ライフサイエンスコーパス: Graves

1 Graves disease (GD) is a common autoimmune thyroid disor

2 Graves disease (GD) is an autoimmune condition caused by

3 Graves disease can involve the thyroid exclusively or it

4 Graves disease is an autoimmune disorder that affects th

5 Graves disease is directly caused by thyroid-stimulating

6 Graves disease is the most common cause of hyperthyroidi

7 Graves disease is the most common cause of persistent hy

8 Graves disease, a common organ-specific autoimmune disea

9 Graves ophthalmopathy (GO) is an autoimmune disease that

10 Graves orbitopathy, also known as thyroid eye disease or

11 Graves' disease (GD) and Hashimoto's thyroiditis (HT) ar

12 Graves' disease (GD) is a common autoimmune disease (AID

13 Graves' disease (GD) is a common thyroid disease, and Gr

14 Graves' disease (GD) is an autoimmune disease that prima

15 Graves' disease (GD) is an autoimmune process involving

16 Graves' disease (GD) is an autoimmune thyroid disease de

17 Graves' disease (GD) is an autoimmune thyroid disorder t

18 Graves' disease (GD) is associated with T cell infiltrat

19 Graves' disease (GD), an autoimmune process involving th

20 Graves' disease is an autoimmune disorder that causes hy

21 Graves' disease is routinely treated with antithyroid dr

22 Graves' disease is the leading cause of hyperthyroidism

23 Graves' Disease results from the production of autoantib

24 Graves' disease results from thyroid-stimulating Abs (TS

25 Graves' disease, which is autoimmune in nature, is the u

26 Graves' hyperthyroidism is caused by autoantibodies to t

27 Graves' hyperthyroidism, a common autoimmune disease cau

28 Graves' ophthalmopathy (GO) affects 50% to 60% of patien

29 Graves' orbitopathy (GO) is an autoimmune inflammatory d

30 100% of TSHR autoantibody activity in all 18 Graves' sera studied.

31 ssues (thyroiditis, n = 3; psoriasis, n = 2; Graves disease, n 1; membranous glomerulonephritis, n =

32 (in total 42 agranulocytosis cases and 1,208 Graves' disease controls), using direct human leukocyte

33 A total of 32 Graves patients and 37 eyelids underwent lower eyelid re

34 eactivity in sera from 45 Hashimoto's and 47 Graves' disease patients.

35 ]), rheumatoid arthritis (1.52 [1.45-1.59]), Graves' disease (1.36 [1.30-1.43]), and systemic lupus e

36 d retinal blood flow in patients with active Graves' orbitopathy (GO).

37 at least 1 member who had both SLE and AITD (Graves' disease or Hashimoto thyroiditis).

38 The autoimmune thyroid diseases (AITD), Graves' disease and chronic lymphocytic thyroiditis (CLT

39 Although Graves hyperthyroidism is relatively common, no causal t

40 ested repatriation under the Native American Graves Protection and Repatriation Act (NAGPRA).

41 disease (OR = 1.53; 95% CI, 1.12-2.10), and Graves' disease (OR = 1.33; 95% CI, 1.03-1.72) and negat

42 , Sjogren's syndrome (2.09 [1.84-2.37]), and Graves' disease (2.07 [1.92-2.22]); pernicious anaemia (

43 Hashimoto's thyroiditis 13.3 [11.8-14.9] and Graves' disease 6.7 [5.1-8.5]), and multiple sclerosis h

44 schizophrenia risk (rheumatoid arthritis and Graves' disease), and DICER1 is pivotal in miRNA process

45 diseases, including rheumatoid arthritis and Graves' disease.

46 tes (T2D), coronary artery disease (CAD) and Graves' disease.

47 loci for schizophrenia, type 1 diabetes, and Graves' disease.

48 une disease, autoimmune thyroid disease (and Graves' disease in particular) contributes disproportion

49 isease (GD) is a common thyroid disease, and Graves ophthalmopathy(GO) is the most common extra-thyro

50 e pathogenesis of Graves hyperthyroidism and Graves orbitopathy that offer several important tools in

51 tis are more common than hyperthyroidism and Graves' disease (strong evidence).

52 iated with both type 1 diabetes mellitus and Graves' disease.

53 abetes mellitus, Hashimoto's thyroiditis and Graves' disease, Sjogren's syndrome, dermatitis herpetif

54 sues involved in Hashimoto's thyroiditis and Graves' disease, we performed ex vivo analysis of lympho

55 ic lymphocytic (Hashimoto's) thyroiditis and Graves' disease.

56 Amiodarone-associated thyrotoxicosis and Graves' disease represented the main thyroid storm etiol

57 uding type 1 diabetes, rheumatoid arthritis, Graves disease, and systemic lupus erythematosus, are as

58 s mellitus, psoriasis, rheumatoid arthritis, Graves disease, Hashimoto thyroiditis, Crohn disease, ul

59 e 1 diabetes mellitus, rheumatoid arthritis, Graves' disease, Hashimoto thyroiditis, autoimmune thyro

60 tions causing endocrine dysfunctions such as Graves disease and hypo- and hyperthyroidism.

61 the common causes of thyrotoxicosis, such as Graves' disease and functioning nodular goiters, there a

62 hat manifest during the acute phase, such as Graves' disease and systemic lupus erythematosus, are di

63 ically to treat autoimmune diseases, such as Graves' disease, may also diminish pathological inflamma

64 In autoimmune Graves' disease (GD), autoantibodies bind to the thyrotr

65 copresence would facilitate AF in autoimmune Graves' hyperthyroidism.

66 umber in cohorts of patients with autoimmune Graves' disease or hepatitis B infection, whereas G138G

67 Because Graves' hyperthyroidism is preferentially induced in BAL

68 ighted MR imaging in differentiation between Graves' disease and painless thyroiditis.

69 ificant difference in the ADC values between Graves' disease and painless thyroiditis (P=0.001).

70 New therapeutic modalities for both Graves' disease and the associated orbitopathy have hast

71 t were analyzed in thyroid lobes affected by Graves' disease (n = 6), thyroid lobes with healthy tiss

72 of hyperthyroidism, most commonly caused by Graves disease, and hypothyroidism, which in iodine suff

73 ld of autoimmune thyroiditis (represented by Graves' disease and Hashimoto's thyroiditis) since Janua

74 signalling of TSHR by autoantibodies causes Graves' disease (hyperthyroidism) and hypothyroidism, bo

75 immune response to the TSHR, thereby causing Graves disease in genetically susceptible individuals.

76 thogenic TSHR Abs as detected using clinical Graves' disease assays.

77 oimmune thyroid diseases (AITDs), comprising Graves disease (GD) and Hashimoto thyroiditis (HT), deve

78 ion has been found in the thyroid condition, Graves' disease, as well as in mothers of homosexual men

79 In 3 of the 14 regions, TCF7L2 (T2D), CTLA4 (Graves' disease) and CDKN2A-CDKN2B (T2D), much of the po

80 Ag-specific immunotherapies aimed at curing Graves' disease in humans.

81 ta, ankylosing spondylitis, dermatomyositis, Graves' disease, Hashimoto thyroiditis, insulin-dependen

82 ely 3% of women and 0.5% of men will develop Graves disease during their lifetime.

83 TSH receptor antibody-ELISA used to diagnose Graves disease ("third-generation assay") and also detec

84 e thyroid gland can be used to differentiate Graves' disease from painless thyroiditis in patients wi

85 sed as a threshold value for differentiating Graves' disease from painless thyroiditis, the best resu

86 tibody generation in the autoimmune disorder Graves disease (GD).

87 f Trp(620) with another autoimmune disorder, Graves' disease, in 1,734 case and control subjects (P =

88 s of risk of the common autoimmune disorders Graves' disease, autoimmune hypothyroidism and type 1 di

89 eases (AITDs) include two related disorders, Graves disease (GD) and Hashimoto thyroiditis, in which

90 his gene with type 1 diabetes mellitus (DM), Graves' disease, rheumatoid arthritis (RA), and multiple

91 h RAIU with scintigraphically diffuse (i.e., Graves disease and diffuse thyroid autonomy) or focal (i

92 revious thyroid disease, particularly either Graves' disease or Hashimoto thyroiditis, suggesting the

93 ance pathogenic Ab production and exacerbate Graves' disease in humans.

94 exon 33 SNP, giving an odds ratio of 6.1 for Graves' disease.

95 os ranging from 1.43 (95% CI=1.30, 1.57) for Graves' disease to 3.48 (95% CI=3.25, 3.72) for type 2 d

96 therefore providing the molecular basis for Graves' disease.

97 excision (n = 6), orbital decompression for Graves ophthalmopathy (n = 3), dacryocystorhinostomy (n

98 Treatment options for Graves' disease include antithyroid drugs, radioactive i

99 n 85 years, the efficacy of radiotherapy for Graves' ophthalmopathy (GO) has not been established con

100 ulation iodine intake do not affect risk for Graves' disease or thyroid cancer, but correction of iod

101 ence of hypoparathyroidism after surgery for Graves disease (GD) is lower after subtotal thyroidectom

102 lly available immunomodulatory therapies for Graves eye disease.

103 d remains a safe and effective treatment for Graves disease after more than 80 y of global clinical u

104 synthesis and secretion, most commonly from Graves' disease or toxic nodular goitre, whereas thyroid

105 pregnancy and should be differentiated from Graves disease.

106 First, that activated T lymphocytes from Graves' patients drive the differentiation of PPAR-gamma

107 D2 mRNA was especially high in thyroids from Graves' patients and in follicular adenomas.

108 rders involving a hyperactive thyroid gland (Graves disease, toxic multinodular goiter, toxic adenoma

109 otoxicosis Therapy Follow-up Study; 91 % had Graves disease, 79% were female, and 65% were treated wi

110 lating variety are the cause of hyperthyroid Graves disease.

111 uptake of RAI in patients with hyperthyroid Graves' disease and thyroid cancer.

112 erthyroidism are autoimmune hyperthyroidism (Graves disease, GD), toxic multinodular goiter (TMNG), a

113 imary antigen in autoimmune hyperthyroidism (Graves' disease) caused by stimulating TSHR antibodies.

114 type 1 diabetes, autoimmune hypothyroidism, Graves disease, psoriatic arthritis, rheumatoid arthriti

115 immune disorders (autoimmune hypothyroidism, Graves' disease, and type 1 diabetes) and non-autoimmune

116 In Graves disease, selenium supplementation might lead to f

117 In Graves' disease a specific combination of polymorphisms

118 In Graves' disease, first-line treatment is a 12-18-month c

119 In Graves' disease, the orbit of the eye can become severel

120 n the genesis of atrial fibrillation (AF) in Graves' hyperthyroidism.

121 ess is important in iodide deficiency and in Graves disease.

122 fficiently and neutralized autoantibodies in Graves' patients' sera.

123 bohydrate that neutralizes autoantibodies in Graves' patients' sera.

124 man tropomodulin and a 64-kDa autoantigen in Graves disease (1D) are related: tropomodulin has 42 and

125 in receptor (TSHR), the major autoantigen in Graves' disease, is posttranslationally modified by intr

126 rst identified as a potential autoantigen in Graves' disease, is similar to the tropomodulin (Tmod) f

127 n's disease, and thyroid follicular cells in Graves' disease (GD).

128 ment of dysthyroid optic neuropathy (DON) in Graves' orbitopathy (GO).

129 The mean ADC value of the thyroid gland in Graves' disease was 2.03+/-0.28x10(-3) mm(2)/sec, and in

130 to localized overproduction of hyaluronan in Graves disease.

131 les are more distal than those identified in Graves' disease and are in LD with Graves' disease prote

132 thyroid function and is targeted by IgGs in Graves' disease (GD-IgG).

133 genes is homologous to a gene implicated in Graves' disease and it, ANT2 and two others are confirme

134 Appearances of and increases in Graves' ophthalmopathy (GO) have been reported after tre

135 DON) is a serious threatening vision loss in Graves' ophthalmopathy (GO).

136 chanistic framework for molecular mimicry in Graves' disease, where early precursor B cells are expan

137 ve involvement of the extraocular muscles in Graves' ophthalmopathy, the absence of N-CAM expression

138 lasts or fat accumulation, such as occurs in Graves' ophthalmopathy, tissue fibrosis, abnormal wound

139 r immune responses localized to the orbit in Graves' disease.

140 Because of the low remission rate in Graves' disease and the inability to cure toxic nodular

141 fibroblasts orchestrate tissue remodeling in Graves disease, at least in part, because they exhibit e

142 Results: In Graves' disease, significantly higher deoxygenated hemog

143 imulating TSHR autoantibodies (TSHR-Ab's) in Graves disease patients may provide a functional explana

144 the basis for the immunologic attack seen in Graves ophthalmopathy.

145 d autoantigens after radio-iodine therapy in Graves patients.

146 thod and effectiveness of primary therapy in Graves' disease.

147 e TSHR on the functional response to TSAb in Graves' patients' sera.

148 angiography (OCTA) in patients with inactive Graves' ophthalmopathy (GO) compared with healthy contro

149 The major AITDs include Graves disease (GD) and Hashimoto's thyroiditis (HT); al

150 Autoimmune thyroid disease (AITD), including Graves' disease (GD) and Hashimoto's thyroiditis (HT), i

151 for imaging of thyroid disorders, including Graves' disease and thyroid nodules.

152 s associated with multiple factors including Graves disease [odds ratio (OR) = 2.06], lateral neck di

153 The most frequent cause is Graves' disease (autoimmune hyperthyroidism).

154 The most common cause of hyperthyroidism is Graves disease, with a global prevalence of 2% in women

155 The most common cause of hyperthyroidism is Graves' disease, followed by toxic nodular goitre.

156 The most common cause of this syndrome is Graves' disease, followed by toxic multinodular goitre,

157 ype 1 diabetes, rheumatoid arthritis, lupus, Graves thyroiditis, Addison disease and other autoimmune

158 This single autoantigenic target makes Graves' disease a prime candidate for Ag-specific immuno

159 ode a protein with homology to the mammalian Graves' disease carrier proteins.

160 overed, paired and differentiated meteorites Graves Nunatak (GRA) 06128 and GRA 06129.

161 Microsomes from normal, Graves', and TSH-stimulated thyroids contained low Km D2

162 cosis (OR = 0.76, p = 1.5 x 10(-3)), but not Graves disease (OR = 1.03, p = 0.82).

163 unction (10 cases of hypothyroidism and 1 of Graves disease) developed in 11 of 19 (57.9%) of the DS

164 e receptor (TSHR), is the primary antigen of Graves disease.

165 mulating autoantibodies (TSAb), the cause of Graves' disease, interact with this region of the TSHR i

166 he thyrotropin receptor (TSHR), the cause of Graves' hyperthyroidism, only develop in humans.

167 for those undergoing the orbital changes of Graves' ophthalmopathy is often challenging, even as our

168 halmopathy (TAO), an autoimmune component of Graves disease.

169 halmopathy (TAO), an autoimmune component of Graves' disease, is associated with profound connective

170 potentially blinding autoimmune component of Graves' disease.

171 8 orbits) with exophthalmos in the course of Graves' orbitopathy were enrolled in the study.

172 one was lost to follow-up, one developed of Graves disease, and one died of sepsis).

173 ons for disease pathogenesis: development of Graves TSHR Abs is limited by the availability of A-subu

174 The etiology of Graves disease is multifactorial, with nongenetic factor

175 and provide new insight into the etiology of Graves disease.

176 iagnosis, pathogenesis, and immunotherapy of Graves' disease.

177 The incidence of Graves disease (GD) is rising in children, and adequate

178 Similarly, the majority of Graves' disease patients develop improved function over

179 Management of Graves disease includes treatment with antithyroid drugs

180 The surgical management of Graves ophthalmopathy includes treatment of globe malpos

181 the field, outline the optimal management of Graves orbitopathy and summarize the research developmen

182 m should be prioritised in the management of Graves' disease and early definitive treatment with radi

183 s a common and debilitating manifestation of Graves disease (GD).

184 athy are connective tissue manifestations of Graves' disease (GD).

185 e link between the orbital manifestations of Graves' disease and those in the pretibial skin, localiz

186 se a new adenovirus-mediated animal model of Graves disease to show that goiter and hyperthyroidism o

187 ween induced and spontaneous mouse models of Graves' disease with implications for potential immunoth

188 secretion) of human TFCOs toward a panel of Graves' disease patient sera, demonstrating that organoi

189 y a role in the etiology and pathobiology of Graves' ophthalmopathy and/or other ocular myopathies.

190 s the new discoveries in the pathogenesis of Graves hyperthyroidism and Graves orbitopathy that offer

191 dvances in understanding the pathogenesis of Graves orbitopathy have allowed the development of new t

192 tions for new studies on the pathogenesis of Graves' disease.

193 of molecular mimicry in the pathogenesis of Graves' disease.

194 understanding the molecular pathogenesis of Graves' disease.

195 The pathophysiology of Graves orbitopathy has also been revised with identifica

196 The presence of Graves orbitopathy can change the management of the dise

197 A prolonged course leads to remission of Graves' hyperthyroidism in about a third of cases.

198 exon 4 that putatively modulates the risk of Graves' disease in East Asian populations.

199 In an important study of Graves hyperthyroidism, treatment with radioactive iodin

200 contributing to the relative T3 toxicosis of Graves' disease.

201 patients who have a history of treatment of Graves disease, a subgroup that is not a target of scree

202 e the preferred therapy for the treatment of Graves' disease during pregnancy.

203 controlled teprotumumab Phase 3 Treatment of Graves' Orbitopathy (Thyroid Eye Disease) to Reduce Prop

204 The Treatment of Graves' Orbitopathy to Reduce Proptosis with Teprotumuma

205 ugs, of potential value for the treatment of Graves' orbitopathy.

206 The classic clinical triad of Graves' disease is hyperthyroidism, diffuse goiter, and

207 leading to the clinical findings typical of Graves ophthalmopathy.

208 Although the European Group on Graves' Ophthalmopathy (EUGOGO) recommend intravenous me

209 The presence of bifoveal fusion and/or Graves orbitopathy were risk factors for these adverse o

210 hyroidism from autonomous thyroid nodules or Graves disease include antithyroid drugs, radioactive io

211 ne thyroid disease (Hashimoto thyroiditis or Graves disease), juvenile RA, inflammatory bowel disease

212 an, hyaluronan, which accumulates in orbital Graves disease.

213 ave relevance to the pathogenesis of orbital Graves disease, an inflammatory autoimmune condition tha

214 py, and is the preferred choice for relapsed Graves' hyperthyroidism.

215 established treatment for moderate-to-severe Graves orbitopathy is intravenous glucocorticoids.

216 serve this association in the organ-specific Graves' disease or Addison's disease.

217 The patients had moderate, symptomatic Graves' ophthalmopathy (mean clinical activity score, 6.

218 fic situations, for example, Duane syndrome, Graves' ophthalmopathy, may be particularly problematic.

219 t from PGP, predictions of Gilbert syndrome, Graves' disease, non-Hodgkin lymphoma, and various blood

220 The Graves' Ophthalmopathy Quality of Life (GO-QOL) scale wa

221 ts for the differences in length between the Graves protein (572 residues) and tropomodulin (359 resi

222 ponder rate, and a larger improvement in the Graves' Ophthalmopathy Quality of Life overall score.

223 homologous repeats in the midsection of the Graves protein, together with the extension of a proline

224 is produces a novel truncated version of the Graves' disease carrier protein-like protein that lacks

225 pared between groups, the mean values of the Graves' patients differed from control at all angles (F

226 and the mean change in overall score on the Graves' ophthalmopathy-specific quality-of-life (GO-QOL)

227 Clinical Activity Score, and results on the Graves' ophthalmopathy-specific quality-of-life question

228 ropomodulin has 42 and 41% identity with the Graves protein in the N-terminal (69 residue) and C-term

229 an increased risk of autoimmune thyroiditis, Graves disease and goitre to low selenium status.

230 thyroiditis) and autoimmune thyrotoxicosis (Graves' disease).

231 pants were patients with exophthalmos due to Graves orbitopathy and other intraorbital conditions and

232 ion and the hyperthyroidism was secondary to Graves' disease.

233 with HLA-DR3 in conferring susceptibility to Graves' disease.

234 elopment of specific ligands useful to treat Graves disease and other dysfunctions of GPHRs.

235 Propylthiouracil (PTU), used to treat Graves' disease, occasionally induces a lupus-like syndr

236 Treating Graves disease with RAI and surgery result in gland dest

237 from a single experimental mouse undergoing Graves' disease, which shared the same H and L chain ger

238 TSHR autoantibodies also underlie Graves' orbitopathy (GO) and pretibial myxoedema.

239 ive iodine therapy in patients with unstable Graves' orbitopathy (GO) after subtotal thyroidectomy.

240 h extrathyroidal manifestations, among which Graves orbitopathy is the most common.

241 ither of the 2 SNPs recently associated with Graves' disease showed evidence for association in the u

242 opathy, a condition commonly associated with Graves' disease, remains inadequately treated.

243 manifestation most commonly associated with Graves' disease.

244 to the intense inflammation associated with Graves' ophthalmopathy.

245 II-encoded HLA-DRB1-DQA1-DQB1 haplotype with Graves' disease (GD) has been known for several years.

246 tified in Graves' disease and are in LD with Graves' disease protective alleles identified in both of

247 [81.5%] females and 775 [18.5%] males) with Graves' disease and 16 756 controls (13 656 [81.5%] fema

248 activating autoantibody from a patient with Graves' disease selects a similar upright orientation of

249 roduced from lymphocytes from a patient with Graves' disease.

250 Patients with Graves disease may be treated with antithyroid drugs, ra

251 Patients with Graves disease may have a diffusely enlarged thyroid gla

252 ue in both normal patients and patients with Graves disease), together with the humoral factors prese

253 actors present in the serum of patients with Graves disease, forms the basis for the immunologic atta

254 antibodies resembling those in patients with Graves disease.

255 was a retrospective review of patients with Graves ophthalmopathy undergoing lower eyelid retraction

256 ommendations only extending to patients with Graves ophthalmopathy, selenium supplementation is widel

257 ent of lower lid retraction in patients with Graves ophthalmopathy.

258 eported recently that IgG from patients with Graves' disease (GD) can induce the expression of the CD

259 are the findings with those of patients with Graves' disease (GD) without orbitopathy (GO-) and healt

260 rbital fibroblasts (GOFB) from patients with Graves' disease (GD), as well as fibrocyte abundance, we

261 most prevalent in hyperthyroid patients with Graves' disease (GD); however, severe cases of orbitopat

262 thyroid drugs as an option for patients with Graves' disease and toxic nodular goitre.

263 ntrol of hyperthyroidism among patients with Graves' disease is associated with improved survival com

264 In patients with Graves' disease, autoantibodies that activate the TSHR p

265 cells to human serum from two patients with Graves' disease, but not control sera, led to secretion

266 Patients with Graves' disease, defined by positive TRAb tests, were se

267 in thyroidal T3 production in patients with Graves' disease, toxic adenomas, and, perhaps, iodine de

268 isease (TED) affects 25-50% of patients with Graves' Disease.

269 unoglobulin G purified from 38 patients with Graves' hyperthyroidism with AF (n=17) or sinus rhythm (

270 When present in patients with Graves' hyperthyroidism, AAbeta1AR and AAM2R facilitate

271 thy (GO) affects 50% to 60% of patients with Graves' hyperthyroidism, resulting in exophthalmos, peri

272 r orbital fat decompression in patients with Graves' ophthalmopathy (GO) by measuring their midpupil

273 ts disfiguring exophthalmos in patients with Graves' orbitopathy (GO).

274 s and choroidal vascularity in patients with Graves' orbitopathy (GO+), and to compare the findings w

275 In patients with Graves' upper eyelid retraction, the method demonstrated

276 of uptake within the thyroid in persons with Graves' disease and lateralized the remnant tissue in pe

277 other patients with thyroiditis and two with Graves' disease recognized only the whole 589-633 fragme

278 are the primary therapy, but some women with Graves disease opt to receive definitive therapy with RA

279 y included all adults (aged >=18 years) with Graves disease in the Intelligent Research in Sight (IRI