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 s in the perigastric mesentery and along the celiac arterial branches).

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

4 e investigated the proportion of adults with celiac autoimmunity at a community medical center and th

5 opic determination of celiac disease (called celiac autoimmunity) have not been thoroughly evaluated.

6 denal biopsies from both non-celiac (NC) and celiac (CD) patients, we explored the contribution of gu

7 sion in 54 pediatric celiac patients and non-celiac controls, and we validate our key findings in two

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

34 Celiac disease (CeD) has characteristics of an autoimmun

35 Celiac disease (CeD) is a food sensitivity characterized

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

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

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

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

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

41 1 (TH1) immunity against dietary gluten and celiac disease (CeD).

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

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

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

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

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

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

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

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

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

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

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

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

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

55 We included 9 celiac disease and 17 IBD articles.

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

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

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

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

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

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

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

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

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

65 Celiac disease and nonceliac gluten sensitivity are comm

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

67 Undiagnosed celiac disease appeared to be clinically silent and rema

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

86 Celiac disease could be treated, and potentially cured,

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

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

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

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

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

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

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

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

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

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

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

98 Celiac disease has a wide range of intestinal and extrai

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

114 Celiac disease is an autoimmune condition characterized

115 Celiac disease is an autoimmune illness activated by glu

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

117 Development of celiac disease is believed to involve the transglutamina

118 Celiac disease is caused by an immune response in person

119 Celiac disease is caused by an immune-mediated reaction

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

121 Potential celiac disease is characterized by positive results from

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

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

124 Celiac disease is often diagnosed in early childhood, bu

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

126 Celiac disease is the most common food-induced enteropat

127 Celiac disease may be associated with a modest but persi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

153 Celiac disease status was not associated with overall su

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

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

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

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

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

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

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

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

162 Celiac disease was defined based on detection of Marsh 2

163 Celiac disease was defined by the presence of small inte

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

165 Patients with celiac disease were compared with controls using stratif

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

167 Autoimmune diseases and celiac disease were excluded.

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

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

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

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

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

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

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

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

176 Screening for celiac disease with tissue transglutaminase autoantibodi

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

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

179 pancreatoduodenectomy, and 1 with potential celiac disease).

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

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

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

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

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

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

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

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

188 Celiac disease, characterized by autoimmune reactions to

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

207 In celiac disease, there is still no therapeutic alternativ

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

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

210 1339 children with genetic risk factors for celiac disease, we found the cumulative incidence of CDA

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

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

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

214 tive IgA deficiency rather than seronegative celiac disease.

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

216 f villous atrophy in children with potential celiac disease.

217 sinus thrombosis unveiling the diagnosis of celiac disease.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

232 velopment of autoimmune disorders, including celiac disease.

233 sures in biopsy specimens from patients with celiac disease.

234 thelial lymphocytes, or serologic markers of celiac disease.

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

236 after oral gluten challenge of patients with celiac disease.

237 r fracture) were associated with undiagnosed celiac disease.

238 blistering condition seen in the context of celiac disease.

239 NPV to populations with lower prevalence of celiac disease.

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

241 ed assay accurately identifies patients with celiac disease.

242 1.1% of participants to avoid gluten without celiac disease.

243 ean level of hemoglobin than persons without celiac disease.

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

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

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

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

248 vement after gluten withdrawal in absence of celiac disease.

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

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

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

252 prevalence of brain injury in patients with celiac disease.

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

254 nity medical center and their progression to celiac disease.

255 h increased risks of subsequent diagnosis of celiac disease.

256 g duodenal biopsy confirmed the diagnosis of celiac disease.

257 organ-specific autoimmune diseases including celiac disease.

258 lantoaxial instability, thyroid disease, and celiac disease.

259 time points and adults later diagnosed with celiac disease.

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

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

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

263 mposite extrudates were formulated to combat celiac enteropathy.

264 iled neurochemical characterization of mouse celiac ganglia and noradrenergic nerves in two target ti

265 Celiac ganglia are important sites of signal integration

266 demonstrate that principal neurons of mouse celiac ganglia have less neurochemical diversity than re

267 eformed fibrils (PFFs) into the stellate and celiac ganglia induces spreading of alpha-Syn pathology

268 ten ataxia (GA), wheat allergy (WA), and non-celiac gluten sensitivity (NCGS) are the five major GRDs

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

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

271 , up to 50% of peptides identified contained celiac-immunogenic motifs, and consumption of wheat beer

272 n structure, conformation, functionality and celiac-immunotoxicity, a central composite design with t

273 been reported regarding the effect on gluten celiac-immunotoxicity.

274 Blood and intestine, mesenterial and celiac lymph nodes were collected; cells and cytokines w

275 veloped from duodenal biopsies from both non-celiac (NC) and celiac (CD) patients, we explored the co

276 A vast majority of mouse celiac neurons express a noradrenergic phenotype, which

277 This profile suggests celiac neurons integrate input from many sources to infl

278 y published datasets providing insights into celiac pathogenesis using clinical pathology FFPE sample

279 -in (Ig KI) mice that express a prototypical celiac patient-derived anti-TG2 B cell receptor equally

280 approach to assess recent gluten exposure in celiac patients and appears to accurately predict the ab

281 et (GFD) is the only effective treatment for celiac patients and assessing adherence to this diet is

282 tic duodenum gene expression in 54 pediatric celiac patients and non-celiac controls, and we validate

283 ) as a biomarker monitoring GFD adherence in celiac patients and to evaluate the concordance of the r

284 Approximately 24% (18 of 76) of the celiac patients consuming a GFD exhibited Marsh II-III m

285 nducted involving 22 de novo CD patients, 77 celiac patients consuming a GFD, and 13 nonceliac subjec

286 s of SBA cases detected in a large cohort of celiac patients diagnosed in a single tertiary care cent

287 for assessing adherence to the GFD in adult celiac patients in Iran.

288 In contrast, 97% (31 of 32) of the celiac patients without duodenal damage had no detectabl

289 of mature epithelial metabolic functions in celiac patients, overlapping substantially with the Croh

290 been claimed to abolish gluten toxicity for celiac patients.

291 sumption of wheat beers would pose risks for celiac patients.

292 e gluten-free sourdough breads, suitable for celiac people and "source of proteins".

293 he clinical scenarios encompassed by the non-celiac self-reported wheat sensitivity (NCSRWS) might be

294 Best Practice Advice 10: Celiac serology has a guarded role in the detection of c

295 und to have CD first by intestinal biopsies, celiac-specific serology should be undertaken as a confi

296 ry young children before the introduction of celiac-specific serology.

297 ferent vagus nerve fibers terminating in the celiac-superior mesenteric ganglia form varicose-like st

298 gic neurons in the DMN, which project to the celiac-superior mesenteric ganglia, significantly increa

299 We aimed to define the core celiac transcriptomic signature and pathologic pathways

300 fice of right renal artery (RRA), orifice of celiac truncus (CT), orifice of superior mesenteric arte

301 dentified as one of the main triggers of non-celiac wheat sensitivity (NCWS).