythematosus, and chron
263 and specific prior autoimmune (polymyositis/dermatomyositis, systemic sclerosis, autoimmune hemolyti
264 ot observed in any patient with polymyositis/dermatomyositis, systemic sclerosis, rheumatoid arthriti
265 an inflammatory myopathies (polymyositis and dermatomyositis), the early, widespread appearance of MH
266 ar to what is observed in human polymyositis/dermatomyositis, the mice developed a strong antinuclear
267 n understanding these mechanisms in juvenile dermatomyositis, the most common form of childhood infla
272 ation, the association of these two genes in dermatomyositis was significantly less than we previousl
273 To further understand the pathophysiology of dermatomyositis, we used microarrays, computational meth
274 sms in patients with rheumatoid arthritis or dermatomyositis were analyzed by polymerase chain reacti
275 A total of 37 patients with polymyositis or dermatomyositis were randomized (19 to creatine, 18 to p
276 factor -308A polymorphism is associated with dermatomyositis, which suggests a pathophysiologic contr
277 18 years or younger with new-onset juvenile dermatomyositis who had received no previous treatment a
278 affect as many as 20% to 30% of adults with dermatomyositis, will not be addressed in this review.
279 crosis factor-alpha, more common in juvenile dermatomyositis with the tumor necrosis factor-alpha-308
281 juvenile idiopathic arthritis, and juvenile dermatomyositis, with special interest on strategies to
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