ライフサイエンスコーパス: giant cell arteritis

1 is accurate in the initial diagnosis of GCA giant cell arteritis .

2 atory vasculopathy affecting large arteries (giant cell arteritis).

3 T-cell activation and granuloma formation in giant cell arteritis.

4 tanding of the underlying pathomechanisms of giant cell arteritis.

5 -vessel involvement in elderly patients with giant cell arteritis.

6 an isolated condition or in association with giant cell arteritis.

7 ral artery biopsy confirmed the diagnosis of giant cell arteritis.

8 t clinical diagnosis or to detect coexistent giant cell arteritis.

9 asculitis mimicking polyarteritis nodosa and giant cell arteritis.

10 ith T cells and monocytes from patients with giant cell arteritis.

11 n the older individuals and in patients with giant cell arteritis.

12 unced in the age-related vasculitic syndrome giant cell arteritis.

13 ic infiltrates in patients with panarteritic giant cell arteritis.

14 rosis factor-alpha is present in arteries in giant cell arteritis.

15 ion of patients with large-vessel disease in giant cell arteritis.

16 Alzheimer's disease, multiple sclerosis and giant-cell arteritis.

17 ucocorticoid-free remission in patients with giant-cell arteritis.

18 ticoid tapering was studied in patients with giant-cell arteritis.

19 n show findings relevant to the diagnosis of giant-cell arteritis.

20 ant to the diagnosis of challenging cases of giant-cell arteritis.

21 ations concerning diagnosis and treatment of giant-cell arteritis.

22 rtitis (118 clinically isolated aortitis, 57 giant cells arteritis, 21 Takayasu arteritis, and 21 wit

23 Results: Ninety-five patients (giant cell arteritis, 52; Takayasu arteritis, 43) contri

24 Giant cell arteritis, a chronic autoimmune disease of th

25 vasculitides, such as Takayasu arteritis and giant cell arteritis, affect vital arteries and cause cl

26 istochemical and gene expression analyses of giant cell arteritis-affected temporal arteries revealed

27 se trials and other recent investigations of giant cell arteritis and idiopathic intracranial hyperte

28 continue to be the mainstay of treatment for giant cell arteritis and its complications.

29 ntreated, including blindness in the case of giant cell arteritis and large artery stenosis and aneur

30 lthough large vessel inflammatory disorders (giant cell arteritis and Takayasu arteritis) are the mos

31 LVV comprises two distinct conditions, giant cell arteritis and Takayasu arteritis, although th

32 ulated in inflamed arteries of patients with giant cell arteritis and Takayasu arteritis, and serum l

33 of large-vessel vasculitides, including both giant cell arteritis and Takayasu arteritis, and the aor

34 common causes of large-vessel vasculitis are giant cell arteritis and Takayasu arteritis, and those o

35 thic arthritis, adult-onset Still's disease, giant cell arteritis and Takayasu arteritis, as well as

36 These conditions include giant cell arteritis and Takayasu arteritis, with isolat

37 arget important mediators of disease in both giant cell arteritis and Takayasu arteritis.

38 e of LVV is often rheumatologic and includes giant cell arteritis and Takayasu arteritis.

39 tivity vasculitis, Wegener's granulomatosis, giant cell arteritis and Takayasu's arteritis in the US

40 n clinically available tests: pentraxin-3 in giant cell arteritis and Takayasu's arteritis; von Wille

41 An unusual case of giant cell arteritis and the most significant symptoms a

42 There were 87,794 patients with giant cell arteritis and/or polymyalgia rheumatica (n =

43 ymptoms and 2 of 203 (1.0%) for treatment of giant cell arteritis, and 1 of 193 (0.5%) for the pathop

44 al detachment, acute angle-closure glaucoma, giant cell arteritis, and central retinal artery occlusi

45 er virus (VZV) vasculopathy produces stroke, giant cell arteritis, and granulomatous aortitis, and it

46 g from the vasculitides (Takayasu arteritis, giant cell arteritis, and polyarteritis nodosa) to ather

47 s (RA), psoriasis, sarcoidosis, scleroderma, giant cell arteritis, and vasculitis.

48 egener granulomatosis, polyarteritis nodosa, giant-cell arteritis, and hypersensitivity vasculitis on

49 f 216 respondents (5.1%; 95% CI, 2.2%-8.0%), giant cell arteritis; and 10 of 218 respondents (4.6%; 9

50 tic arthritis, polymyalgia rheumatica (PMR), giant cell arteritis, ankylosing spondylitis, and Sjogre

51 ostic clues in helping make the diagnosis of giant cell arteritis are discussed.

52 dia and intima where pathological changes in giant cell arteritis are most pronounced.

53 Subsets of giant cell arteritis are probably caused by variations i

54 Because intracerebral VZV vasculopathy and giant cell arteritis are strongly associated with produc

55 cans of 20 patients with A-AION secondary to giant cell arteritis (biopsy-proven), 20 patients with N

56 enting to a metropolitan hospital and having giant cell arteritis, carotid artery disease, atrial fib

57 k factors for RAO in cardiac surgery include giant cell arteritis, carotid stenosis, stroke, hypercoa

58 Giant-cell arteritis commonly relapses when glucocortico

59 Giant cell arteritis continues to be a common cause of v

60 ological aortic involvement in patients with giant cell arteritis correlates with the significant det

61 In temporal arteries affected by giant cell arteritis, DCs are highly enriched and activa

62 disorder; multiple myeloma; acute leukemia; giant cell arteritis; dialysis; esophageal, stomach, pan

63 In giant cell arteritis, distinct clinical phenotypes with

64 sculitis, systemic granulomatous vasculitis, giant cell arteritis, diverse connective tissue disorder

65 a-producing T cells in vasculitic lesions of giant cell arteritis express several markers that identi

66 This issue provides a clinical overview of giant cell arteritis, focusing on diagnosis, treatment,

67 267 patients with polymyalgia rheumatica or giant cell arteritis found a GIAI prevalence of 1.9% aft

68 Giant-cell arteritis frequently poses diagnostic and the

69 Giant cell arteritis (GCA) and polymyalgia rheumatica (P

70 ) and medium-sized vessel vasculitis such as giant cell arteritis (GCA) and Takayasu arteritis (TAK).

71 Giant cell arteritis (GCA) and Takayasu's arteritis (TAK

72 ermine whether an association exists between giant cell arteritis (GCA) and the presence of varicella

73 Polymyalgia rheumatica (PMR) and giant cell arteritis (GCA) are related inflammatory diso

74 Giant cell arteritis (GCA) causes autoimmune inflammatio

75 Giant cell arteritis (GCA) causes severe inflammation of

76 This article aims to provide a review of giant cell arteritis (GCA) clinical features, differenti

77 Granuloma formation in giant cell arteritis (GCA) emphasizes the role of adapti

78 Giant cell arteritis (GCA) is a granulomatous and occlus

79 Giant cell arteritis (GCA) is a systemic vasculitis pref

80 Giant cell arteritis (GCA) is a vasculitic syndrome that

81 Giant cell arteritis (GCA) is a vasculitis of large and

82 Giant cell arteritis (GCA) is an immune-mediated disease

83 Giant cell arteritis (GCA) is an inflammatory vasculopat

84 Glucocorticoid (GC) therapy for giant cell arteritis (GCA) is effective but requires pro

85 Arterial wall damage in giant cell arteritis (GCA) is mediated by several differ

86 Giant cell arteritis (GCA) is the most common form of sy

87 Giant cell arteritis (GCA) is the most common form of va

88 Giant cell arteritis (GCA) is the most common systemic v

89 Giant cell arteritis (GCA) is the most common type of pr

90 Giant cell arteritis (GCA) is the most common type of pr

91 ies suggest that extracranial involvement of giant cell arteritis (GCA) may be more extensive than pr

92 conducted a large-scale genetic analysis on giant cell arteritis (GCA), a polygenic immune-mediated

93 In giant cell arteritis (GCA), inflammatory lesions typical

94 tion between rheumatology care and age, sex, giant cell arteritis (GCA), PMR relapses, corticosteroid

95 Giant cell arteritis (GCA), the most common form of syst

96 In giant cell arteritis (GCA), vasculitic damage of the aor

97 racteristic of polymyalgia rheumatica and/or giant cell arteritis (GCA).

98 artery biopsies taken from individuals with giant cell arteritis (GCA).

99 (ESR), and bilateral AION were suggestive of giant cell arteritis (GCA).

100 lasms, inflammation, pituitary apoplexy, and giant cell arteritis (GCA).

101 of adjunctive low-dose methotrexate (MTX) in giant cell arteritis (GCA).

102 d cerebrovascular accidents often complicate giant cell arteritis (GCA).

103 Giant cell arteritis (GCA, also called temporal arteriti

104 Giant-cell arteritis (GCA) is a large-vessel vasculitis

105 ment of large arteries is well-documented in giant-cell arteritis (GCA), but the risk for cardiovascu

106 n the subclavian or axillary vessels; aortic giant-cell arteritis; giant-cell arteritis presenting as

107 ous arteritis characterizes the pathology of giant cell arteritis, granulomatous aortitis, and intrac

108 Giant cell arteritis has supplanted temporal arteritis a

109 biopsy (TAB), performed for the diagnosis of giant cell arteritis, has a low reported rate of complic

110 Studies in giant cell arteritis have shown that differences in the

111 and herpesviruses in temporal arteries with giant cell arteritis have yielded contradictory results.

112 In patients with giant cell arteritis, imaging often spares the use of in

113 lege leads to autoimmune vasculitis, such as giant cell arteritis, in which CD8+ Treg cells fail to c

114 Inflammation of the arterial wall in giant cell arteritis induces a series of structural chan

115 Giant cell arteritis is a granulomatous vasculitis of th

116 Visual loss caused by giant cell arteritis is a medical emergency that require

117 Giant cell arteritis is a systemic condition with a stro

118 the vascular lesions support the model that giant cell arteritis is a T-cell-driven disease.

119 The immunopathogenesis of giant cell arteritis is an accumulative process in which

120 Giant cell arteritis is an autoimmune disease of medium

121 Giant cell arteritis is associated with a markedly incre

122 ortic aneurysm formation in association with giant cell arteritis is discussed, along with the implic

123 Although survival in giant cell arteritis is generally good, subsets of patie

124 The clinical presentation of giant cell arteritis is occasionally nonspecific; patien

125 rticoid-induced remission of newly diagnosed giant cell arteritis is of no benefit and may be harmful

126 Giant cell arteritis is the most common form of LVV affe

127 Giant-cell arteritis is an immune-mediated disease chara

128 Giant-cell arteritis is associated with increased risks

129 In general, the clinical outcome of giant-cell arteritis is excellent, and efforts must now

130 In other vascular territories, giant-cell arteritis is most commonly diagnosed by vascu

131 es are discussed here, and scalp necrosis in giant-cell arteritis is reviewed.

132 -positive results than in patients with GCA giant cell arteritis -negative results ( TAB temporal ar

133 Large-vessel involvement in giant cell arteritis occurs in over a quarter of patient

134 Giant cell arteritis occurs in those aged 50 years and o

135 Associated with increased RAO were giant cell arteritis (odds ratio [OR], 7.73; CI, 2.78-21

136 Methods: Patients with giant cell arteritis or Takayasu arteritis underwent ind

137 , Sweet's syndrome, polyarteritis nodosa, or giant-cell arteritis) or a hematologic condition (myelod

138 ring peripheral blood mononuclear cells from giant cell arteritis patients into immunodeficient NSG m

139 tokine transcription in temporal arteries of giant cell arteritis patients with and without up-regula

140 re significantly higher in patients with GCA giant cell arteritis -positive results than in patients

141 illary vessels; aortic giant-cell arteritis; giant-cell arteritis presenting as an intense systemic i

142 As in giant cell arteritis, recent evidence supports the role

143 tis, polyarteritis nodosa, Kawasaki disease, giant cell arteritis, Takayasu arteritis, and Behcet's d

144 by large vessel vasculitis (LVV), including giant cell arteritis, Takayasu's arteritis, immunoglobul

145 Most frequently encountered are giant cell arteritis (temporal arteritis) and vasculitis

146 o study the regulation of neoangiogenesis in giant cell arteritis, temporal arteries were examined fo

147 Although much less common than giant cell arteritis, the different forms of antineutrop

148 ive criteria for a positive biopsy result in giant cell arteritis, the imaging characteristics of pri

149 range 1.52 for polymyalgia rheumatica and/or giant cell arteritis to 2.82 for systemic lupus erythema

150 reports have highlighted etiologies such as giant cell arteritis, trauma, neuro-syphilis and demyeli

151 00 have polymyalgia rheumatica, 228,000 have giant cell arteritis, up to 3.0 million have had self-re

152 n temporal arteries (TAs) from patients with giant cell arteritis, varicella zoster virus (VZV) is se

153 In giant cell arteritis, vessel-wall infiltrating CD4 T cel

154 Giant cell arteritis was also identified in 5 patients.

155 GCA giant cell arteritis was diagnosed or excluded clinicall

156 bilateral amaurosis in whom the diagnosis of giant cell arteritis was suggested by perineural enhance

157 Giant cell arteritis was unlikely given the patient's la

158 Temporal artery specimens from patients with giant cell arteritis were analyzed bu two-color immunohi

159 onsent, 185 patients suspected of having GCA giant cell arteritis were included in a prospective thre

160 rely affect the temporal arteries, mimicking giant cell arteritis, while, to our knowledge, the assoc

161 patients with polymyalgia rheumatica and/or giant cell arteritis who were investigated a median (IQR

162 nical subtypes can be distinguished: cranial giant-cell arteritis with ischemic complications in the

163 and the central nervous system; large-vessel giant-cell arteritis with occlusions in the subclavian o

164 rease likelihood of stroke or visual loss in giant-cell arteritis without increasing bleeding complic