ライフサイエンスコーパス: celiac disease

1 ts and harms of treatment of screen-detected celiac disease.

2 ptoms and the natural history of subclinical celiac disease.

3 the inflamed tissue state observed in human celiac disease.

4 bodies before the appearance of anti-TG2A or celiac disease.

5 ty of oats as part of a GFD in patients with celiac disease.

6 l intestinal mucosal injury in patients with celiac disease.

7 from 2009 through 2012) than persons without celiac disease.

8 iac disease, cases were classified as proven celiac disease.

9 c disease, compared with individuals without celiac disease.

10 d the risk of celiac disease autoimmunity or celiac disease.

11 ment of celiac disease autoimmunity (CDA) or celiac disease.

12 ts and harms of treatment of screen-detected celiac disease.

13 Serology findings were negative for celiac disease.

14 tTGA for at least 3 months or development of celiac disease.

15 om 6 adults (26-55 years old) with untreated celiac disease.

16 n diagnostic accuracy of serologic tests for celiac disease.

17 icating celiac disease were classified as no celiac disease.

18 e first months of life might affect risk for celiac disease.

19 ts of including oats in GFD of patients with celiac disease.

20 sures in biopsy specimens from patients with celiac disease.

21 stinguishable from those of patients with D2 celiac disease.

22 e compared between D1 vs D2 in patients with celiac disease.

23 (D1) have not been delineated in adults with celiac disease.

24 e increases the sensitivity of detection for celiac disease.

25 y trigger of the abnormal immune response in celiac disease.

26 ingle-nucleotide polymorphisms contribute to celiac disease.

27 l intestinal mucosal injury in patients with celiac disease.

28 t sleep complaints may be a manifestation of celiac disease.

29 potential effects on epithelial pathology in celiac disease.

30 ppropriateness of the GFD for people without celiac disease.

31 uten-containing foods in relation to risk of celiac disease.

32 , present in people with a predisposition to celiac disease.

33 thelial lymphocytes, or serologic markers of celiac disease.

34 y peptides as T-cell clones from adults with celiac disease.

35 after oral gluten challenge of patients with celiac disease.

36 segments by epitope 1-specific antibodies in celiac disease.

37 sis, 359 (5%) of the 6546 children developed celiac disease.

38 r fracture) were associated with undiagnosed celiac disease.

39 blistering condition seen in the context of celiac disease.

40 NPV to populations with lower prevalence of celiac disease.

41 ein associated with both type 1 diabetes and celiac disease.

42 ed assay accurately identifies patients with celiac disease.

43 1.1% of participants to avoid gluten without celiac disease.

44 ean level of hemoglobin than persons without celiac disease.

45 GL) could identify patients with and without celiac disease.

46 rce (USPSTF) recommendation on screening for celiac disease.

47 ants observed, 10 (4.3%) were diagnosed with celiac disease.

48 vement after gluten withdrawal in absence of celiac disease.

49 ty and specificity both >90%) for diagnosing celiac disease.

50 to a gluten-free diet without a diagnosis of celiac disease.

51 otoxic T cells mediate tissue destruction in celiac disease.

52 lts and children at the time of diagnosis of celiac disease.

53 nity, or serologic features of patients with celiac disease.

54 iatric celiac disease is distinct from adult celiac disease.

55 Of the participants, 592 were found to have celiac disease, 345 were found not to have celiac diseas

56 ian age, 6.2 years), 645 were diagnosed with celiac disease, 46 were found not to have celiac disease

57 nses by T cells from 30 of the children with celiac disease (73%).

58 ts assessed, 268 (19.4%) were diagnosed with celiac disease; 9.7% of these patients had villous atrop

59 effectiveness of screening and treatment for celiac disease, accuracy of screening tests in asymptoma

60 ral polyclonal Treg cells from patients with celiac disease, after a short in vitro expansion, the gl

61 contextual information on the prevalence of celiac disease among patients without obvious symptoms a

62 We found 0.7% of participants to have celiac disease and 1.1% of participants to avoid gluten

63 ed up, 66 developed CDA and met criteria for celiac disease and 46 developed only CDA.

64 f comorbidities between undiagnosed cases of celiac disease and age- and sex-matched seronegative con

65 Furthermore, patients with celiac disease and concomitant type 1 or type 2 diabetes

66 The CD-DIET Study (Celiac Disease and Diabetes - Dietary Intervention and E

67 ntial pathophysiological relevance of TRX in celiac disease and establish the Cys(370)-Cys(371) disul

68 AIMS: The association between prevalence of celiac disease and geographic region is incompletely und

69 inical factors associated with prevalence of celiac disease and gluten-free diet in the United States

70 a phase 2 study of patients with symptomatic celiac disease and histologic evidence of significant du

71 Celiac disease and nonceliac gluten sensitivity are comm

72 Clinicians cannot distinguish between celiac disease and nonceliac gluten sensitivity by sympt

73 h a gluten-free diet, distinguishing between celiac disease and nonceliac gluten sensitivity is impor

74 ding screening, diagnosis, and treatment for celiac disease and nonceliac gluten sensitivity.

75 icacy of a GFD in patients with asymptomatic celiac disease and T1D on key diabetes and patient-cente

76 -DQ-gluten tetramer test, 2 had unrecognized celiac disease and the remaining 2 had T cells that prol

77 Association between celiac disease and type 1 diabetes in adults is still so

78 Subjects with susceptibility genotypes for celiac disease and type 1 diabetes were followed up for

79 is still somewhat unclear, and that between celiac disease and type 2 diabetes even less known.

80 th celiac disease, 46 were found not to have celiac disease, and 16 had inconclusive results.

81 e celiac disease, 345 were found not to have celiac disease, and 24 had no final diagnosis.

82 te are lower in individuals with undiagnosed celiac disease, and levels of hemoglobin are lower in pa

83 ls), healthy family members of patients with celiac disease, and potential celiac disease patients.

84 itis, rheumatoid arthritis, type 1 diabetes, celiac disease, and psoriasis using summary data from ge

85 gh at lower levels than patients with active celiac disease, and without loss of inhibitory receptors

86 Undiagnosed celiac disease appeared to be clinically silent and rema

87 Although sarcoidosis and celiac disease are both chronic immunologic disorders in

88 of tissue destruction during progression of celiac disease are poorly defined.

89 Associations of sarcoidosis and celiac disease are rare but do occur.

90 ated use of hypnotics among individuals with celiac disease as a proxy measure for poor sleep.

91 nesota (<50 y), without a prior diagnosis of celiac disease assay using an assay for IgA against tiss

92 erization of a lncRNA, lnc13, that harbors a celiac disease-associated haplotype block and represses

93 denal biopsy analysis to confirm or rule out celiac disease at 13 centers in Europe.

94 ive incidence of a subsequent diagnosis with celiac disease at 5 years after testing was 10.8% in per

95 Outcomes were the development of celiac disease autoimmunity (CDA) or celiac disease.

96 ively hydrolyzed formula reduced the risk of celiac disease autoimmunity or celiac disease.

97 of asymptomatic adults with screen-detected celiac disease based on positive serologic findings foun

98 We identified persons with celiac disease based on results of serum tests for IgA a

99 A diagnosis of celiac disease based on serologic and histologic evidenc

100 developed an assay to identify patients with celiac disease based on the ability of antibodies from t

101 aired growth is a well-known complication in celiac disease, but factors associated with it are poorl

102 IECs from subjects with a family history of celiac disease, but not from subjects who already had im

103 ocal and central results were concordant for celiac disease, cases were classified as proven celiac d

104 Ingestion of gluten by persons with celiac disease causes immune-mediated inflammatory damag

105 d with those from patients with conventional celiac disease (CCD) (villous atrophy beyond D1) and ind

106 Wheat allergy (WA) and celiac disease (CD) are well-defined entities, but are b

107 tween early-life antibiotic use and islet or celiac disease (CD) autoimmunity in genetically at-risk

108 type II (RCDII) is a severe complication of celiac disease (CD) characterized by the presence of an

109 at 4-6 mo of age did not reduce the risk of celiac disease (CD) in a group of high-risk children.

110 Celiac disease (CD) is a disease of the small intestine

111 Celiac disease (CD) is an HLA-associated disorder charac

112 Celiac disease (CD) is an immune-mediated disorder chara

113 Celiac disease (CD) is an immune-mediated enteropathy tr

114 Celiac disease (CD) is an inflammatory disease of the sm

115 We assessed how the diagnosis of Celiac Disease (CD) is made and how the new ESPGHAN guid

116 wheat peptides responsible for the onset of Celiac Disease (CD) is their high content in proline res

117 Celiac disease (CD) is underdiagnosed in the pediatric p

118 Celiac disease (CD) may affect healthcare use in childre

119 Celiac disease (CD) patients mount an abnormal immune re

120 Celiac disease (CD) patients usually present high levels

121 2)-specific VH:VL autoantibody repertoire of celiac disease (CD) patients.

122 d the HLA class I A*01 and B*08 alleles with celiac disease (CD) susceptibility.

123 e for its involvement in the pathogenesis of celiac disease (CD), a T helper 1 cell-mediated enteropa

124 egraded gluten peptides from cereals trigger celiac disease (CD), an autoimmune enteropathy occurring

125 the small intestine of patients with active celiac disease (CD), and their number drops in patients

126 st in wheat sensitivity among people without celiac disease (CD), but little is known about any risks

127 In HLA-DQ8-associated celiac disease (CD), the pathogenic T cell response is d

128 are associated with increased risk for later celiac disease (CD).

129 the serologic test of choice for diagnosing celiac disease (CD).

130 The only treatment for celiac disease (CeD) is a lifelong gluten-free diet (GFD

131 Celiac disease (CeD) is a prevalent autoimmune condition

132 1 (TH1) immunity against dietary gluten and celiac disease (CeD).

133 a range of inflammatory disorders, including celiac disease (CeD); however, the mechanisms by which h

134 Patients were assigned to categories of no celiac disease, celiac disease, or biopsy required, base

135 re lower in participants with a diagnosis of celiac disease, compared with individuals without celiac

136 gluten-free diet (GFD) without exclusion of celiac disease complicates its detection.

137 s atrophy beyond D1) and individuals without celiac disease (controls).

138 Celiac disease, Crohn disease and ulcerative colitis are

139 ple sclerosis, systemic lupus erythematosus, celiac disease, Crohn's disease, Addison's disease, prim

140 rom any D1 site increased the sensitivity of celiac disease detection by 9.3%-10.8% (P < .0001).

141 isk for celiac disease who were followed for celiac disease development.

142 Poor sleep was also more common after celiac disease diagnosis as compared with matched contro

143 ymptoms or classic consequences of diagnosed celiac disease (diarrhea, anemia, or fracture) were asso

144 e 1 diabetes was markedly overrepresented in celiac disease, especially in men, whereas the prevalenc

145 areness and reducing the diagnostic delay of celiac disease even in the elderly population.

146 n-specific T cells in blood of patients with celiac disease, even if they are on a GFD.

147 oxic T cells from relatives of patients with celiac disease expressed higher levels of activating NK

148 re studies of subjects with biopsy-confirmed celiac disease, follow-up biopsies, and measurement of s

149 conclusive cases were regarded as not having celiac disease for calculation of diagnostic accuracy.

150 rder to protect people with wheat allergy or celiac disease from the accidental ingestion of gliadin.

151 use of CE in patients with Crohn's disease, celiac disease, gastrointestinal bleeding, and anemia.

152 For patients with celiac disease, gliadin detoxification via the use of gl

153 nts with a health care provider diagnosis of celiac disease had a lower mean level of hemoglobin than

154 Patients with celiac disease had a median of 50 IELs/100 enterocytes i

155 a self-instituted gluten-free diet, for whom celiac disease had been excluded.

156 or omega-gliadin peptides from children with celiac disease had comparable levels of reactivity to wh

157 Children who developed celiac disease had increased titers of cow's milk antibo

158 he effector T-cell response in patients with celiac disease has been well characterized, the role of

159 We sought to define whether patients with celiac disease have a dysfunction or lack of gluten-spec

160 1.14; 95% confidence interval, 0.51-2.54) or celiac disease (hazard ratio, 4.13; 95% confidence inter

161 artment has been proposed as a treatment for celiac disease; however, no protease has been shown to s

162 Participants with undiagnosed celiac disease (identified by positive results from sero

163 Patients were assigned to categories of no celiac disease if all assays found antibody concentratio

164 antibody concentrations <1-fold the ULN, or celiac disease if at least 1 assay measured antibody con

165 imed to estimate the cumulative incidence of celiac disease in adolescents born in the Denver metropo

166 dence on benefits and harms of screening for celiac disease in asymptomatic adults, adolescents, and

167 lated to benefits and harms of screening for celiac disease in asymptomatic individuals.

168 lance of benefits and harms of screening for celiac disease in asymptomatic persons.

169 the prevalence and morbidity of undiagnosed celiac disease in individuals younger than age 50 in a c

170 out the prevalence and burden of undiagnosed celiac disease in individuals younger than age 50.

171 out the prevalence and burden of undiagnosed celiac disease in individuals younger than age 50.

172 utaminase (tTG) were developed to screen for celiac disease in patients consuming gluten.

173 d barley can trigger IgE-mediated allergy or Celiac disease in sensitive individuals.

174 consumption was not associated with risk of celiac disease in the child after adjustment for country

175 we highlight the incidence and prevalence of celiac disease in the elderly, the patterns of clinical

176 AIMS: Little is known about the incidence of celiac disease in the general population of children in

177 ate pregnancy is not associated with risk of celiac disease in the offspring.

178 of cow's milk antibody before anti-TG2A and celiac disease indicates that subjects with celiac disea

179 gic sensitization, type 1 diabetes mellitus, celiac disease, inflammatory bowel disease, autoimmune t

180 Only 2 studies of serologic tests for celiac disease involving 62 and 158 patients were conduc

181 Celiac disease is a chronic immune-mediated inflammatory

182 BACKGROUND & AIMS: Celiac disease is a chronic small intestinal inflammator

183 Observations: Celiac disease is a gluten-induced immune-mediated enter

184 Celiac disease is a human T cell-mediated autoimmune-lik

185 signs or symptoms, or both, suggesting that celiac disease is a systemic disease.

186 exaggerated response to an unknown antigen, celiac disease is a T cell-driven disease triggered by i

187 Celiac disease is caused by an immune response in person

188 BACKGROUND & AIMS: Celiac disease is characterized by HLA-DQ2/8-restricted

189 Celiac disease is characterized by intestinal inflammati

190 It is uncertain whether pediatric celiac disease is distinct from adult celiac disease.

191 BACKGROUND & AIMS: A diagnosis of celiac disease is made based on clinical, genetic, serol

192 nt initiates a gluten-free diet, testing for celiac disease is no longer accurate.

193 Celiac disease is often diagnosed in early childhood, bu

194 lk-based formula would decrease the risk for celiac disease later in life.

195 ota in modulating gluten immune response and celiac disease-like pathology in a humanized mouse model

196 d regarding diagnostic accuracy of tests for celiac disease, little or no evidence was identified to

197 eukocyte antigen genotype, family history of celiac disease, maternal education, and sex of the child

198 Silent or subclinical celiac disease may result in potentially avoidable adver

199 onsecutive patients with a high suspicion of celiac disease (mean age, 46.5 y; 64% female).

200 celiac disease indicates that subjects with celiac disease might have increased intestinal permeabil

201 Therefore, screening for celiac disease must occur before a gluten-free diet is i

202 MA, and any symptom identified children with celiac disease (n = 399) with a PPV of 99.75 (95% confid

203 89), idiopathic achalasia (ncases = 727) and celiac disease (ncases = 11,115).

204 s made by the pediatric gastroenterologists (celiac disease, no celiac disease, or no final diagnosis

205 celiac disease on a GFD, 19 subjects without celiac disease on a GFD [due to self-reported gluten sen

206 mized cutoff values identified subjects with celiac disease on a GFD with 97% sensitivity (95% CI 0.9

207 ssion model that identified individuals with celiac disease on a GFD with an area under the receiver

208 143 HLA-DQ2.5(+) subjects (62 subjects with celiac disease on a GFD, 19 subjects without celiac dise

209 icity (95% CI 0.84-1.00) vs subjects without celiac disease on a GFD.

210 interval [CI] 0.89-1.00) vs subjects without celiac disease on a GFD.

211 The assay detected individuals with celiac disease on a gluten-containing diet vs controls w

212 The values identified subjects with celiac disease on a gluten-containing diet with 100% sen

213 ported gluten sensitivity], 10 subjects with celiac disease on a gluten-containing diet, and 52 presu

214 type, except for samples from subjects with celiac disease on a gluten-containing diet.

215 ant type 1 or type 2 diabetes and those with celiac disease only underwent comparisons of clinical an

216 % vs 3 %, P < 0.001) than the patients with celiac disease only.

217 oncomitant type 2 diabetes and patients with celiac disease only.

218 ealthy individuals with no family history of celiac disease or antibodies against tissue transglutami

219 atitudes of 35 degrees North or greater have celiac disease or avoid gluten than persons living south

220 ce a period of CDA, not all children develop celiac disease or require gluten-free diets.

221 s and harms of screening vs no screening for celiac disease or treatment vs no treatment for screen-d

222 Individuals with celiac disease or type 1 diabetes have been reported to

223 is diagnosed in individuals who do not have celiac disease or wheat allergy but who have intestinal

224 assigned to categories of no celiac disease, celiac disease, or biopsy required, based entirely on an

225 t a diagnosis of inflammatory bowel disease, celiac disease, or liver disease, endoscopy during pregn

226 tric gastroenterologists (celiac disease, no celiac disease, or no final diagnosis).

227 In human celiac disease patient samples, increased levels of the

228 atory end points including a 26% decrease in celiac disease patient-reported outcome symptomatic days

229 n enzyme-linked immunosorbent assays against celiac disease patients' sera versus normal blood donors

230 aptive antigluten immunity, and in potential celiac disease patients, who have antibodies against tis

231 eshold of 20mg/kg of gluten is essential for celiac disease patients.

232 in the development of gluten-free pasta for celiac disease patients.

233 ) monitoring as well as therapy follow-up of celiac disease patients.

234 died these issues in a large cohort of adult celiac disease patients.

235 patients with celiac disease, and potential celiac disease patients.

236 ices may have contributed to the increase in celiac disease prevalence during the latter half of the

237 e, ulcerative colitis, rheumatoid arthritis, celiac disease, psoriasis, and multiple sclerosis.

238 ve individuals (59.1%) were seropositive for celiac disease-related alleles compared with 8 (28.6%) o

239 ic approaches for diagnosis and treatment of celiac disease requires a detailed understanding of the

240 gluten introduction was not associated with celiac disease risk, and timing of allergenic food intro

241 Although dietary gluten is the trigger for celiac disease, risk is strongly influenced by genetic v

242 tices, presented higher amounts of potential celiac disease's immunostimulatory epitopes when compare

243 Using celiac disease sera as a discovery set, IMUNE identified

244 To diagnose celiac disease, serological tests were used, and duodena

245 Patients with celiac disease should be followed up closely for dietary

246 BACKGROUND & AIMS: Patients with celiac disease should maintain a gluten-free diet (GFD),

247 fty patients and 20 controls were tested for celiac disease-specific HLA antigen alleles; 13 of 22 TG

248 Celiac disease status was not associated with overall su

249 reatment vs no treatment for screen-detected celiac disease; studies on diagnostic accuracy of serolo

250 In conclusion, individuals with celiac disease suffer an increased risk of poor sleep, b

251 nt TG2 activity is thought to play a role in celiac disease, suggesting that a better understanding o

252 Subjects completed the Celiac Disease Symptom Diary each day for 28 days and un

253 ty of D1 biopsy analysis in the detection of celiac disease, the number and sites of biopsies require

254 te evidence on the accuracy of screening for celiac disease, the potential benefits and harms of scre

255 litus, systemic lupus erythematosus, RA, and celiac disease, these results suggest a general mechanis

256 test would allow individuals with suspected celiac disease to avoid gluten challenge and duodenal bi

257 this finding, we estimated the prevalence of celiac disease to be 1.1% (95% confidence interval, 1.0%

258 , we estimated the prevalence of undiagnosed celiac disease to be 1.1%.

259 we found the cumulative incidence of CDA and celiac disease to be high within the first 10 years.

260 Refractory celiac disease type II (RCDII) is a severe complication

261 a-analysis of patients with biopsy-confirmed celiac disease undergoing follow-up biopsy on a GFD, we

262 r analysis excluded subjects with refractory celiac disease, undergoing gluten challenge, or consumin

263 Treated patients with celiac disease underwent oral wheat challenge to stimula

264 s of biopsies required to detect ultra-short celiac disease (USCD, villous atrophy limited to D1), an

265 esting was 10.8% in persons with undiagnosed celiac disease vs 0.1% in seronegative persons (P < .01)

266 Undiagnosed celiac disease was associated with increased rates of hy

267 ase; in subjects with positive test results, celiac disease was confirmed using an assay for endomysi

268 Gluten avoidance without celiac disease was defined as adherence to a gluten-free

269 Celiac disease was defined based on detection of Marsh 2

270 The risk of poor sleep in celiac disease was essentially not influenced by adjustm

271 The phenotype of IELs from patients with D1 celiac disease was indistinguishable from those of patie

272 Gluten avoidance without celiac disease was more common among individuals who liv

273 Celiac disease was more common among individuals who liv

274 of 230 infants with genetic risk factors for celiac disease, we did not find evidence that weaning to

275 erologic tests of a community population for celiac disease, we estimated the prevalence of undiagnos

276 1339 children with genetic risk factors for celiac disease, we found the cumulative incidence of CDA

277 5.1%, respectively, and incidence values for celiac disease were 1.6%, 2.8%, and 3.1%, respectively.

278 ess the ULN) but no other results indicating celiac disease were classified as no celiac disease.

279 enotype, the cumulative incidence of CDA and celiac disease were determined.

280 No trials of screening for celiac disease were identified.

281 an increased risk of ulcerative colitis and celiac disease, whereas children delivered by elective C

282 intestinal biopsy samples from patients with celiac disease, which suggests that down-regulation of l

283 f mucosal damage in children and adults with celiac disease who are following a GFD.

284 EMA IgA assays in identifying patients with celiac disease who have persistent villous atrophy despi

285 CE was recommended to assess patients with celiac disease who have unexplained symptoms despite app

286 14 children (2-5 years old) at high risk for celiac disease who were followed for celiac disease deve

287 strointestinal bleeding, Crohn's disease, or celiac disease, who have had negative or inconclusive en

288 c T cells in family members of patients with celiac disease, who were without any signs of adaptive a

289 T cells identifies patients with and without celiac disease with a high level of accuracy, regardless

290 nonbiopsy approach identifies children with celiac disease with a positive predictive value (PPV) ab

291 e TTG-IgA procedure identified patients with celiac disease with a PPV of 0.988 and an NPV of 0.934;

292 e TTG-DGL procedure identified patients with celiac disease with a PPV of 0.988 and an NPV of 0.958.

293 hibition assay that identifies patients with celiac disease with high levels of specificity and sensi

294 safety of latiglutenase in 494 patients with celiac disease (with moderate or severe symptoms) in Nor

295 ts with USCD may have early stage or limited celiac disease, with a mild clinical phenotype and infre

296 t of the patients with anti-TG2 IgA-negative celiac disease without a significant decrease in specifi

297 tology, and Nutrition allow for diagnosis of celiac disease without biopsies in children with symptom

298 Children can be accurately diagnosed with celiac disease without biopsy analysis.

299 cation of pediatric patients with or without celiac disease, without biopsy.

300 doscopy for more than half the children with celiac disease worldwide.