ライフサイエンスコーパス: morphea

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 seen in 32 cases (68.1%) of SSc and none in morphea.

10 es (80.5%) of SSc and no such abnormality in morphea.

11 linear scleroderma (30%) and 6 patients with morphea (26%) had IgG autoantibodies to fibrillin 1 (rFb

12 was not associated with clinical measures of morphea activity.

13 PURPOSE OF REVIEW: Morphea, also known as localized scleroderma, is a disor

14 Morphea, also known as localized scleroderma, is charact

15 a case-control study of 87 participants with morphea and 26 healthy control subjects.

16 Cases of localized scleroderma (morphea and linear disease) were excluded.

17 e will provide better care for patients with morphea and understanding its pathophysiology will lay g

18 erma (27 with linear scleroderma and 23 with morphea) and 51 normal controls were tested for IgG and

19 is [SSc], 16 with linear SSc, 14 with linear morphea, and 17 with morphea) were examined in the large

20 FN-related pathways have not been studied in morphea, and biomarkers are needed.

21 lopments in the evaluation and management of morphea as well as its pathophysiology.

22 AHAs are more prevalent among patients with morphea but are of limited clinical utility except in li

23 ntibodies (ANAs) and other autoantibodies in morphea but found they are of limited significance.

24 hree (5.3%); while only four cases (7.1%) of morphea had esophageal symptoms all of which were mild i

25 n the past year, a revised classification of morphea has been presented.

26 The involvement of esophagus in morphea has been studied very scarcely.

27 cipants included individuals enrolled in the Morphea in Adults and Children (MAC) cohort and Sclerode

28 The promise of evidence-based treatments for morphea in the near future will provide better care for

29 ssociated with clinical indicators of severe morphea including functional limitation (ssDNA ab, P = .

30 In summary, inflammatory morphea is characterized by T helper type 1 cytokine imb

31 e incidence rate of localized scleroderma or morphea is reported at 27 new cases per million per year

32 need of upper gastrointestinal evaluation in morphea (localized scleroderma) patients.

33 ts with linear scleroderma and in those with morphea, mean levels of IgM and IgG binding to rFbn-1 we

34 lassified, ranging from localized plaques of morphea of cosmetic importance only, to deep lesions of

35 ized scleroderma, which may take the form of morphea or linear scleroderma.

36 Sc skin biopsies, but was not found in lSSc, morphea, or healthy control biopsies.

37 rom 17 dSSc, seven limited SSc (lSSc), three morphea patients, and six healthy controls.

38 newly and already diagnosed cases of SSc and morphea respectively were taken up for the study.

39 tients of SSc; and 28, 25 and 20 patients of morphea respectively.

40 9 was present at increased concentrations in morphea serum (P < 0.0001), as were other T helper type

41 We sought to characterize morphea serum cytokine imbalance and IFN-related gene ex

42 f autoantibodies with clinical indicators of morphea severity.

43 was also increased in inflammatory lesional morphea skin (fold change = 30.6, P = 0.006), and prelim

44 tional profiling of whole blood and lesional morphea skin, and used double-staining immunohistochemis

45 association of specific autoantibodies with morphea subtype or severity, but no large-scale studies

46 re was no difference in ANA prevalence among morphea subtypes.

47 Among patients with linear morphea, the presence of autoantibodies was associated w

48 ce of ANAs, AHAs, ssDNA abs in patients with morphea vs matched controls and association of the prese

49 f ANAs, AHAs, and ssDNA abs in patients with morphea was 34%, 12%, and 8%, respectively.

50 ear SSc, 14 with linear morphea, and 17 with morphea) were examined in the largest cohort of such pat

51 of limited clinical utility except in linear morphea, where their presence, although infrequent, is a