ライフサイエンスコーパス: celiac

1 We conducted a survey of members of Beyond Celiac (a PAG), collecting responses from 1832 U.S. adul

2 e wall, dextran biotin was injected into the celiac and superior mesenteric ganglia (CSMG) of rats.

3 had lower hemoglobin (p = 0.016) and higher celiac antibody (p < 0.001), alanine aminotransferase (p

4 FV after the meal remained unaffected in the celiac artery and cerebral circulation.

5 maging techniques can be used to demonstrate celiac artery compression by the MAL including mesenteri

6 y terms median arcuate ligament syndrome and celiac artery compression syndrome.

7 ligament release; celiac ganglionectomy; and celiac artery revascularization.

8 was noted at the superior mesenteric artery, celiac artery, or common hepatic artery.

9 calcifications of the aorta (score of 0-2), celiac axis (score of 0-2), right postceliac arteries (c

10 vely distant lymph node metastases along the celiac axis and/or the proximal field have a negative im

11 re disease resulting from compression of the celiac axis by fibrous attachments of the diaphragmatic

12 el flavoured GF bread can be included in the celiac diet.

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

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

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

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

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

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

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

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

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

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

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

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

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

26 Celiac disease (CD) patients usually present high levels

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

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

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

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

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

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

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

34 1 (TH1) immunity against dietary gluten and celiac disease (CeD).

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

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

37 1.14; 95% confidence interval, 0.51-2.54) or celiac disease (hazard ratio, 4.13; 95% confidence inter

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

53 Celiac disease and nonceliac gluten sensitivity are comm

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

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

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

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

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

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

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

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

62 Undiagnosed celiac disease appeared to be clinically silent and rema

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

100 Celiac disease is a chronic immune-mediated inflammatory

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

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

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

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

105 Celiac disease is caused by an immune response in person

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

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

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

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

110 Celiac disease is often diagnosed in early childhood, bu

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

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

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

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

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

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

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

118 143 HLA-DQ2.5(+) subjects (62 subjects with celiac disease on a GFD, 19 subjects without celiac dise

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

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

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

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

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

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

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

126 % vs 3 %, P < 0.001) than the patients with celiac disease only.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

144 Celiac disease status was not associated with overall su

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

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

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

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

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

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

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

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

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

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

155 Undiagnosed celiac disease was associated with increased rates of hy

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

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

158 Celiac disease was defined based on detection of Marsh 2

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

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

161 Celiac disease was more common among individuals who liv

162 5.1%, respectively, and incidence values for celiac disease were 1.6%, 2.8%, and 3.1%, respectively.

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

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

165 No trials of screening for celiac disease were identified.

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

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

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

169 14 children (2-5 years old) at high risk for celiac disease who were followed for celiac disease deve

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

191 Celiac disease, Crohn disease and ulcerative colitis are

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

211 1339 children with genetic risk factors for celiac disease, we found the cumulative incidence of CDA

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

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

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

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

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

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

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

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

220 iatric celiac disease is distinct from adult celiac disease.

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

222 ptoms and the natural history of subclinical celiac disease.

223 the inflamed tissue state observed in human celiac disease.

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

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

226 l intestinal mucosal injury in patients with celiac disease.

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

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

229 c disease, compared with individuals without celiac disease.

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

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

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

233 Serology findings were negative for celiac disease.

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

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

236 n diagnostic accuracy of serologic tests for celiac disease.

237 icating celiac disease were classified as no celiac disease.

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

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

240 sures in biopsy specimens from patients with celiac disease.

241 stinguishable from those of patients with D2 celiac disease.

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

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

244 e increases the sensitivity of detection for celiac disease.

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

246 ingle-nucleotide polymorphisms contribute to celiac disease.

247 l intestinal mucosal injury in patients with celiac disease.

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

249 thelial lymphocytes, or serologic markers of celiac disease.

250 potential effects on epithelial pathology in celiac disease.

251 ppropriateness of the GFD for people without celiac disease.

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

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

254 after oral gluten challenge of patients with celiac disease.

255 r fracture) were associated with undiagnosed celiac disease.

256 blistering condition seen in the context of celiac disease.

257 NPV to populations with lower prevalence of celiac disease.

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

259 ed assay accurately identifies patients with celiac disease.

260 1.1% of participants to avoid gluten without celiac disease.

261 ean level of hemoglobin than persons without celiac disease.

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

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

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

265 vement after gluten withdrawal in absence of celiac disease.

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

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

268 otoxic T cells mediate tissue destruction in celiac disease.

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

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

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

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

273 ed with a variety of interventions including celiac ganglionectomy as well as open, laparoscopic, or

274 Lowering blood pressure with celiac ganglionectomy in SHRs did not alter the increase

275 , laparoscopic, or robotic ligament release; celiac ganglionectomy; and celiac artery revascularizati

276 Non-celiac gluten sensitivity (NCGS) is still an undefined s

277 The mechanisms of non-celiac gluten sensitivity are unclear, and there are no

278 BACKGROUND & AIMS: Non-celiac gluten sensitivity is characterized by symptom im

279 study of individuals with self-reported non-celiac gluten sensitivity, we found fructans to induce s

280 by evaluating urine samples from healthy and celiac individuals with different dietary gluten conditi

281 s that have been additionally diagnosed with celiac-like enteropathy.

282 T4 disease, 215 (66%) N1, and 62 (19%) with celiac nodal involvement.

283 sing peripheral blood mononuclear cells from celiac patients after receiving a 3-day gluten challenge

284 e 1 diabetes (men/women) was 8.0 % /1.8 % in celiac patients and 0.7 % /0.3 % in the population, and

285 -TG2 mAbs generated from gut plasma cells of celiac patients and identified four epitopes (epitopes 1

286 mitant type 1 or type 2 diabetes predisposes celiac patients to severe co-morbidities and type 1 diab

287 alence of type 1 and type 2 diabetes in 1358 celiac patients was compared with the population-based v

288 Celiac patients with concomitant type 1 diabetes were yo

289 % vs 95 % and 96 %, P < 0.001) compared with celiac patients with concomitant type 2 diabetes and pat

290 icient methods for dietary gluten control of celiac patients, we have developed a simple and highly s

291 ell as by stimulation assays of T-cells from celiac patients.

292 th those with the highest immunoactivity for celiac patients.

293 argeting plasma cells seems to be favored in celiac patients.

294 Faecal calprotectin, thyroid tests, celiac serology, breath tests were more frequently sugge

295 Celiac sprue is a chronic disease, which usually occurs

296 in a population-based birth cohort of young celiac subjects and references matched by maternal educa

297 ssion Scale (HADS), and the disease-specific Celiac Symptom Index (CSI) questionnaires.

298 f life scores improved (46.3-40.6; P = .05); celiac symptom indices (24.3-24.3; P = .53), intra-epith

299 ive GIP is desirable to assess the potential celiac toxicity of food.

300 ases in the upper mediastinum and around the celiac trunk after neoadjuvant therapy and resection doe