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1 ctive Crohn's, treated coeliac and untreated coeliac.
2 tential to mitigate the problems confronting coeliacs.
3 ts were stratified by adenopathy (no vs yes [coeliac absent] vs yes [coeliac present <=2 cm]) and ran
5 erent activity is carried in the coeliac and coeliac accessory branches of the subdiaphragmatic vagus
6 e results indicate that afferent activity in coeliac and accessory coeliac vagal branches is involved
7 is vagal afferent activity is carried in the coeliac and coeliac accessory branches of the subdiaphra
14 CI: 0.740 to 1.984, p < 0.001), (3) treated coeliacs and untreated coeliacs (SMD = 0.722 95% CI: 0.2
15 of the descending aorta at the level of the coeliac arteries, a stimulus that elevated blood pressur
18 Glossodynia on GFD was more prevalent in the coeliac cohort than in the controls (14% vs 6%, p < 0.00
22 RD0.1), Urticaria (1.58[1.57-1.60], RD1.9), Coeliac disease (1.42[1.37-1.47], RD0.1), Ulcerative col
23 ad positive antibody results, of whom 14 had coeliac disease (11 EMA positive, three EMA negative).
25 son's disease (IRR 26.5 [95% CI 17.3-40.7]), coeliac disease (28.4 [25.2-32.0]), and thyroid disease
26 ildren with IgE-mediated wheat allergy (WA), coeliac disease (CD) and Helicobacter pylori infection (
30 studies have shown that the knowledge about coeliac disease (CD) is not satisfactory among healthcar
33 for proteins with epitopes that can trigger coeliac disease (CD), and several contain a 33-mer pepti
35 Despite the considerable health impact of coeliac disease (CD), reliable estimates of the impact o
40 loci shared between two autoimmune diseases: coeliac disease (CeD) and rheumatoid arthritis (RA).
46 l syndrome was significantly associated with coeliac disease (p=0.004, odds ratio=7.0 [95% CI 1.7-28.
47 osed with active CD, CD on a GFD, Refractory coeliac disease (RCD) type I and II, and enteropathy ass
51 lude the association of Down's syndrome with coeliac disease and Alzheimer's disease, and improved me
52 enes at HLA-unlinked loci also predispose to coeliac disease and are probably stronger determinants o
55 nded to occur rapidly after the diagnosis of coeliac disease and cumulative survival dropped in the f
57 ersensitivity (FHS), including food allergy, coeliac disease and food intolerance, is a major public
58 falls of vitamin A supplementation in active coeliac disease and have enabled identification of oat a
59 untries experienced: poor dietary intake for coeliac disease and inflammatory bowel disease, cultural
60 ng, the well established association between coeliac disease and insulin dependent diabetes mellitus,
64 tic susceptibilities that are both unique to coeliac disease and overlap with other autoimmune diseas
65 mall bowel Crohn's disease, complications of coeliac disease and surveillance of polyposis syndromes.
66 e the possible concealed burden of untreated coeliac disease and the effects of a gluten-free diet.
67 especially regarding the natural history of coeliac disease and the effects on long-term health for
72 designed for the selective amplification of coeliac disease associated alleles (DQA1*05, DQB1*02, DQ
73 ies against tissue transglutaminase (marking coeliac disease autoimmunity) also appeared early (2-4 y
76 gliadin antibodies are a marker of untreated coeliac disease but can also be found in individuals wit
77 eurological syndromes may be associated with coeliac disease but it is unclear whether these are dire
78 (age and sex matched) were investigated for coeliac disease by analysis of serum IgA antigliadin, Ig
82 y of the mechanism of the immune response in coeliac disease could provide insight into the mechanism
85 resence of abdominal symptoms at the time of coeliac disease diagnosis, long diagnostic delay and fem
89 iopsy did not identify any causes other than coeliac disease for iron deficiency anaemia, suggesting
90 astrointestinal symptom rating scale (GSRS), coeliac disease GSRS, and Bristol stool form scale (BSFS
91 as lost, at which point 25% of patients with coeliac disease had detectable gluten in faeces, whilst
92 in developing new strategies for preventing coeliac disease has motivated efforts to identify cereal
93 manifestations in patients with established coeliac disease have been reported since 1966, it was no
97 barley and rye, or gluten protein, can cause coeliac disease in individuals not tolerating gluten.
98 g offers additional sensitivity in detecting coeliac disease in individuals who have self-prescribed
100 om group 1 revealed histological evidence of coeliac disease in nine (35%), non-specific duodenitis i
105 Currently, the only effective treatment for coeliac disease is a lifelong strict gluten-free diet; h
111 Epidemiological studies have shown that coeliac disease is as common in parts of Asia, Africa an
122 e molecular basis for the HLA association in coeliac disease is well defined, and B cells have a clea
123 was to determine the cost-effectiveness of a coeliac disease mass screening at 12 years of age, takin
125 ion is difficult because occult sub-clinical coeliac disease occurs commonly and background prevalenc
127 d with deteriorated health, and persons with coeliac disease often wait a long time for their diagnos
129 with cerebellar ataxia and SG diagnosed with coeliac disease or gluten sensitivity, 15% had RFC1 expa
131 gate these issues in a large cohort of adult coeliac disease patients both at diagnosis and while on
132 d messenger RNA (mRNA) expression changes in coeliac disease patients challenged with gluten using PA
137 a cytokine greatly upregulated in the gut of coeliac disease patients, retinoic acid rapidly activate
144 of coeliac disease is achieved by combining coeliac disease serology and small intestinal mucosal hi
148 to assess changes over time in prevalence of coeliac disease symptoms/associated medical conditions,
149 was higher in patients with newly diagnosed coeliac disease than Controls (median [Q1, Q3] coeliac d
150 t, at diagnosis and on GFD, in patients with coeliac disease than in the controls, and they were asso
151 of course: patients with a new diagnosis of coeliac disease that do not improve despite a strict glu
153 ee diet, rapid progression from symptom-free coeliac disease to coeliac disease with symptoms, long d
159 after 12 weeks of treatment in patients with coeliac disease undergoing gluten challenge, was not sig
162 significant evidence in favour of linkage to coeliac disease was obtained for chromosomes 3q27, 5q33.
163 gical dysfunction is a known complication of coeliac disease we have investigated the frequency of an
165 coeliac disease type 2 is a rare subtype of coeliac disease with high mortality rates; interleukin 1
167 ression from symptom-free coeliac disease to coeliac disease with symptoms, long delay from celiac di
168 in our understanding of the pathogenesis of coeliac disease(4), the respective roles of disease-pred
169 orwegian Human Milk Study, and Prevention of Coeliac Disease) that collaborate in the European Union-
171 opsy samples from 42 patients with untreated coeliac disease, 37 treated patients, and 18 controls, w
172 gluten-free diet is the only means to manage coeliac disease, a permanent immune intolerance to glute
173 ren participated and 240 were diagnosed with coeliac disease, and a study involving members of the Sw
174 ed age 18-80 years, a confirmed diagnosis of coeliac disease, and adherence to a gluten-free diet for
175 d urine of children with ulcerative colitis, coeliac disease, and Crohn's disease at diagnosis and fr
176 tunity to both increase our understanding of coeliac disease, and develop new therapeutic strategies.
178 or all immune recognition of wheat gluten in coeliac disease, and to explore if the tissue transgluta
179 ases such as systemic lupus erythematosus or coeliac disease, antibodies to specific membrane targets
180 esis and improving diagnostic strategies for coeliac disease, but further work into the treatment of
181 s have mainly been studied: Turner syndrome, coeliac disease, cystic fibrosis, growth hormone deficie
182 -related extra-intestinal diseases including coeliac disease, diabetes mellitus type 1, bronchial ast
183 n our genetic and immunological knowledge of coeliac disease, early introduction of a gluten-free die
184 ore, similar to the involvement of gluten in coeliac disease, Epstein-Barr virus (EBV) infection is n
185 ina propria that is characteristic of active coeliac disease, expresses the predisposing HLA-DQ8 mole
186 ociated with systemic lupus erythematosus or coeliac disease, have not in general disclosed consisten
187 erstanding of inflammatory bowel disease and coeliac disease, hindered by language and literacy barri
188 nded our knowledge of the long-term risks of coeliac disease, in addition to excluding infertility as
190 testinal and endocrine diseases, focusing on coeliac disease, inflammatory bowel disease, diabetes, a
192 and sent to 4000 individuals with diagnosed coeliac disease, requesting information on respondents'
193 present in cereal proteins that do not cause coeliac disease, Shan and colleagues suggest that genera
194 data, clinical presentation and treatment of coeliac disease, time and place of diagnosis and presenc
196 diseases including asthma, Crohn's disease, coeliac disease, vitiligo, multiple sclerosis and type 1
198 ultiple sclerosis (MS) is similar to that of coeliac disease, with human leukocyte antigen (HLA) bein
240 eliac disease than Controls (median [Q1, Q3] coeliac disease: 2104 pg/mL 1493, 2457] vs Controls: 938
241 re), 58% a TSH dosage (7%) and 8% a test for coeliac diseases (1%) and the year after: 44% (8%), 43%
242 selected members of the Swedish Society for Coeliacs, divided into equal-sized age- and sex strata;
244 nosis and presence of thyroidal disease, non-coeliac food intolerance or gastrointestinal co-morbidit
245 in isolated superior cervical ganglia (SCG), coeliac ganglia (CG), and superior mesenteric ganglia (S
250 DiI crystals were placed bilaterally on the coeliac ganglia, labeled piriform and fusiform pregangli
251 dominal sympathetic (mesenteric) nerves, the coeliac ganglia, or on the rostral three somatic spinal
252 in parallel to disease progression, whereas coeliac ganglionectomy led to the disintegration of adve
256 be a potential alternative for reduction of coeliac immunological activities in gluten proteins.
257 tomach (nucleus gelatinosus); 5) hepatic and coeliac nerves (nucleus subpostrema); and 6) carotid bod
258 se-specific mortality compared to those with coeliac node metastasis (HR 0.71, 95% CI 0.40-1.27).
260 patients with distal oesophageal cancer with coeliac node metastasis seem to have a similarly poor su
263 d no coeliac node metastasis, 56 (12.6%) had coeliac node metastasis, and 44 (9.9%) had more distant
265 Compared to coeliac node negative patients, coeliac node positive patients were at a 52% increased r
270 diet (type A cases) and previously diagnosed coeliac patients that initially improved on a gluten-fre
275 ons (A and B cases) and sex- and age-matched coeliac patients who normally responded to a gluten-free
280 how unequivocally that: (a) receptors in the coeliac-portal circulation are more sensitive in amplify
281 enopathy (no vs yes [coeliac absent] vs yes [coeliac present <=2 cm]) and randomly assigned (1:1) to
283 ties and cost effectiveness of pre-endoscopy coeliac screening with Simtomax in anaemia; 3) whether o
284 high risk, but those found to have negative coeliac serology are very unlikely to develop the diseas
286 blood count and C-reactive protein, negative coeliac serology, and no evidence of suicidal ideation.
287 MR between: (1) healthy controls and treated coeliacs (SMD = 0.409 95% CI 0.034 to 0.783, p = 0.032),
288 < 0.001), (3) treated coeliacs and untreated coeliacs (SMD = 0.722 95% CI: 0.286 to 1.157, p = 0.001)
289 = 0.032), (2) healthy controls and untreated coeliacs (SMD = 1.362 95% CI: 0.740 to 1.984, p < 0.001)
291 ical, stellate, paravertebral chain ganglia, coeliac/superior mesenteric and inferior mesenteric gang
292 aled that the mean time between the onset of coeliac symptoms and being diagnosed was above 13 years.
293 Resected arterial segments included the coeliac trunk (50), hepatic artery (29), superior mesent
294 ere also obtained across the aorta above the coeliac trunk, superior mesenteric vein, splenic vein an
295 ositive in 8/9 first-degree relatives having coeliac-type mucosal lesions of grade Marsh 2 (n = 3) or
296 t afferent activity in coeliac and accessory coeliac vagal branches is involved in the regulation of
298 ents were activated: splenic sympathetic and coeliac vagus nerve activities increased in parallel to
299 ) while pooled LMRs in untreated and treated coeliac were 0.133 (95% CI: 0.089-0.178) and 0.037 (95%
300 n help improve the total dietary intake of a coeliac while not negating on the quality properties of