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1 ocalized scleroderma (linear scleroderma and morphea).
2 aluation is justified only in SSc and not in morphea.
3 (32.7%) of SSc and only two cases (7.14%) of morphea.
4 in SSc, no such motility disorder is seen in morphea.
5 vestigate the immunological underpinnings of morphea.
6 h atrophic disorders such as lipoatrophy and morphea.
7 rmatofibromas, but not in sclerotic areas of morphea.
8 a promising biomarker of disease activity in morphea.
9 e expression showed significant overlap with morphea.
10 51 upstream regulators were shared in EF and morphea.
11  seen in 32 cases (68.1%) of SSc and none in morphea.
12  the sera and lesional skin of patients with morphea.
13 upregulated in EF, and 9 were upregulated in morphea.
14 es (80.5%) of SSc and no such abnormality in morphea.
15 t of SSc are also promising for treatment of morphea.
16 , and immune dysregulation observed in human morphea.
17 d by generalized morphea (244 [26%]), plaque morphea (141 [15%]), mixed morphea (38 [4%]), and panscl
18 morphea (474 [50%]), followed by generalized morphea (244 [26%]), plaque morphea (141 [15%]), mixed m
19 linear (474 [50%]) or generalized subtype of morphea (244 [26%]).
20 linear scleroderma (30%) and 6 patients with morphea (26%) had IgG autoantibodies to fibrillin 1 (rFb
21 ), mixed morphea (38 [4%]), and pansclerotic morphea (3 [0.3%]).
22 44 [26%]), plaque morphea (141 [15%]), mixed morphea (38 [4%]), and pansclerotic morphea (3 [0.3%]).
23 most patients were classified to have linear morphea (474 [50%]), followed by generalized morphea (24
24 orphea and 500 patients with pediatric-onset morphea; 741 female participants [78%]; median age at on
25 items that experts agreed were indicative of morphea activity (new lesion in the past 3 months, enlar
26                                          The Morphea Activity Measure (MAM) was recently validated, b
27 was not associated with clinical measures of morphea activity.
28  valid, and viable tool to measure pediatric morphea activity.
29                           PURPOSE OF REVIEW: Morphea, also known as localized scleroderma, is a disor
30                                              Morphea, also known as localized scleroderma, is charact
31 a case-control study of 87 participants with morphea and 26 healthy control subjects.
32  participants (444 patients with adult-onset morphea and 500 patients with pediatric-onset morphea; 7
33 tifies shared molecular mechanisms of EF and morphea and demonstrates strong pathophysiologic similar
34 rly in terms of generalized and pansclerotic morphea and descriptors such as morphea profunda.
35              Cases of localized scleroderma (morphea and linear disease) were excluded.
36                       The similarity between morphea and the inflammatory subset of SSc on transcript
37 e will provide better care for patients with morphea and understanding its pathophysiology will lay g
38 erma (27 with linear scleroderma and 23 with morphea) and 51 normal controls were tested for IgG and
39 is [SSc], 16 with linear SSc, 14 with linear morphea, and 17 with morphea) were examined in the large
40 FN-related pathways have not been studied in morphea, and biomarkers are needed.
41       Although some subtypes, such as linear morphea, are present across all the classification schem
42 lopments in the evaluation and management of morphea as well as its pathophysiology.
43  AHAs are more prevalent among patients with morphea but are of limited clinical utility except in li
44 ntibodies (ANAs) and other autoantibodies in morphea but found they are of limited significance.
45 sought to examine the molecular landscape of morphea by examining lesional skin gene expression and b
46                        Detecting activity of morphea can be complex but is crucial for adequate treat
47 ermining disease progression in craniofacial morphea (CM) is challenging, as clinical findings of dis
48 yzed skin biopsies from patients with EF and morphea compared with those from adult healthy skin usin
49 reed that the tool was easy to use, measured morphea disease activity at a single time point, and sho
50 oint, and should be responsive to changes in morphea disease activity over multiple time points.
51                       Disabling pansclerotic morphea (DPM) is a rare systemic inflammatory disorder,
52             During the development phase, 14 morphea experts (dermatologists and pediatric dermatolog
53 dered aggressive in terms of growth pattern (morphea form, infiltrative and micronodular features) as
54 hree (5.3%); while only four cases (7.1%) of morphea had esophageal symptoms all of which were mild i
55 n the past year, a revised classification of morphea has been presented.
56              The involvement of esophagus in morphea has been studied very scarcely.
57 immune bullous diseases, systemic sclerosis, morphea, hidradenitis, and dermatomyositis.
58 cipants included individuals enrolled in the Morphea in Adults and Children (MAC) cohort and Sclerode
59  and children from 2 prospective cohorts-the Morphea in Adults and Children at the University of Texa
60 rolled in two prospective cohort registries (Morphea in Children and Adults Cohort [n = 750] and Nati
61 The promise of evidence-based treatments for morphea in the near future will provide better care for
62 ssociated with clinical indicators of severe morphea including functional limitation (ssDNA ab, P = .
63 or their ability to categorize patients with morphea into demographically and clinically coherent gro
64  Taken together, these results indicate that morphea is a skin-directed process characterized by T he
65                                              Morphea is an autoimmune condition of the skin associate
66                                              Morphea is an inflammatory fibrotic disorder of the skin
67                                              Morphea is an insidious inflammatory disorder of the ski
68                                              Morphea is characterized by initial inflammation followe
69                     In summary, inflammatory morphea is characterized by T helper type 1 cytokine imb
70 s substantial morbidity, the pathogenesis of morphea is poorly studied.
71 hogenesis of eosinophilic fasciitis (EF) and morphea is poorly understood.
72 e incidence rate of localized scleroderma or morphea is reported at 27 new cases per million per year
73 ions affecting joint and bone with overlying morphea lesions using cross-sectional analysis of 1,058
74 need of upper gastrointestinal evaluation in morphea (localized scleroderma) patients.
75  single-cell transcriptomic profiles of SSc, morphea (localized scleroderma), and sclerotic GVHD (Scl
76 ts with linear scleroderma and in those with morphea, mean levels of IgM and IgG binding to rFbn-1 we
77 lassified, ranging from localized plaques of morphea of cosmetic importance only, to deep lesions of
78 ized scleroderma, which may take the form of morphea or linear scleroderma.
79 Sc skin biopsies, but was not found in lSSc, morphea, or healthy control biopsies.
80 K molecule upregulated in EF (P = .0007) and morphea (P = .0002).
81 rom 17 dSSc, seven limited SSc (lSSc), three morphea patients, and six healthy controls.
82 pansclerotic morphea and descriptors such as morphea profunda.
83 ollaboration with 14 patients with pediatric morphea (recruited from a referral center [Medical Colle
84 newly and already diagnosed cases of SSc and morphea respectively were taken up for the study.
85 tients of SSc; and 28, 25 and 20 patients of morphea respectively.
86 9 was present at increased concentrations in morphea serum (P < 0.0001), as were other T helper type
87                    We sought to characterize morphea serum cytokine imbalance and IFN-related gene ex
88 f autoantibodies with clinical indicators of morphea severity.
89                                       EF and morphea shared signatures of necroptosis; self-DNA recog
90  was also increased in inflammatory lesional morphea skin (fold change = 30.6, P = 0.006), and prelim
91                                   Unaffected morphea skin also differed from unaffected SSc skin beca
92         Specifically, expression profiles of morphea skin clustered with the SSc inflammatory subset
93 tional profiling of whole blood and lesional morphea skin, and used double-staining immunohistochemis
94             In this cross-sectional study of morphea subtype classification systems, the Padua criter
95  association of specific autoantibodies with morphea subtype or severity, but no large-scale studies
96         Patient demographic characteristics, morphea subtype, quality-of-life measures, disease activ
97          Numerous classification systems for morphea subtypes exist, but none have been systematicall
98 re was no difference in ANA prevalence among morphea subtypes.
99                   Among patients with linear morphea, the presence of autoantibodies was associated w
100 oderma skin from a patient with pansclerotic morphea to humanized mice engrafted with unmatched allog
101                                 We found the morphea transcriptome is dominated by IFN-gamma-mediated
102 ne survey items were evaluated by experts in morphea using a Likert scale (score range, 0-10, with 0
103 ce of ANAs, AHAs, ssDNA abs in patients with morphea vs matched controls and association of the prese
104 f ANAs, AHAs, and ssDNA abs in patients with morphea was 34%, 12%, and 8%, respectively.
105 ear SSc, 14 with linear morphea, and 17 with morphea) were examined in the largest cohort of such pat
106 of limited clinical utility except in linear morphea, where their presence, although infrequent, is a
107          Consecutive pediatric patients with morphea who were available for data collection at baseli

 
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