ライフサイエンスコーパス: Graves disease

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

2 lating variety are the cause of hyperthyroid Graves disease.

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

4 antibodies resembling those in patients with Graves disease.

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

6 pregnancy and should be differentiated from Graves disease.

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

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

9 to localized overproduction of hyaluronan in Graves disease.

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

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

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

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

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

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

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

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

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

19 understanding the molecular pathogenesis of Graves' disease.

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

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

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

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

24 therefore providing the molecular basis for Graves' disease.

25 potentially blinding autoimmune component of Graves' disease.

26 most common extra-thyroidal presentation of graves' disease.

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

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

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

30 manifestation most commonly associated with Graves' disease.

31 diseases, including rheumatoid arthritis and Graves' disease.

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

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

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

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

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

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

38 In Graves' disease a specific combination of polymorphisms

39 Graves disease, a common organ-specific autoimmune disea

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

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

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

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

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

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

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

47 [81.5%] females and 775 [18.5%] males) with Graves' disease and 16 756 controls (13 656 [81.5%] fema

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

77 Graves disease can involve the thyroid exclusively or it

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

134 Management of Graves disease includes treatment with antithyroid drugs

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

136 Graves disease is an autoimmune disorder that affects th

137 Graves disease is directly caused by thyroid-stimulating

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

139 Graves disease is the most common cause of hyperthyroidi

140 Graves disease is the most common cause of persistent hy

141 Graves' disease is an autoimmune disorder that causes hy

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

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

144 Graves' disease is routinely treated with antithyroid dr

145 Graves' disease is the leading cause of hyperthyroidism

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

176 Graves' Disease results from the production of autoantib

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

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

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

180 In Graves disease, selenium supplementation might lead to f

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

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

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

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

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

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

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

188 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

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

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

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

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

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

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

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

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

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

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

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