ライフサイエンスコーパス: ANCA-associated vasculitis

1 ctivation is involved in the pathogenesis of ANCA-associated vasculitis.

2 ipheral granulocytes of patients with active ANCA-associated vasculitis.

3 ents with biopsy-proven renal involvement of ANCA-associated vasculitis.

4 ibitor of metalloproteinase-1, and CXCL13 in ANCA-associated vasculitis.

5 n be detected in most European patients with ANCA-associated vasculitis.

6 a central pathogenic feature of proteinase 3 ANCA-associated vasculitis.

7 o cyclophosphamide for inducing remission in ANCA-associated vasculitis.

8 m the development of focal necrotizing GN in ANCA-associated vasculitis.

9 ith cyclophosphamide as induction therapy in ANCA-associated vasculitis.

10 idase (MPO) is a well defined autoantigen in ANCA-associated vasculitis.

11 dard intravenous cyclophosphamide for severe ANCA-associated vasculitis.

12 other autoimmune diseases, including classic ANCA-associated vasculitis.

13 ESR or ANCA levels to monitor patients with ANCA-associated vasculitis.

14 minocycline as agents capable of inducing an ANCA-associated vasculitis.

15 pondents for SLE, and 64% of respondents for ANCA-associated vasculitis.

16 gain access to PMN granule components during ANCA-associated vasculitis.

17 8(+) T cells mediate disease in experimental ANCA-associated vasculitis.

18 clinical antineutrophil cytoplasm antibody (ANCA) associated vasculitis.

19 E), and antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis.

20 In patients with severe ANCA-associated vasculitis, a single course of rituximab

21 ies for antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) are limited by partial

22 Antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) constitutes life-threa

23 Antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) is a common cause of r

24 seases, antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV), a chronic, severe dis

25 The differences between PR3-ANCA-associated vasculitis (AAV) and MPO-AAV described i

26 The two salient features of ANCA-associated vasculitis (AAV) are the restricted micr

27 ANCA-associated vasculitis (AAV) is a highly inflammator

28 in experimental murine myeloperoxidase (MPO)-ANCA-associated vasculitis (AAV) show mast cells degranu

29 rine (AZA) for remission-induction in severe ANCA-associated vasculitis (AAV), but renal outcomes are

30 ADAM17 in active proteinase-3 (PR3)-positive ANCA-associated vasculitis (AAV).

31 ral to disease pathogenesis in patients with ANCA-associated vasculitis (AAV).

32 severe antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis, ANCA positivity, and resist

33 discovery cohort of 1233 U.K. patients with ANCA-associated vasculitis and 5884 controls and was rep

34 -complex (MHC) and non-MHC associations with ANCA-associated vasculitis and also that granulomatosis

35 fibrosis, noncystic fibrosis bronchiectasis, ANCA-associated vasculitis and bronchiectasis.

36 eroxidase (MPO) underlies the development of ANCA-associated vasculitis and GN, but the mechanisms un

37 ht have therapeutic benefit in patients with ANCA-associated vasculitis and GN.

38 of 80 to 90% among patients with refractory ANCA-associated vasculitis and may be safer than cycloph

39 eatment for induction of remission in severe ANCA-associated vasculitis and may be superior in relaps

40 ry support for the concept that proteinase 3 ANCA-associated vasculitis and myeloperoxidase ANCA-asso

41 ivation of these cells by ANCA is central to ANCA-associated vasculitis and necrotizing crescentic gl

42 ffective and safe new treatment modality for ANCA-associated vasculitis and possibly other autoimmune

43 3:1 ratio, 44 patients with newly diagnosed ANCA-associated vasculitis and renal involvement to a st

44 immunodominant epitopes in the pathology of ANCA-associated vasculitis and suggest that autoantibody

45 free in antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis, and a pair of urinary prote

46 hat CD8(+) cells are a therapeutic target in ANCA-associated vasculitis, and suggest that a molecular

47 ens for antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis are effective in 70 to 90% o

48 CA-associated vasculitis and myeloperoxidase ANCA-associated vasculitis are distinct autoimmune syndr

49 ANCAs) may contribute to the pathogenesis of ANCA-associated vasculitis are not well understood.

50 patients receiving rituximab for refractory ANCA-associated vasculitis at 4 centers in the UK was us

51 350 patients who received a new diagnosis of ANCA-associated vasculitis between 1985 and 2003 and wer

52 cheme with which to categorize patients with ANCA-associated vasculitis, but adding the percentage of

53 ANCA-associated vasculitis can be induced in various for

54 elial growth factor, in patients with active ANCA-associated vasculitis compared with patients during

55 icroparticles in the plasma of children with ANCA-associated vasculitis compared with that in healthy

56 tudinal analysis revealed that patients with ANCA-associated vasculitis could be divided into two gro

57 Serum from patients with acute ANCA-associated vasculitis disrupted blood flow in the c

58 Antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis exhibits endothelial damage,

59 severe antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis for 40 years.

60 ctively, among three groups of patients with ANCA-associated vasculitis from Vienna, Austria (n=19);

61 This study confirms that the pathogenesis of ANCA-associated vasculitis has a genetic component, show

62 be controlled with immunosuppressive drugs, ANCA-associated vasculitis has become a chronic and rela

63 neutrophil cytoplasmic antibodies (ANCAs) in ANCA-associated vasculitis has been debated for some tim

64 peroxidase (MPO) ANCA and proteinase 3 (PR3) ANCA associated vasculitis have been developed, which ha

65 ractory antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis in small studies.

66 ine the efficacy and safety of rituximab for ANCA-associated vasculitis in a larger multicenter cohor

67 , microscopic polyangiitis, or renal-limited ANCA-associated vasculitis in complete remission after a

68 e remission induction therapy for refractory ANCA-associated vasculitis in this study.

69 Management of eye disease in ANCA-associated vasculitis includes local anti-inflammat

70 ltured neutrophils from patients with active ANCA-associated vasculitis, indicating that increased tr

71 Antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis is a severe condition encomp

72 -2) in anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis is controversial because of

73 Anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis is the most common cause of

74 tening) antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis is unknown.

75 ANCA-associated vasculitis is an autoimmune condition ch

76 ANCA-associated vasculitis is the most frequent cause of

77 -MPO antibodies, increase sFlt1 during acute ANCA-associated vasculitis, leading to an antiangiogenic

78 r necrosis and crescent formation in a renal ANCA-associated vasculitis model.

79 ase 3 (PRTN3) in leukocytes of patients with ANCA-associated vasculitis observed longitudinally (n=82

80 hundred sixty-six consecutive patients with ANCA-associated vasculitis, positive for either proteina

81 rophil microparticles in the pathogenesis of ANCA-associated vasculitis, potentially providing a targ

82 Participants in the Rituximab in ANCA-Associated Vasculitis (RAVE) trial were excluded fr

83 is of patients enrolled in the Rituximab for ANCA-Associated Vasculitis (RAVE) Trial who had renal in

84 copic polyangiitis, and 5 with renal-limited ANCA-associated vasculitis) received azathioprine (58 pa

85 Observations in patients with ANCA-associated vasculitis suggest that CD8(+) T cells p

86 V: 163 subjects enrolled in the Rituximab in ANCA-Associated Vasculitis trial were screened for the p

87 rial of Rituximab versus Cyclophosphamide in ANCA-Associated Vasculitis trial.

88 histopathological classification system for ANCA-associated vasculitis was recently published, but w

89 The benefit of infliximab (a mAb to TNF) in ANCA-associated vasculitis was recently reported in a pr

90 ntigen gene expression and disease status in ANCA-associated vasculitis, we measured gene-specific DN