ライフサイエンスコーパス: arteritis

1 e in the initial diagnosis of GCA giant cell arteritis .

2 lopathy affecting large arteries (giant cell arteritis).

3 attractive for arterial lesions of Takayasu arteritis.

4 nd lumen pathologies resulting from Takayasu arteritis.

5 revascularization in patients with Takayasu arteritis.

6 es of its main branches, indicating Takayasu arteritis.

7 red the gold standard in imaging of Takayasu arteritis.

8 s disease and the first GWAS of equine viral arteritis.

9 cute inflammatory illness marked by coronary arteritis.

10 tion, a response resembling clinical intimal arteritis.

11 tes in patients with panarteritic giant cell arteritis.

12 ic cells (DC) in the development of coronary arteritis.

13 and regulate the patterning of the emerging arteritis.

14 ells are required for LCCWE-induced coronary arteritis.

15 s in the pathological mechanisms of coronary arteritis.

16 ings relevant to the diagnosis of giant-cell arteritis.

17 diagnosis of challenging cases of giant-cell arteritis.

18 erning diagnosis and treatment of giant-cell arteritis.

19 dulating inflammation in atherosclerosis and arteritis.

20 r-alpha is present in arteries in giant cell arteritis.

21 ents with large-vessel disease in giant cell arteritis.

22 lesion described as endotheliitis or intimal arteritis.

23 nd devised a genetic risk score for Takayasu arteritis.

24 ar signaling in this mouse model of coronary arteritis.

25 chymal invasion and abscesses, and meningeal arteritis.

26 vation and granuloma formation in giant cell arteritis.

27 rom latent infection or induction of chronic arteritis.

28 the underlying pathomechanisms of giant cell arteritis.

29 s disease, multiple sclerosis and giant-cell arteritis.

30 , is the cause of gamma HV68-induced elastic arteritis.

31 during follow-up, with 1 caused by temporal arteritis.

32 olvement in elderly patients with giant cell arteritis.

33 re also diagnosed with giant cell (temporal) arteritis.

34 weanling mice exhibited milder large-vessel arteritis.

35 biopsy confirmed the diagnosis of giant cell arteritis.

36 idenced a worldwide distribution of Takayasu arteritis.

37 se in both giant cell arteritis and Takayasu arteritis.

38 condition or in association with giant cell arteritis.

39 d-free remission in patients with giant-cell arteritis.

40 ring was studied in patients with giant-cell arteritis.

41 and monocytes from patients with giant cell arteritis.

42 imicking polyarteritis nodosa and giant cell arteritis.

43 ils and monocytes that precipitates coronary arteritis.

44 individuals and in patients with giant cell arteritis.

45 A agonists may provide effective therapy for arteritis.

46 e age-related vasculitic syndrome giant cell arteritis.

47 s and tocilizumab) in patients with Takayasu arteritis.

48 omes are affected by the severity of intimal arteritis.

49 ains important in the management of Takayasu arteritis.

50 proach, prognosis, and treatment of brucella arteritis.

51 roles for monocytes and B cells in Takayasu arteritis.

52 ary embolism, transitory ischemic attacks to arteritis.

53 rimary sclerosing cholangitis and Takayasu's arteritis(3-6)-we identify that the causal gene, ETS2, i

54 cs and outcomes of 49 patients with Takayasu arteritis (80% female; median age, 42 years [20-55 years

55 Giant cell arteritis, a chronic autoimmune disease of the aorta and

56 s, such as Takayasu arteritis and giant cell arteritis, affect vital arteries and cause clinical comp

57 l and gene expression analyses of giant cell arteritis-affected temporal arteries revealed abundant e

58 me of whose phenotypes included large-vessel arteritis and cranial neuropathy.

59 equired for IL-1beta maturation) in coronary arteritis and evaluated the efficacy of IL-1 receptor an

60 r levels of chimerism, moderate CR including arteritis and fibrosis in the Peyer's patches and mesent

61 Large vessel vasculitides, such as Takayasu arteritis and giant cell arteritis, affect vital arterie

62 ecrotizing vasculitis, including necrotizing arteritis and hemorrhagic pulmonary capillaritis.

63 nd other recent investigations of giant cell arteritis and idiopathic intracranial hypertension is cl

64 A small number of patients with Takayasu arteritis and IgG4-related aortitis have also been succe

65 be the mainstay of treatment for giant cell arteritis and its complications.

66 ecessary to regulate MCMV-associated elastic arteritis and latency in vivo and reactivation of a herp

67 a systemic lymphoplasmacytic and histiocytic arteritis and periarteritis in guinea pigs more than 2 m

68 enetic basis and pathophysiology of Takayasu arteritis and provides clues for potential new therapeut

69 fection, limiting chronic diseases including arteritis and pulmonary fibrosis.

70 ge vessel inflammatory disorders (giant cell arteritis and Takayasu arteritis) are the most common fo

71 nflamed arteries of patients with giant cell arteritis and Takayasu arteritis, and serum levels of th

72 ssel vasculitides, including both giant cell arteritis and Takayasu arteritis, and the aortitis of Co

73 tis, adult-onset Still's disease, giant cell arteritis and Takayasu arteritis, as well as other condi

74 tant mediators of disease in both giant cell arteritis and Takayasu arteritis.

75 ulitis, Wegener's granulomatosis, giant cell arteritis and Takayasu's arteritis in the US amounted to

76 y available tests: pentraxin-3 in giant cell arteritis and Takayasu's arteritis; von Willebrand facto

77 ce are protected from LCCWE-induced coronary arteritis and that this protection is mediated through t

78 An unusual case of giant cell arteritis and the most significant symptoms and diagnost

79 cessful monitoring of patients with Takayasu arteritis and to plan possible interventional treatment.

80 There were 87,794 patients with giant cell arteritis and/or polymyalgia rheumatica (n = 25,581), in

81 countered are giant cell arteritis (temporal arteritis) and vasculitis secondary to infections.

82 2 of 203 (1.0%) for treatment of giant cell arteritis, and 1 of 193 (0.5%) for the pathophysiologic

83 It correlated with tubulitis, arteritis, and antibody markers within concurrent histol

84 nt, acute angle-closure glaucoma, giant cell arteritis, and central retinal artery occlusion.

85 inophilic bronchiolitis, NCGN, capillaritis, arteritis, and granulomatosis.

86 ZV) vasculopathy produces stroke, giant cell arteritis, and granulomatous aortitis, and it develops a

87 ulomatosis, polyarteritis nodosa, giant-cell arteritis, and hypersensitivity vasculitis on the basis

88 teritis, in 1 of 1 cases of nongranulomatous arteritis, and in 5 of 18 control aortas (28%) obtained

89 is, the nongranulomatous variant of temporal arteritis, and Kawasaki's disease.

90 vasculitides (Takayasu arteritis, giant cell arteritis, and polyarteritis nodosa) to atherosclerosis,

91 ients with giant cell arteritis and Takayasu arteritis, and serum levels of this cytokine mirror dise

92 uding both giant cell arteritis and Takayasu arteritis, and the aortitis of Cogan syndrome and relaps

93 riasis, sarcoidosis, scleroderma, giant cell arteritis, and vasculitis.

94 ndents (5.1%; 95% CI, 2.2%-8.0%), giant cell arteritis; and 10 of 218 respondents (4.6%; 95% CI, 1.8%

95 is, polymyalgia rheumatica (PMR), giant cell arteritis, ankylosing spondylitis, and Sjogren's syndrom

96 in helping make the diagnosis of giant cell arteritis are discussed.

97 ima where pathological changes in giant cell arteritis are most pronounced.

98 Subsets of giant cell arteritis are probably caused by variations in the patho

99 ntracerebral VZV vasculopathy and giant cell arteritis are strongly associated with productive VZV in

100 The long-term effects of the acute coronary arteritis are unknown.

101 disorders (giant cell arteritis and Takayasu arteritis) are the most common form of systemic vasculit

102 the category of acute rejection with intimal arteritis (ARV) is relevant to short- and long-term clin

103 Giant cell arteritis has supplanted temporal arteritis as the preferred term for chronic granulomatou

104 s disease, giant cell arteritis and Takayasu arteritis, as well as other conditions such as Castleman

105 e, our data demonstrate that in the coronary arteritis associated with KD, TGF-beta suppresses elasti

106 Intimal arteritis (Banff v-lesion) was an independent histologic

107 patients with A-AION secondary to giant cell arteritis (biopsy-proven), 20 patients with NA-AION, and

108 dy-mediated rejection ("mixed") activity and arteritis but little hyalinosis, whereas TCMR2 had less

109 be effective for the treatment of Takayasu's arteritis, but their role in the treatment of other form

110 metropolitan hospital and having giant cell arteritis, carotid artery disease, atrial fibrillation,

111 or RAO in cardiac surgery include giant cell arteritis, carotid stenosis, stroke, hypercoagulable sta

112 Granulomatous arteritis characterizes the pathology of giant cell arte

113 lammatory vascular disease, such as Takayasu arteritis, chemotherapy- or radiation-induced vascular i

114 c rejection grade, endotheliitis, transplant arteritis, coagulation necrosis, acute pancreatitis, pre

115 Giant-cell arteritis commonly relapses when glucocorticoids are tap

116 We performed a genetic study in Takayasu arteritis comprising 6,670 individuals (1,226 affected i

117 Giant cell arteritis continues to be a common cause of visual loss.

118 rtic involvement in patients with giant cell arteritis correlates with the significant detection of V

119 In temporal arteries affected by giant cell arteritis, DCs are highly enriched and activated and hav

120 multiple myeloma; acute leukemia; giant cell arteritis; dialysis; esophageal, stomach, pancreas, lung

121 ystemic granulomatous vasculitis, giant cell arteritis, diverse connective tissue disorders; viral, s

122 (EAV) is the causative agent of equine viral arteritis (EVA), a reproductive and respiratory disease

123 ustry as the causative agent of equine viral arteritis (EVA), a respiratory, systemic, and reproducti

124 T cells in vasculitic lesions of giant cell arteritis express several markers that identify them as

125 with such unusual manifestations of temporal arteritis facilitates early diagnosis and treatment, the

126 ontrol group, with significant reductions of arteritis, fibrosis, and cellular infiltration, includin

127 e provides a clinical overview of giant cell arteritis, focusing on diagnosis, treatment, and practic

128 thologic studies proposing an acute coronary arteritis followed by healing fail to account for the co

129 Giant-cell arteritis frequently poses diagnostic and therapeutic ch

130 Giant cell arteritis (GCA) and Takayasu's arteritis (TAK) are major

131 her an association exists between giant cell arteritis (GCA) and the presence of varicella-zoster vir

132 Polymyalgia rheumatica (PMR) and giant cell arteritis (GCA) are related inflammatory disorders occur

133 Giant cell arteritis (GCA) causes autoimmune inflammation of the ao

134 ticle aims to provide a review of giant cell arteritis (GCA) clinical features, differential diagnosi

135 Granuloma formation in giant cell arteritis (GCA) emphasizes the role of adaptive immunity

136 Giant cell arteritis (GCA) is a granulomatous and occlusive vasculi

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

138 Giant cell arteritis (GCA) is a systemic vasculitis preferentially

139 Giant cell arteritis (GCA) is a vasculitic syndrome that preferenti

140 Giant cell arteritis (GCA) is an immune-mediated disease of unknown

141 Giant cell arteritis (GCA) is an inflammatory vasculopathy in which

142 Glucocorticoid (GC) therapy for giant cell arteritis (GCA) is effective but requires prolonged admi

143 Arterial wall damage in giant cell arteritis (GCA) is mediated by several different macroph

144 Giant cell arteritis (GCA) is the most common form of systemic vasc

145 Giant cell arteritis (GCA) is the most common form of vasculitis in

146 Giant cell arteritis (GCA) is the most common systemic vasculitis i

147 Giant cell arteritis (GCA) is the most common type of primary vascu

148 Giant cell arteritis (GCA) is the most common type of primary vascu

149 that extracranial involvement of giant cell arteritis (GCA) may be more extensive than previously ap

150 a large-scale genetic analysis on giant cell arteritis (GCA), a polygenic immune-mediated vasculitis.

151 ge arteries is well-documented in giant-cell arteritis (GCA), but the risk for cardiovascular events

152 In giant cell arteritis (GCA), inflammatory lesions typically produce

153 n rheumatology care and age, sex, giant cell arteritis (GCA), PMR relapses, corticosteroid complicati

154 Giant cell arteritis (GCA), the most common form of systemic vascul

155 In giant cell arteritis (GCA), vasculitic damage of the aorta and its

156 ammation, pituitary apoplexy, and giant cell arteritis (GCA).

157 ve low-dose methotrexate (MTX) in giant cell arteritis (GCA).

158 scular accidents often complicate giant cell arteritis (GCA).

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

160 psies taken from individuals with giant cell arteritis (GCA).

161 bilateral AION were suggestive of giant cell arteritis (GCA).

162 Giant cell arteritis (GCA, also called temporal arteritis) is a rar

163 ies, ranging from the vasculitides (Takayasu arteritis, giant cell arteritis, and polyarteritis nodos

164 avian or axillary vessels; aortic giant-cell arteritis; giant-cell arteritis presenting as an intense

165 is characterizes the pathology of giant cell arteritis, granulomatous aortitis, and intracerebral var

166 The outlook in Takayasu arteritis has improved over the last decade, reflecting

167 Giant cell arteritis has supplanted temporal arteritis as the prefe

168 ), performed for the diagnosis of giant cell arteritis, has a low reported rate of complications.

169 , and some patients with refractory Takayasu arteritis have responded to the immunomodulator leflunom

170 Studies in giant cell arteritis have shown that differences in the immunomodul

171 viruses in temporal arteries with giant cell arteritis have yielded contradictory results.

172 ted during the 1984 outbreak of equine viral arteritis in central Kentucky subsequently became long-t

173 the diagnostic procedure of choice to detect arteritis in cranial vessels.

174 We conclude that (i) the induction of arteritis in gammaHV68-infected IFN-gammaR-deficient mic

175 the preferred term for chronic granulomatous arteritis in older adults.

176 iption of a premortum diagnosis of pulmonary arteritis in PAN in which the patient had a response to

177 lmonary capillaritis and splenic necrotizing arteritis in some.

178 Mild arteritis in the 150 day allografts of both strain combi

179 matosis, giant cell arteritis and Takayasu's arteritis in the US amounted to $150 million per year.

180 tion of LCCWE produced severe focal coronary arteritis in TLR4(-/-) and C57BL/6 control mice but not

181 s with pathologically verified granulomatous arteritis, in 1 of 1 cases of nongranulomatous arteritis

182 to autoimmune vasculitis, such as giant cell arteritis, in which CD8+ Treg cells fail to contain CD4+

183 nd postoperative immunosuppression to render arteritis inactive.

184 f some of these conditions, such as Takayasu arteritis, includes a very long period of low level symp

185 urvival, parenchymal rejection, or occlusive arteritis, indicating that these processes are IFN-gamma

186 lammation of the arterial wall in giant cell arteritis induces a series of structural changes, includ

187 Giant cell arteritis is a granulomatous vasculitis of the aorta and

188 Visual loss caused by giant cell arteritis is a medical emergency that requires prompt re

189 Takayasu arteritis is a rare inflammatory disease of large arteri

190 Giant cell arteritis is a systemic condition with a strong predilec

191 ar lesions support the model that giant cell arteritis is a T-cell-driven disease.

192 Giant-cell arteritis is an immune-mediated disease characterized by

193 Takayasu arteritis is an inflammatory disease of large-diameter a

194 Giant cell arteritis is associated with a markedly increased risk o

195 Giant-cell arteritis is associated with increased risks for MI, CVA

196 We show here that LCCWE-induced coronary arteritis is dependent on intact TLR2 and MyD88 signalin

197 ysm formation in association with giant cell arteritis is discussed, along with the implications of r

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

199 Although survival in giant cell arteritis is generally good, subsets of patients with an

200 In other vascular territories, giant-cell arteritis is most commonly diagnosed by vascular imaging

201 The clinical presentation of giant cell arteritis is occasionally nonspecific; patients can have

202 uced remission of newly diagnosed giant cell arteritis is of no benefit and may be harmful.

203 ussed here, and scalp necrosis in giant-cell arteritis is reviewed.

204 nt cell arteritis (GCA, also called temporal arteritis) is a rare and Takayasu arteritis (TA) is an e

205 Arteritis may be found with acute TCMR, active antibody-

206 mes of 79 consecutive patients with Takayasu arteritis (median age, 39 years; interquartile range [IQ

207 ary arteries: acute self-limited necrotizing arteritis (NA), subacute/chronic (SA/C) vasculitis, and

208 results than in patients with GCA giant cell arteritis -negative results ( TAB temporal artery biopsy

209 Large-vessel involvement in giant cell arteritis occurs in over a quarter of patients with this

210 Takayasu arteritis occurs mainly in young women and, if left untr

211 ssociated with increased RAO were giant cell arteritis (odds ratio [OR], 7.73; CI, 2.78-21.52; P < 0.

212 were more likely to have had rejection with arteritis, odds ratio (OR): 4.83 (1.47-15.87), p = 0.009

213 -documented classic PAN was found to have an arteritis of medium-sized muscular pulmonary arteries.

214 ) Systemic vasculitis disorders (necrotizing arteritis of the polyarteritis type, hypersensitivity va

215 Fungal arteritis of the Y graft used to revascularize the whole

216 were associated with allograft loss, whereas arteritis (OR=0.5, 95% CI=0.2-1.2, P=0.11) and glomeruli

217 yndrome, polyarteritis nodosa, or giant-cell arteritis) or a hematologic condition (myelodysplastic s

218 eral blood mononuclear cells from giant cell arteritis patients into immunodeficient NSG mice engraft

219 scription in temporal arteries of giant cell arteritis patients with and without up-regulated neoangi

220 sfer experiments, CCR6(+) T cells produce an arteritis pattern with media-invasive T cells damaging v

221 aled discrete, superficial, white retinitis; arteritis; phlebitis; and retinal hemorrhages with or wi

222 (PET Imaging of Giant Cell and Takayasu Arteritis [PITA], NCT04071691; Residual Inflammation and

223 antly higher in patients with GCA giant cell arteritis -positive results than in patients with GCA gi

224 els; aortic giant-cell arteritis; giant-cell arteritis presenting as an intense systemic inflammatory

225 red for the cellular activation and coronary arteritis produced by LCCWE.

226 As in giant cell arteritis, recent evidence supports the role of aspirin

227 t virus replication is necessary for chronic arteritis, since antiviral therapy of mice with establis

228 and radiographic manifestations of Takayasu arteritis (TA) in a cohort from the US, evaluate the res

229 d temporal arteritis) is a rare and Takayasu arteritis (TA) is an even rarer autoimmune disease (AID)

230 nflammation is a typical feature of Takayasu arteritis (TA), and tumor necrosis factor (TNF) is impor

231 ng been the standard for diagnosing temporal arteritis (TA), but in practice this test is less than 1

232 the wide variation in the course of Takayasu arteritis (TA), predicting outcome is challenging.

233 ust be able to confidently diagnose temporal arteritis (TA), since failure to make a correct diagnosi

234 in the assessment of patients with Takayasu arteritis (TA).

235 roximately 50% of all patients with Takayasu arteritis (TA).

236 clinical and laboratory features of Takayasu arteritis (TAK) and explore the risk factors that associ

237 Giant cell arteritis (GCA) and Takayasu's arteritis (TAK) are major forms of large-vessel vasculit

238 Takayasu's arteritis (TAK) is a large-vessel vasculitis with a chro

239 elp accurately diagnose and monitor Takayasu arteritis (TAK).

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

241 regulation of neoangiogenesis in giant cell arteritis, temporal arteries were examined for the exten

242 ei (LCCWE) into mice causes a focal coronary arteritis that histopathologically mimics the coronary l

243 tract (LCCWE), mice develop a focal coronary arteritis that histopathologically resembles Kawasaki di

244 Giant cell vasculitis is an arteritis that predominantly affects medium- and large-s

245 Intimal arteritis (the presence of v-lesions) in kidney transpla

246 Although much less common than giant cell arteritis, the different forms of antineutrophil cytopla

247 a for a positive biopsy result in giant cell arteritis, the imaging characteristics of primary angiit

248 Temporal arteritis, the most common form of systemic vasculitis i

249 imilar to the lesions observed in Takayasu's arteritis, the nongranulomatous variant of temporal arte

250 for polymyalgia rheumatica and/or giant cell arteritis to 2.82 for systemic lupus erythematosus).

251 ve highlighted etiologies such as giant cell arteritis, trauma, neuro-syphilis and demyelination seco

252 ymyalgia rheumatica, 228,000 have giant cell arteritis, up to 3.0 million have had self-reported gout

253 AMR: T cell-mediated rejection with intimal arteritis (v) lesion (TCMRV; n = 78), total antibody-med

254 cording to the Banff classification, intimal arteritis (v-lesion) contributes to diagnosing T cell-me

255 The Banff scores of intimal arteritis (v1, v2 and v3) represented low, moderate, and

256 arteries (TAs) from patients with giant cell arteritis, varicella zoster virus (VZV) is seen in perin

257 In giant cell arteritis, vessel-wall infiltrating CD4 T cells and macr

258 Equine arteritis virus (EAV) and porcine reproductive and respi

259 ved in all known arteriviruses except equine arteritis virus (EAV) and wobbly possum disease virus (W

260 espiratory syndrome virus (PRRSV) and equine arteritis virus (EAV) are economically important veterin

261 apted virulent Bucyrus (VB) strain of equine arteritis virus (EAV) established persistent infection i

262 Equine arteritis virus (EAV) has a global impact on the equine

263 eptibility of CD3(+) T lymphocytes to equine arteritis virus (EAV) infection and establishment of per

264 Equine arteritis virus (EAV) is the causative agent of equine v

265 f the virulent Bucyrus (VB) strain of equine arteritis virus (EAV) to produce the modified live virus

266 is the critical natural reservoir of equine arteritis virus (EAV), as venereal infection of mares fr

267 jor envelope proteins (G(L) and M) of equine arteritis virus (EAV), both individually and in heterodi

268 nalysis of CD3+ T cells infected with equine arteritis virus (EAV).

269 and possible cell entry receptor for equine arteritis virus (EAV).

270 so bind to the LDV-C 3'(-)NCR RNA and equine arteritis virus 3'(-)NCR RNA.

271 e determined the crystal structure of equine arteritis virus PLP2 in complex with ubiquitin (1.45 A).

272 s for processing of glycoprotein 3 of equine arteritis virus.

273 xin-3 in giant cell arteritis and Takayasu's arteritis; von Willebrand factor antigen in childhood ce

274 Giant cell arteritis was also identified in 5 patients.

275 Arteritis was associated with inclusion bodies and MCMV

276 Arteritis was associated with subsequent antibody-mediat

277 Acute KD coronary arteritis was characterized by transmural infiltration o

278 Takayasu arteritis was compared to hundreds of other traits, reve

279 GCA giant cell arteritis was diagnosed or excluded clinically in all pa

280 An arteritis was identified in the lung, which was further

281 Arteritis was observed only in the medium to large size

282 licted the immunosuppressed patients whereas arteritis was restricted to the immunocompetent ones.

283 te necrosis was seen in 6 of 7 patients; and arteritis was seen in 3 of 7 patients.

284 , a significantly milder rejection with less arteritis was seen in the allografts of the recipient ma

285 maurosis in whom the diagnosis of giant cell arteritis was suggested by perineural enhancement on orb

286 s casei wall extract (LCWE) induces coronary arteritis, we show that LCWE increased TGF-beta signalin

287 ematosus (SLE), systemic sclerosis, Takayasu arteritis, Wegener granulomatosis, Behcet syndrome, and

288 tery specimens from patients with giant cell arteritis were analyzed bu two-color immunohistochemistr

289 ghty-eight percent of patients with Takayasu arteritis were inadequately controlled with or were into

290 patients suspected of having GCA giant cell arteritis were included in a prospective three-universit

291 ant role in the pathogenesis of equine viral arteritis when horses are infected with the virulent str

292 one of the RAG1(-/-) mice developed coronary arteritis, whereas 70% of WT and 100% of B cell(null) mi

293 the temporal arteries, mimicking giant cell arteritis, while, to our knowledge, the association betw

294 atments in refractory patients with Takayasu arteritis with an acceptable safety profile.

295 pes can be distinguished: cranial giant-cell arteritis with ischemic complications in the eye, the fa

296 An occlusive CD45+ arteritis with medial necrosis occurred with IL-10 defic

297 tral nervous system; large-vessel giant-cell arteritis with occlusions in the subclavian or axillary

298 t advances in medical management of Takayasu arteritis, with a special focus on the rationale and evi

299 Heterozygotes do not die from arteritis within a year of birth but do develop small le

300 ihood of stroke or visual loss in giant-cell arteritis without increasing bleeding complications.