ライフサイエンスコーパス: celiac disease

1 pancreatoduodenectomy, and 1 with potential celiac disease).

2 sinus thrombosis unveiling the diagnosis of celiac disease.

3 rs in the development of type 1 diabetes and celiac disease.

4 f villous atrophy in children with potential celiac disease.

5 disease autoimmunity and 447 (7%) developed celiac disease.

6 temic antibiotics could be a risk factor for celiac disease.

7 ger durations of any human milk feeding with celiac disease.

8 not have led to the increased prevalence of celiac disease.

9 the first year of life and risk of diagnosed celiac disease.

10 e to be associated with a later diagnosis of celiac disease.

11 is a promising strategy for the treatment of celiac disease.

12 children, including 3346 with a diagnosis of celiac disease.

13 nicians as well as researchers, this must be celiac disease.

14 -Wiedemann syndrome, and 17 individuals with celiac disease.

15 r changes in the brains of participants with celiac disease.

16 n intake during childhood may confer risk of celiac disease.

17 rotein) making it suitable for patients with celiac disease.

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

19 sures in biopsy specimens from patients with celiac disease.

20 velopment of autoimmune disorders, including celiac disease.

21 thelial lymphocytes, or serologic markers of celiac disease.

22 after oral gluten challenge of patients with celiac disease.

23 tegy might be developed for the treatment of celiac disease.

24 r fracture) were associated with undiagnosed celiac disease.

25 blistering condition seen in the context of celiac disease.

26 NPV to populations with lower prevalence of celiac disease.

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

28 ed assay accurately identifies patients with celiac disease.

29 1.1% of participants to avoid gluten without celiac disease.

30 ean level of hemoglobin than persons without celiac disease.

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

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

33 s are essential for an accurate diagnosis of celiac disease.

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

35 vement after gluten withdrawal in absence of celiac disease.

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

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

38 otoxic T cells mediate tissue destruction in celiac disease.

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

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

41 iatric celiac disease is distinct from adult celiac disease.

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

43 ptoms and the natural history of subclinical celiac disease.

44 the inflamed tissue state observed in human celiac disease.

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

46 l intestinal mucosal injury in patients with celiac disease.

47 to transglutaminase 2 (TG2) are hallmarks of celiac disease.

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

49 prevalence of brain injury in patients with celiac disease.

50 T cells from patients with active or treated celiac disease.

51 nity medical center and their progression to celiac disease.

52 h increased risks of subsequent diagnosis of celiac disease.

53 g duodenal biopsy confirmed the diagnosis of celiac disease.

54 organ-specific autoimmune diseases including celiac disease.

55 lantoaxial instability, thyroid disease, and celiac disease.

56 time points and adults later diagnosed with celiac disease.

57 s disease (CD), ulcerative colitis (UC), and celiac disease.

58 din protein (TIMP-GLIA) in 3 mouse models of celiac disease.

59 tive IgA deficiency rather than seronegative celiac disease.

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

61 om intestinal biopsies from 40 patients with celiac disease (35 untreated and 5 on a gluten-free diet

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

63 with inflammatory bowel diseases (9.4%) and celiac disease (7.3%) were higher than those in the gene

64 oint, 31 (20%) had a subsequent diagnosis of celiac disease, 81 (53%) remained positive for tTGA with

65 verall mortality was increased in those with celiac disease (9.7 vs 8.6 deaths per 1000 person-years;

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

67 Celiac disease Adherence Test (CDAT) is a valid English-

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

69 ased risk of celiac disease autoimmunity and celiac disease among genetically predisposed children.

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

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

72 We included 9 celiac disease and 17 IBD articles.

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

74 red dietitian nutritionist with expertise in celiac disease and a gastroenterologist who specializes

75 The incidence of both celiac disease and a related condition called nonceliac

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

77 ed with tissues from patients with potential celiac disease and controls.

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

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

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

81 ty of TG2 is involved in the exacerbation of celiac disease and in at least 1 case of hemoglobinopath

82 man milk to mixed-fed infants with diagnosed celiac disease and inflammatory bowel disease (IBD).

83 and a gastroenterologist who specializes in celiac disease and malabsorptive disorders, and they sho

84 Celiac disease and nonceliac gluten sensitivity are comm

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

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

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

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

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

90 ive for tTGA without a clinical diagnosis of celiac disease, and 41 (27%) had negative test results f

91 Undiagnosed celiac disease appeared to be clinically silent and rema

92 The criteria for the diagnosis of celiac disease are changing, but in adults, diagnosis st

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

94 ange, 8.0-10.0 years]), 1216 (18%) developed celiac disease autoimmunity and 447 (7%) developed celia

95 f life was associated with increased risk of celiac disease autoimmunity and celiac disease among gen

96 en intake was associated with higher risk of celiac disease autoimmunity for every 1-g/d increase in

97 The primary outcome was celiac disease autoimmunity, defined as positive tissue

98 llected data from the clinic on diagnoses of celiac disease based on duodenal biopsy analysis.

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

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

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

102 ng-term study of 280 children with suspected celiac disease (based on anti-TG2 and anti-EMA) on glute

103 For patients with suspected celiac disease but negative results from serologic tests

104 these specific plasma cells in patients with celiac disease but was observed in an average 30% of gut

105 human milk is associated with higher risk of celiac disease, but concerns about reverse causality pre

106 is and management of patients with suspected celiac disease, but negative results from serologic test

107 s (tTGA) without endoscopic determination of celiac disease (called celiac autoimmunity) have not bee

108 el functional food is presented here and for celiac disease can be a path towards the development of

109 Celiac disease can develop at any age, but outcomes of a

110 A diagnosis of seronegative celiac disease can then be confirmed based on clinical a

111 type data on control samples and CD, UC, and celiac disease cases were provided by the respective con

112 Associations have been made between celiac disease (CD) and small bowel cancers, but there h

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

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

115 n the intestinal microbiota of children with celiac disease (CD) cause the disease or are a result of

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

117 odalities in the diagnosis and monitoring of celiac disease (CD) in adults as well as in children and

118 The treatment of celiac disease (CD) is a lifelong gluten-free diet (GFD)

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

120 Celiac disease (CD) is an immune-mediated disorder trigg

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

122 Celiac disease (CD) is triggered by gluten and related p

123 explanation for the increasing prevalence of celiac disease (CD) over the past decades is that breedi

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

125 ted the presence of an ID/anti-ID network in celiac disease (CD), a condition in which antitissue tra

126 Celiac disease (CD), dermatitis herpetiformis (DH), glut

127 In contrast to the well-characterized Celiac Disease (CD), the clinical scenarios encompassed

128 gallate) in a nutritional context to prevent Celiac Disease (CD).

129 d immune-mediated intestinal disorders, e.g. celiac disease (CD).

130 s between healthy controls and patients with celiac disease (CD).

131 o detected a shared genetic risk between CC, celiac disease, CD, and UC, which supports clinical obse

132 Gluten challenge is used to diagnose celiac disease (CeD) and for clinical research.

133 is controversy over the association between celiac disease (CeD) and inflammatory bowel diseases (IB

134 DQ2.2, are implicated in the pathogenesis of celiac disease (CeD) by presenting gluten peptides to CD

135 Celiac disease (CeD) has characteristics of an autoimmun

136 Celiac disease (CeD) is a food sensitivity characterized

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

138 HLA-DQ2.5-mediated celiac disease (CeD) is triggered by the ingestion of gl

139 Celiac disease (CeD) provides an opportunity to study th

140 In the setting of celiac disease (CeD), where exposure to dietary antigen

141 on the risk of COVID-19 and its outcomes in celiac disease (CeD).

142 1 (TH1) immunity against dietary gluten and celiac disease (CeD).

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

144 Celiac disease, characterized by autoimmune reactions to

145 Crohn's disease, inflammatory bowel disease, celiac disease, chronic pancreatitis, and primary sclero

146 uodenal tissues from patients with untreated celiac disease compared with controls.

147 tudied between 1969 and 2017, a diagnosis of celiac disease compared with the general population was

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

149 The secondary outcome was celiac disease confirmed by intestinal biopsy or persist

150 ree diet), as well as 43 individuals without celiac disease (controls).

151 Celiac disease could be treated, and potentially cured,

152 x diseases, including asthma, breast cancer, celiac disease, Crohn's disease, Parkinson's disease and

153 PARTICIPANTS: All individuals in Sweden with celiac disease diagnosed between 1969 and 2017 were iden

154 eliac disease, for a cumulative incidence of celiac disease diagnosis of 0.06% (95% confidence interv

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

156 in the blood and intestines of patients with celiac disease display a surprisingly rare phenotype.

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

158 ls from intestinal biopsies of patients with celiac disease express MHCII; this is the most abundant

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

160 en (ages 2-18 years) in Italy with suspected celiac disease, followed for up to 12 years (range, 18-1

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

162 en intake was associated with higher risk of celiac disease for every 1-g/d increase in gluten consum

163 cords, 6 individuals received a diagnosis of celiac disease, for a cumulative incidence of celiac dis

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

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

166 uodenal tissues from patients with untreated celiac disease had increased levels of messenger RNAs en

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

168 with control individuals, participants with celiac disease had significant deficits in reaction time

169 Celiac disease has a wide range of intestinal and extrai

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

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

172 Patients with celiac disease have gluten-specific immune responses, bu

173 Strategies to reduce the development of celiac disease have not been proven successful in random

174 n for SBCE) to newer ones such as refractory celiac disease, hereditary polyposis syndromes and Crohn

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

176 Among tests for celiac disease, IgA tissue transglutaminase presented th

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

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

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

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

181 Negative results can be used to rule out celiac disease in seronegative patients.

182 ife was positively associated with diagnosed celiac disease in the Danish and Norwegian cohorts (pool

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

184 lieved to be involved in the pathogenesis of celiac disease, in addition to genetic variants and diet

185 uropsychological dysfunction in persons with celiac disease included in the National UK Biobank, whic

186 There were 49 829 patients with celiac disease, including 24% who were diagnosed between

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

188 emory T-cell enteropathy (model 3) models of celiac disease, intravenous injections of TIMP-GLIA sign

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

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

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

192 Celiac disease is an autoimmune condition characterized

193 Celiac disease is an autoimmune illness activated by glu

194 These findings support the concept that celiac disease is associated with neurologic and psychol

195 Development of celiac disease is believed to involve the transglutamina

196 Celiac disease is caused by an immune response in person

197 Celiac disease is caused by an immune-mediated reaction

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

199 Potential celiac disease is characterized by positive results from

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

201 The incidence of celiac disease is increasing, partly because of improved

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

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

204 Celiac disease is often diagnosed in early childhood, bu

205 Celiac disease is provoked by gluten exposure, but the c

206 Celiac disease is the most common food-induced enteropat

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

208 Celiac disease may be associated with a modest but persi

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

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

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

212 villous atrophy and genetic risk factors for celiac disease must undergo endoscopic evaluation after

213 Biobank participants with celiac disease (n = 104; mean age, 63 years; 65% female)

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

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

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

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

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

219 illous atrophy), and 5 patients with treated celiac disease (on a gluten-free diet), as well as 43 in

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

221 stent increases in tTGA without diagnoses of celiac disease or have negative results from second test

222 s of management of patients believed to have celiac disease or other enteropathies unrelated to glute

223 the consumption of such food by people with celiac disease or other gluten-related disorders.

224 ain intestinal inflammation in patients with celiac disease or other inflammatory disorders.

225 gluten proteins to symptoms in patients with celiac disease or other wheat-related disorders is contr

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

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

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

229 ), psoriasis (OR = 1.70; 95% CI, 1.51-1.91), celiac disease (OR = 1.53; 95% CI, 1.12-2.10), and Grave

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

231 DQ2-restricted gliadin epitopes, relevant to celiac disease, or DQ2-restricted viral epitopes, releva

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

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

234 Genomic regions for celiac disease (P = 0.22) and primary sclerosing cholang

235 sue transglutaminase is critical to activate celiac disease pathogenesis making the addition of mTG t

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

237 ainst the enzyme transglutaminase 2 (TG2) in celiac disease patients by generating recombinant antibo

238 enerated from intestinal biopsy specimens of celiac disease patients, this treatment showed the poten

239 cy as a treatment to detoxify the gluten for celiac disease patients.

240 ber of dispensed antibiotics and the risk of celiac disease (pooled odds ratio for each additional di

241 enal biopsies from 9 patients with potential celiac disease (positive results from tests for anti-TG2

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

243 years, range 18-80 years), diagnosed at the Celiac Disease Referral Center of our University Hospita

244 ase were randomly selected from the national celiac disease registry database.

245 m gluten-containing grains for patients with celiac disease remains controversial.

246 ciates with higher risk of diagnosed IBD and celiac disease, respectively.

247 ut negative results from serologic tests for celiac disease (seronegative enteropathy).

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

249 All patients with celiac disease should be referred to a registered dietit

250 to determine whether children with suspected celiac disease should immediately start a gluten-free di

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

252 However, we also identified a celiac disease specific signature linked to increased ce

253 Celiac disease status was not associated with overall su

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

255 rin, fecal calprotectin, serologic tests for celiac disease, tests for bile acid diarrhea, the commer

256 FXIIIa in acquired FXIII deficiency, TG2 in celiac disease, TG3 in dermatitis herpetiformis, TG4 in

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

258 for tTGA, only 20% are later diagnosed with celiac disease; the remaining individuals maintain persi

259 In celiac disease, there is still no therapeutic alternativ

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

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

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

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

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

265 m the UK Biobank, we found participants with celiac disease to have cognitive deficit, indications of

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

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

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

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

270 Undiagnosed celiac disease was associated with increased rates of hy

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

272 Celiac disease was defined based on detection of Marsh 2

273 Celiac disease was defined by the presence of small inte

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

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 Individuals with celiac disease were at increased risk of death from card

279 Patients with celiac disease were compared with controls using stratif

280 enotypes associated with type 1 diabetes and celiac disease were enrolled.

281 Autoimmune diseases and celiac disease were excluded.

282 No trials of screening for celiac disease were identified.

283 ss the construct validity, 230 patients with celiac disease were randomly selected from the national

284 nvironmental triggers of type 1 diabetes and celiac disease, were followed up at 6 clinical centers i

285 Gluten-related disorders, including celiac disease, wheat allergy, and nonceliac gluten sens

286 The findings lend credence to a model of celiac disease where gluten-reactive T cells provide hel

287 T PRACTICE ADVICE 6: Patients with suspected celiac disease who are seronegative but have villous atr

288 from intestinal biopsies from patients with celiac disease who consume gluten, but not from patients

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

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

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

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

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

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

295 ysial antibody, should be considered to have celiac disease with selective IgA deficiency rather than

296 Screening for celiac disease with tissue transglutaminase autoantibodi

297 villous atrophy), 30 patients with untreated celiac disease (with villous atrophy), and 5 patients wi

298 l ages, some children receive a diagnosis of celiac disease without a biopsy.

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

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

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