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      Frequently Asked Questions About Celiac Disease   04/07/2018

      This Celiac.com FAQ on celiac disease will guide you to all of the basic information you will need to know about the disease, its diagnosis, testing methods, a gluten-free diet, etc.   Subscribe to Celiac.com's FREE weekly eNewsletter   What are the major symptoms of celiac disease? Celiac Disease Symptoms What testing is available for celiac disease?  Celiac Disease Screening Interpretation of Celiac Disease Blood Test Results Can I be tested even though I am eating gluten free? How long must gluten be taken for the serological tests to be meaningful? The Gluten-Free Diet 101 - A Beginner's Guide to Going Gluten-Free Is celiac inherited? Should my children be tested? Ten Facts About Celiac Disease Genetic Testing Is there a link between celiac and other autoimmune diseases? Celiac Disease Research: Associated Diseases and Disorders Is there a list of gluten foods to avoid? Unsafe Gluten-Free Food List (Unsafe Ingredients) Is there a list of gluten free foods? Safe Gluten-Free Food List (Safe Ingredients) Gluten-Free Alcoholic Beverages Distilled Spirits (Grain Alcohols) and Vinegar: Are they Gluten-Free? Where does gluten hide? Additional Things to Beware of to Maintain a 100% Gluten-Free Diet What if my doctor won't listen to me? An Open Letter to Skeptical Health Care Practitioners Gluten-Free recipes: Gluten-Free Recipes
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    DIAGNOSTIC VALUE OF CONFOCAL ENDOMICROSCOPY IN CELIAC DISEASE


    Jefferson Adams

    Celiac.com 04/27/2010 - A team of clinicians recently assessed the diagnostic value of confocal endomicroscopy in celiac disease.


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    Clinicians U. Günther, S. Daum, F. Heller, M. Schumann, C. Loddenkemper, M. Grünbaum, M. Zeitz, and C. Bojarski made up the research team. They are variously affiliated with the  Medical Clinic of Gastroenterology, Rheumatology and Infectious Diseases, and with the Department of Pathology, Charité of the Campus Benjamin Franklin of University Medicine Berlin, Germany.

    Studies by Gutschmidt, by Henker and others have shown that, even in the face of greater awareness and more widespread blood testing, a number of countries suffer from low rates of celiac disease detection.

    Patchiness of the mucosal and submucosal changes associated with celiac disease impedes proper celiac diagnosis, and contributes to a small, but important sampling error among those assessed.

    Some clinicians feel that the problem might be resolved somewhat by modifying the endoscopic screening process to include real-time assessment of the duodenal morphology. Better endoscopic and imaging procedures will mean better diagnostic accuracy of biopsy specimens.

    One early step toward improved gathering of targeted biopsies in celiac disease patients lies in using magnification endoscopy, either alone, or together with high-resolution narrow-band imaging. This method offers better ability to detect patchy villous atrophy sites in the duodenum.

    However, neither magnification, nor narrow-band imaging techniques can detect increased number of intraepithelial lymphocytes (IELs).

    Confocal endomicroscopy (CEM) permits live, real-time histology with a 1000x magnification during endoscopy. Recently, a prospective pilot study for the first time showed CEM to enable effective live, real-time diagnosis and evaluation of celiac disease.  Researchers compared endomicroscopic findings during live, real-time endoscopy with histological findings graded according to Marsh classification.

    The research team used CEM to examine twenty-four patients with celiac disease and six patients with refractory celiac disease, all following a gluten-free diet.

    The team evaluated duodenal mucosa by CEM and by conventional histological analysis for villous atrophy, crypt hyperplasia, and increased numbers of intraepithelial lymphocytes (IELs > 40/100 enterocytes).

    They then compared the CEM to the histology results for sensitivity, specificity, and inter-observer variability using Marsh classification scores.

    As control subjects, the team used thirty patients without celiac disease, but who were undergoing routine upper gastrointestinal endoscopy.

    Using conventional histology on the 30 patients with celiac disease, the team found 23 cases with villous atrophy and crypt hyperplasia, and 27 cases of increased IELs.

    Using CEM, the team found 17 cases of villous atrophy, 12 cases of crypt hyperplasia, and 22 cases of increased IELs. The CEM results compared favorably to those of conventional histology for villous atrophy, for which CEM showed a sensitivity of 74%, and for increased numbers of IELs, for which CEM showed a sensitivity of 81%. However, the CEM results were lacking for detecting crypt hyperplasia, for which CEM showed a sensitivity of 52%. 

    The κ values for determination of inter-observer variability were 0.90 for villous atrophy, 1.00 for crypt hyperplasia, and 0.84 for IEL detection. For the 30 control patients, both traditional histology and CEM revealed normal duodenal architecture with overall specificity of 100%.

    From these results, the team concluded that the assessment of duodenal histology by CEM in patients with celiac disease is sensitive and specific in determining increased numbers of IELs and villous atrophy, but inadequate for detecting crypt hyperplasia. Until improvements are made, CEM is not suitable for use in diagnosing celiac disease.


    SOURCE: Endoscopy 2010; 42:197–202.


    Image Caption: Confocal Endomicroscopy in Celiac Disease
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    admin

    The following abstract was submitted to celiac.com directly by William Dickey, Ph.D., a leading celiac disease researcher and gastroenterologist who practices at Altnagelvin Hospital, Londonderry, Northern Ireland.
    Scandinavian Journal of Gastroenterology 2005; 40: 1240-3.
    Dickey W, Hughes DF, McMillan SA.
    Celiac.com 09/27/2005 - What does a positive endomysial antibody (EmA) test mean if the biopsy does not show villous atrophy? The authors studied 35 patients where this was the case. In the authors practice, these patients account for 10% of all EmA positives.
    Firstly, the lack of villous atrophy did not necessarily mean a normal biopsy: 14 patients had excess inflammatory cells (lymphocytes) consistent with a mild abnormality of gluten sensitivity.
    Secondly, many of these patients had typical celiac features: twelve had a family history of celiac, five had dermatitis herpetiformis and thirteen had osteopenia or osteoporosis on DEXA scan.
    After discussion, 27 patients opted to take a gluten-free diet from the first biopsy: 26 of these had clinical improvement. Seven of eight patients who persisted with a normal diet developed villous atrophy on follow-up biopsies.
    The authors conclude that a positive EmA result indicates gluten sensitivity even if biopsies do not show villous atrophy. While a biopsy remains important as a baseline reference, these patients should be offered a gluten-free diet to allow clinical improvement and prevent the development of villous atrophy. There may be no such thing as a "false positive" EmA, although the authors emphasise that the same conclusion cannot yet be applied to tissue transglutaminase antibody results.

    Jefferson Adams
    Celiac.com 05/11/2012 - Horses are susceptible to inflammatory small bowel disease, and the condition effects horses in much the same way as it effects humans.
    As with its human counterpart, equine inflammatory small bowel disease (ISBD) is an idiopathic pathologic condition that seems to be growing more and more common.
    A research team recently conducted a study to examine the possibility that gluten may play a role in equine ISBD.
    The researchers were J.H. van der Kolk, L.A. van Putten, C.J. Mulder, G.C. Grinwis, M. Reijm, C.M. Butler, B.M. von Blomberg of the Department of Equine Sciences, Medicine Section, Faculty of Veterinary Medicine at the University of Utrecht, in Utrecht, in the Netherlands.
    For their study, the team assessed antibodies that are known to be important in the diagnosis of human celiac disease: IgA antibodies to human recombinant and guinea pig tissue-transglutaminase (TGA), native gliadin (AGA), deamidated-gliadin-peptides (DGPA), and primate and equine endomysium (EMA).
    The team measured these antibodies using blood samples from three different groups of horses: Twelve ISBD affected horses on a gluten-rich diet, along with two control groups.
    The first control group included 22 horses on a gluten-rich diet, and the second included 25 horses on a gluten-poor diet.
    The researchers measured differences (p < 0.05) in the groups using the Wilcoxon test.
    They found that both ISBD-affected horses and gluten-rich control group had significantly (p < 0.0004) higher hrTGA titers than gluten-poor control group.
    However, ISBD horses did not show significantly higher levels of any of the celiac disease related antibodies when compared to gluten-rich controls.
    Still, They found significantly higher antibody levels (TGA, EMA and DGPA) in one of the ISBD horses.
    They put that horse, 14-year-old stallion, on a gluten-free ration for 6 months. They then reassessed his antibodies and found a significant reduction of antibody levels, along with clinical recovery associated with improved duodenal histopathology.
    The researchers write that this is the first such study assessing gluten-related antibodies in horses and that the results suggest a potential pathogenic role of gluten in at least some cases of equine ISBD.
    These clinical results suggest that further study into the immunologic basis of possible gluten-sensitive enteropathy in horses might have important implications for the human manifestation of the disease.
    Source:
    Vet Q. 2012 Apr 10.

    Jefferson Adams
    Celiac.com 05/09/2013 - Previous studies have shown an immunologic response primarily directed against transglutaminase (TG)6 in patients with gluten ataxia (GA). A team of researchers set out to see if Transglutaminase 6 antibodies could be helpful in the diagnosis of gluten ataxia.
    The team included M. Hadjivassiliou, P. Aeschlimann, D.S. Sanders, M. Mäki, K. Kaukinen, R.A. Grünewald, O. Bandmann, N. Woodroofe, G. Haddock, and D.P. Aeschlimann.
    They are variously affiliated with the Departments of Neurology (M.H., R.A.G., O.B.) and Gastroenterology (D.S.S.) at Royal Hallamshire Hospital in Sheffield, UK, the Matrix Biology & Tissue Repair Research Unit (P.A., D.P.A.) of the School of Dentistry at Cardiff University in Cardiff, UK, the Department of Paediatrics (M.M., K.K.) of the School of Medicine at University of Tampere in Finland, and the Department of Biological Sciences (N.W., G.H.) at Sheffield Hallam University in Sheffield, UK.
    For their prospective cohort study, the team looked at patients from the ataxia, gluten/neurology, celiac disease (celiac disease), and movement disorder clinics based at Royal Hallamshire Hospital (Sheffield, UK) and from the celiac disease clinic at Tampere University Hospital in Tampere, Finland.
    Patients were broken into groups that included idiopathic sporadic ataxia, gluten ataxia, celiac disease, and neurology, along with healthy control subjects.
    The team screened all subjects for TG6 antibodies, and conducted duodenal biopsies on all patients with positive blood screens. In addition, they analyzed biopsies from 15 consecutive patients with idiopathic sporadic ataxia and negative serology for gluten-related disorders for immunoglobulin A deposits against TG.
    They found TG6 antibodies in 21 of 65 (32%) patients with idiopathic sporadic ataxia, in 35 of 48 (73%) patients with GA, in 16 of 50 (32%) patients with celiac disease, in 4 of 82 (5%) neurological control subjects, and in just 2 of 57 (4%) healthy control subjects.
    The results showed that forty-two percent of patients with GA had enteropathy, as did 51% of patients with ataxia and TG6 antibodies.
    Five of 15 consecutive patients with idiopathic sporadic ataxia had immunoglobulin A deposits against TG2, 4 of which subsequently tested positive for TG6 antibodies.
    Follow-up screens showed that one year of gluten-free diet left TG6 antibody levels greatly reduced or undetectable.
    The study shows that antibodies against TG6 are gluten-dependent and that they seem to be a sensitive and specific indicator of gluten ataxia.
    Source:
    Neurology. 2013 Apr 10.

    Jefferson Adams
    Celiac.com 07/21/2014 - The presence of HLA haplotype DR3–DQ2 or DR4–DQ8 is associated with an increased risk of celiac disease. In addition, nearly all children with celiac disease have serum antibodies against tissue transglutaminase (tTG).
    A research team recently set out to determine the risk of celiac disease autoimmunity and celiac disease, by age and by halpotype, in children. The research team included Edwin Liu, M.D., Hye-Seung Lee, Ph.D., Carin A. Aronsson, M.Sc., William A. Hagopian, M.D., Ph.D., Sibylle Koletzko, M.D., Ph.D., Marian J. Rewers, M.D., M.P.H., George S. Eisenbarth, M.D., Ph.D., Polly J. Bingley, M.D., Ezio Bonifacio, Ph.D., Ville Simell, M.Sc., and Daniel Agardh, M.D., Ph.D. for the TEDDY Study Group.
    The team studied 6403 children with HLA haplotype DR3–DQ2 or DR4–DQ8 prospectively from birth in the United States, Finland, Germany, and Sweden. The study’s primary end point was the development of celiac disease autoimmunity, which the team defined as the presence of tTG antibodies on two consecutive tests at least 3 months apart. The secondary end point was the development of celiac disease itself, which they defined as either a diagnosis on biopsy or persistently high levels of tTG antibodies.
    The average follow-up was 5 years, with an overall range of 46 to 77 months. A total of 786 children (12%) developed celiac disease autoimmunity. A total of 350 children underwent biopsy, and 291 of those were diagnosed with celiac disease. Another 21 children did not undergo biopsy, but showed persistently high levels of tTG antibodies.
    For children with a single DR3–DQ2 haplotype, rates of celiac disease autoimmunity and celiac disease by the age of 5 years were 11% and 3%, respectively. For those with two copies (DR3–DQ2 homozygosity) rates of celiac disease autoimmunity and celiac disease by the age of 5 years were 26% and 11%, respectively.
    The adjusted hazard ratios for celiac disease autoimmunity were 2.09 (95% confidence interval [CI], 1.70 to 2.56) among children with one gene, and 5.70 (95% CI, 4.66 to 6.97) among children with both genes, as compared with children who had the lowest-risk genotypes (DR4–DQ8 heterozygotes or homozygotes).
    Living in Sweden was also independently associated with an increased risk of celiac disease autoimmunity (hazard ratio, 1.90; 95% CI, 1.61 to 2.25). Children with the HLA haplotype DR3–DQ2, especially homozygotes, were found to be at high risk for celiac disease autoimmunity and celiac disease early in childhood.
    People in Sweden face a higher risk for celiac disease autoimmunity and celiac disease than residents of other countries. These finding highlight the importance of studying environmental factors associated with celiac disease.
    Source:
    N Engl J Med 2014; 371:42-49July 3, 2014. DOI: 10.1056/NEJMoa1313977

  • Recent Articles

    Jefferson Adams
    Celiac.com 04/23/2018 - A team of researchers recently set out to learn whether celiac disease patients commonly suffer cognitive impairment at the time they are diagnosed, and to compare their cognitive performance with non-celiac subjects with similar chronic symptoms and to a group of healthy control subjects.
    The research team included G Longarini, P Richly, MP Temprano, AF Costa, H Vázquez, ML Moreno, S Niveloni, P López, E Smecuol, R Mazure, A González, E Mauriño, and JC Bai. They are variously associated with the Small Bowel Section, Department of Medicine, Dr. C. Bonorino Udaondo Gastroenterology Hospital; Neurocience Cognitive and Traslational Institute (INECO), Favaloro Fundation, CONICET, Buenos Aires; the Brain Health Center (CESAL), Quilmes, Argentina; the Research Council, MSAL, CABA; and with the Research Institute, School of Medicine, Universidad del Salvador.
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    J Clin Gastroenterol. 2018 Mar 1. doi: 10.1097/MCG.0000000000001018.

    Connie Sarros
    Celiac.com 04/21/2018 - Dear Friends and Readers,
    I have been writing articles for Scott Adams since the 2002 Summer Issue of the Scott-Free Press. The Scott-Free Press evolved into the Journal of Gluten Sensitivity. I felt honored when Scott asked me ten years ago to contribute to his quarterly journal and it's been a privilege to write articles for his publication ever since.
    Due to personal health reasons and restrictions, I find that I need to retire. My husband and I can no longer travel the country speaking at conferences and to support groups (which we dearly loved to do) nor can I commit to writing more books, articles, or menus. Consequently, I will no longer be contributing articles to the Journal of Gluten Sensitivity. 
    My following books will still be available at Amazon.com:
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    Jefferson Adams
    Celiac.com 04/20/2018 - A digital media company and a label data company are teaming up to help major manufacturers target, reach and convert their desired shoppers based on dietary needs, such as gluten-free diet. The deal could bring synergy in emerging markets such as the gluten-free and allergen-free markets, which represent major growth sectors in the global food industry. 
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    "Brands with very specific product benefits, gluten-free for example, require precise targeting to efficiently reach and convert their desired shoppers,” says Todd Morris, President of Catalina's Go-to-Market organization, adding that “Catalina offers the only purchase-based targeting solution with this capability.” 
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    Source:
    fdfworld.com

    Jefferson Adams
    Celiac.com 04/19/2018 - Previous genome and linkage studies indicate the existence of a new disease triggering mechanism that involves amino acid metabolism and nutrient sensing signaling pathways. In an effort to determine if amino acids might play a role in the development of celiac disease, a team of researchers recently set out to investigate if plasma amino acid levels differed among children with celiac disease compared with a control group.
     
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    Source:
    PLoS One. 2018; 13(3): e0193764. doi: & 10.1371/journal.pone.0193764

    Jefferson Adams
    Celiac.com 04/18/2018 - To the relief of many bewildered passengers and crew, no more comfort turkeys, geese, possums or other questionable pets will be flying on Delta or United without meeting the airlines' strict new requirements for service animals.
    If you’ve flown anywhere lately, you may have seen them. People flying with their designated “emotional support” animals. We’re not talking genuine service animals, like seeing eye dogs, or hearing ear dogs, or even the Belgian Malinois that alerts its owner when there is gluten in food that may trigger her celiac disease.
    Now, to be honest, some of those animals in question do perform a genuine service for those who need emotional support dogs, like veterans with PTSD.
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    Fresh from an unsavory incident with an “emotional support” peacock incident, United Airlines has followed Delta’s lead and set stricter rules for emotional support animals. United’s rules also took effect March 1, 2018.
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    Source:
    cnbc.com