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      Frequently Asked Questions About Celiac Disease   04/24/2018

      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 is Celiac Disease and the Gluten-Free Diet? 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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Found 35 results

  1. I was wondering if someone can help me understand my results. I got wishy washy responses from two different doctors and I am still pretty confused. I attached an image of my results, but in case you aren't able to view it, my Gliadin IgA is high, but everything else seems to be in low and in normal range. Anyone know what this means? At the time of this test, I was on a pretty low to no-gluten diet. I'd appreciate any insight you all can provide!
  2. Celiac.com 04/17/2018 - Could the holy grail of gluten-free food lie in special strains of wheat that lack “bad glutens” that trigger the celiac disease, but include the “good glutens” that make bread and other products chewy, spongey and delicious? Such products would include all of the good things about wheat, but none of the bad things that might trigger celiac disease. A team of researchers in Spain is creating strains of wheat that lack the “bad glutens” that trigger the autoimmune disorder celiac disease. The team, based at the Institute for Sustainable Agriculture in Cordoba, Spain, is making use of the new and highly effective CRISPR gene editing to eliminate the majority of the gliadins in wheat. Gliadins are the gluten proteins that trigger the majority of symptoms for people with celiac disease. As part of their efforts, the team has conducted a small study on 20 people with “gluten sensitivity.” That study showed that test subjects can tolerate bread made with this special wheat, says team member Francisco Barro. However, the team has yet to publish the results. Clearly, more comprehensive testing would be needed to determine if such a product is safely tolerated by people with celiac disease. Still, with these efforts, along with efforts to develop vaccines, enzymes, and other treatments making steady progress, we are living in exciting times for people with celiac disease. It is entirely conceivable that in the not-so-distant future we will see safe, viable treatments for celiac disease that do not require a strict gluten-free diet. Read more at Digitaltrends.com , and at Newscientist.com
  3. Hey guys! Recently diagnosed officially after aoiding gluten for 12 years. It took me 3 doctors to find someone who would come at the issue with a non-biased POV. I ended up doing a gluten challenge and got a blood test and biopsy. Today I got a blood test I took last year prior to the gluten challenge and the Gliadin IGA was 78.0. I have two questions; 1) Dr who ordered the blood test told me a lot of things that were not accurate abt celiac and ruled it out totally. With a Gliadin IGA of 78, that’s just flat out wrong, isn’t it? I mean doesn’t it indicate a liklihood of celiac of like 97%? 2) Whatever diet I was eating for 14 yrs was not adequate to what I need to live with celiac based on this test, right? Just checking. I think that’s what it means and that I need to tighten up my gluten-free diet a little in light of the dx? I know a lotta you guys are serious blood test gurus so I’ll put this out there. Thanks, fam!
  4. So a couple years ago I was tested for celiac... Ttg IgG/IgA were all negative DGA IgG/IgA were all negative AGA IgG: Positive AGA IgA Negative HLADQB1*02 Negative HLADQB1*03:02 Negative HLADQA1*05 Positive Biopsies have all been negative. I suffer from Hashimoto's thyroiditis and I just feel miserable with all the body aches and brain fog. My son was born back in July and I'm just so tired of not feeling well and I really want to finally feel good and enjoy life to the fullest. I'm thinking of asking for my labs to be repeated again and see. I'm just wondering if it is possible for me to still have celiac or if I'm just looking for something that just isn't there because I'm desperate for answers... Appreciate any input!! Thank you
  5. Iron: 17 mcg/dL (Low) November 11, 2016 Ferritin: 1.8 ng/mL (Low) November 11, 2016 RBC: 4.05x10^6/uL (Low) November 11, 2016 Hemoglobin: 8.5 gm/dL (Low) November 11, 2016 Vitamin D: 25.7 ng/mL (Low) February 22, 2017 ANA Profile : February 27, 2017 FANA: Positive FANA Titer: 1:640 FANA Pattern: Homogenous Gliadin IgA: 2 units June 29, 2017 Gliadin IgG: 3 units June 29,2017 TTG Ab IgA: <1 units/mL June 29, 2017 TTG Ab IgG: <1 units/mL June 29, 2017 Immunoglobulin A: 59.1 mg/Dl (Low) July 10, 2017 Immunoglobulin M: 44.2 mg/Dl (Low) July 10,2017 Immunoglobulin G: 1010.0 mg/Dl (Normal?) July 10, 2017 Immunoglobulin E: 5 KU/L July 10,2017 My RBC and Hemoglobin have come up and are normal. My iron levels will get high (too high) when I take 65 mg elemental iron twice a day for several weeks but my ferritin has never gotten over 42 ng/mL. When I stop taking my iron supplement my iron and ferritin plummet in just a matter of weeks. My hair is falling out, I get rapid heartbeat when I get too low on iron and if I get my iron too high. My whole body hurts especially my finger joints, back , knees and really all of my joints. Going to the bathroom at least 2 times day and sometimes up to 5 times a day. Extreme fatigue, Brain fog, extremely emotional and irritable. I just went gluten free July 1, 2017 and am starting to feel better. Joints feel better, I can sleep better, my mood is better. Celiac or maybe just gluten sensitive? Any thoughts? What do my labs say about me?
  6. Hello! This is my first post. My big question is about Gliadin IgG. I was tested in 2004 and had a high positive at 64 (24 being positive). My Dr at the time told me I should cut back on gluten and diagnosed me with Sjogrens Syndrome (even though I was B12 deficient, anemic, and having such bad acid reflux that I would get sores all over the back of my throat). Recently I was diagnosed with Lupus (SLE) and asked to be tested for Celiacs. My Gliadin tests came back negative, but TtG IgG was 6 (6-9 weak positive). TtG IgA was 1.4. Tomorrow I get the endoscopy and biopsy. I'm so confused as to why I tested so high for Gliadin IgG and now it is negative. I am not gluten free. The Dr said she has no idea and they are just trying to figure it out. Ive read Celiacs does not go into remission unless you are gluten free. Does anyone know how I could have been positive 12 yrs ago and now be negative?
  7. Celiac.com 03/27/2017 - A number of researchers are looking to provide alternative or adjunct treatments to the gluten-free diet in celiac disease. Meanwhile, a number of companies are currently developing a wide variety of such options, ranging from various kinds of enzyme therapies, to treatments that eliminate celiac disease reactions, even to vaccines to inoculate celiac sufferers against their condition, perhaps allowing for full recovery and a return to non-gluten-free eating habits, as desired. At least, that's one dream. More likely will be the development of enzymes or other treatments that offer celiacs varying degrees of protection from gluten ingestion. Most likely, such treatments would be designed to augment an existing gluten-free diet, and to provide protection against moderate gluten-contamination when eating out. One particular enzyme that shows strong potential in breaking down toxic peptides in A-gliadin, the main culprit in celiac reactions, is caricain. A recent paper discusses the scientific principles behind the use of caricain for enzyme therapy. The paper is based on a recent study, in which a team of researchers set out to review the structures of the toxic peptides in A-gliadin for key sequences of amino acids or motifs related to toxicity, especially with respect to digestive difficulties, or immunogenicity. The research team included Hugh J. Cornell and Teodor Stelmasiak. They are affiliated with the RMIT University, School of Applied Sciences, Melbourne, Australia, and with Glutagen Pty Ltd, Maribyrnong, Victoria, Australia. For their study, they first evaluated structures of synthetic A-gliadin peptides shown to be toxic in the fetal chick assay, both before and after digestion with duodenal mucosa from patients in long remission. They also measured synthetic peptides corresponding to the undigested residues, and compared the key amino acid sequences, to see if they might be related to direct toxicity and immunogenicity of the peptides. They found that the smallest toxic peptides from celiac mucosal digestion were octa-peptides, which they found in greater amounts than similar products from normal digestion. One of those peptides corresponded to residues 12-19 of A-gliadin and contained the key motifs PSQQ and QQQP of De Ritis et al., while the other corresponded to residues 72-79, and contained the key motif PYPQ (extending to PYPQPQ). These key motifs have been noted by other workers, especially those investigating immunological activity over the past two decades. Their in undigested residues from celiac mucosal digestion These motifs, along with the greater prevalence of these residues, as compared with residues from normal digestion, supports the basic notions underpinning enzyme therapy for celiac disease. These study also supports the basic scientific merits of research and development of the enzyme caricain to break down gliadin peptides with two different types of toxicity, and thus to potentially benefit people with celiac disease. Source: International Journal of Celiac Disease. Vol. 4, No. 4, 2016, pp 113-120. doi: 10.12691/ijcd-4-4-2 Previous study: NCBI
  8. Hi, See if any experts here can help. My test result in May 2016 was Total igA normal anti ttg igA 42 (20 is cutoff) anti gliadin igA 55 (20 cutoff) I didnt choose to have a biopsy so I just went gluten-free I took repeated test about 50 days apart and the anti ttg igA went from 42--20---36---20---17. It has become negative. Antigliadin igA went from 55--50---47---70. Anyone can explain what the hell is going on with these numbers?
  9. Celiac.com 08/20/2015 - Celiac disease is frequently mis-diagnosed. Even when patients received endoscopy, celiac disease is often missed or not detected. A team of researchers recently assessed the accuracy of finger prick-based point-of-care tests in the detection of celiac disease, and developed an algorithm for diagnosis. The research team included PD Mooney, SH Wong, AJ Johnston, M Kurien, A Avgerinos, and DS Sanders. They are variously affiliated with the Royal Hallamshire Hospital, Sheffield, United Kingdom and the University of Sheffield, Sheffield, United Kingdom. Their team conducted a prospective study of two groups of celiac disease patients evaluated at the Royal Hallamshire Hospital in Sheffield UK from March 2013 through February 2014. In group one, the team evaluated 55 patients at high risk for celiac disease, and who tested positive for endomysial antibody, using the Biocard test (BHR Pharmaceuticals, Nuneaton, UK) and the Celiac Quick Test (Biohit Healthcare UK, Ellesmere Port, UK), which measure antibodies to tissue transglutaminase (anti-tTG), and the Simtomax test (Tillotts Pharma, Rheinfelden, Switzerland), which measures deamidated gliadin peptide antibodies (DGP). Group 2 included 508 consecutive patients who received an endoscopy for any reason, received the DGP test, and also were evaluated using a diagnostic algorithm that incorporated results from the DGP test and data on symptoms. For both groups, point-of-care tests were administered at the time of endoscopy, and the results compared against results from histologic analyses of duodenal biopsy specimens from all patients. In group 1, the DGP test identified patients with celiac disease with 94.4% sensitivity, the Celiac Quick Test identified patients with 77.8% sensitivity (P = .03 vs the DGP test), while the Biocard test identified patients with 72.2% sensitivity (P = .008 vs the DGP test). In group 2, the DGP test identified patients with celiac disease with 92.7% sensitivity (95% confidence interval, 83.0-97.3), 85.2% specificity (95% confidence interval, 81.5-88.3), a positive predictive value of 49.2% (95% confidence interval, 40.3-58.2), and a negative predictive value of 98.7% (95% confidence interval, 96.8-99.5). Measurement of serum anti-tTG identified patients with celiac disease with 91.2% sensitivity (95% confidence interval, 81.1-96.4), 87.5% specificity (95% confidence interval, 84.0-90.4), a positive predictive value of 53.0% (95% confidence interval, 43.6-62.2), and a negative predictive value of 98.5% (95% confidence interval, 96.5-99.4). The algorithm identified patients with celiac disease with 98.5% sensitivity, and has the potential to reduce duodenal biopsies by 35%. In this prospective study, the test for DGP identified celiac patients with comparable sensitivity and specificity as standard serologic analysis of anti-tTG. Conducting the DGP test before endoscopy might increase the accuracy of the diagnosis of celiac disease. These results look promising, but further study is needed, in lower-prevalence populations, to more accurately determine the potential benefits of the DGP test in celiac screening. Source: Clin Gastroenterol Hepatol. 2015 Jul;13(7):1278-1284.e1. doi: 10.1016/j.cgh.2015.01.010. Epub 2015 Jan 26.
  10. Hi all, Last week I underwent extensive blood, urine, and skin testing for psychiatric purposes. I had previously been diagnosed by a psychologist with depression (dysthymia), generalized anxiety disorder, and ADHD inattentive type. When I saw a psychiatrist, he suggested that my illness may be due to food reaction. Today I got back my test results, some of which pertain to gluten intolerance. Gliadin (deamidated) IGA: 7 units <20 antibody not detected Gliadin (deamidated) IGG: 3 units <20 antibody not detected Transglutaminase IGG: 3 U/ml <6 no antibody detected Transglutaminase IGG: 1 U/ml <4 no antibody detected (To me it seems if the antibody is not detected, then gluten intolerance/sensitivity shouldn't necessarily be the issue. Am I correct, or do I have it the other way around?) I was also administered injections of diluted (not concentrated, not sure if that matters) gluten and wheat that produced no symptoms or immediate reaction, but gave a very mild delayed reaction after 24 hours. Milk and corn, by contrast, produced more noticeable reactions. Still, the psychiatrist recommended immediately cutting all gluten out of my diet (along with dairy and corn, among some other dietary changes). I plan on taking his suggestion, but I have never had any of the common symptoms of gluten intolerance/sensitivity in the past to my knowledge. I am 22 years old. Not asking for medical advice but possibly some anecdotal comparisons: do my gliadin and transglutaminase results seem to significantly suggest gluten intolerance/sensitivity? Other posters in this forum have used more stringent reference ranges, but even then, my results seem low. Even though this diagnosis is coming from a medical professional with much greater expertise on the matter than I have, it seems to rely on a reading of my results as >0 automatically equating to gluten intolerance/sensitivity. I study statistics, so I'm skeptical of using rejection ranges that liberally. Curious what you all think. Thanks, Matt
  11. Celiac.com 01/29/2015 - Testing for tissue transglutaminase antibodies (TGA) is currently a common part of attempting to diagnose celiac disease. A research team wanted to find out if determination of antibodies to synthetic deamidatedgliadin peptides (anti-DGP) might work as an alternative or complement to TGA testing. To find out, the team assessed the performance of a time-resolved immunofluorometry (TR-IFMA) based anti-DGP assay in the diagnosis of celiac disease in children, and also retrospectively analyzed the appearance of anti-DGP antibodies before TGA seroconversion. The research team included A. Lammi, P. Arikoski, S. Simell, T. Kinnunen, V. Simell, S. Paavanen-Huhtala, A. Hinkkanen, R. Veijola, M. Knip, J. Toppari, O. Vaarala, O. Simell, and J. Ilonen. They are variously affiliated with the Department of Clinical Microbiology and the A.I. Virtanen Institute for Molecular Sciences at the University of Eastern Finland in Kuopio, Finland, the Department of Pediatrics at Kuopio University Hospital and University of Eastern Finland, Kuopio, Finland, the Department of Pediatrics at the University of Oulu and Oulu University Hospital in Oulu, Finland, the Children's Hospital, and the Institute of Clinical Medicine at the University of Helsinki in Helsinki, Finland, the Folkhälsan Research Center in Helsinki, Finland, the Department of Pediatrics at Tampere University Hospital in Tampere, Finland, the Immunogenetics Laboratory, and the Department of Physiology at the University of Turku, and with the Department of Pediatrics and Adolescent Medicine at the University of Turku and Turku University Hospital in Turku, Finland. For their study, the team assessed 92 children with biopsy-confirmed celiac disease. The team took blood samples at the time of, or just prior to, clinical diagnosis. The team also assessed a control group of 82 TGA-negative children who were positive for HLA-DQ2 or -DQ8. Based on receiver operating characteristics (ROC) curves, they found that the optimal cut-off value for IgA anti-DGP positivity was 153 arbitrary units (AU) with a sensitivity of 92.4% and specificity of 97.6%, while the optimal cut-off value for IgG anti-DGP 119 AU, with a sensitivity of 97.8% and specificity of 97.6%. They found that all 92 children with celiac disease tested positive for either IgA or IgG anti-DGP at the time of diagnosis. Blood results from 48 children with celiac disease, analyzed retrospectively before the diagnosis, showed that anti-DGP antibodies preceded TGA positivity in 35 of 48 celiac disease children and appeared an average of one year earlier. From these results, the TR-IFMA test for detecting anti-DGP antibodies shows high sensitivity and specificity for celiac disease in children. For most of the patients, anti-DGP seropositivity preceded TGA positivity, which means that monitoring anti-DGP antibodies frequently in genetically susceptible children might allow doctors to spot celiac disease earlier than allowed by current tests. Source: J Pediatr Gastroenterol Nutr. 2014 Dec 16.
  12. Hello everyone!! Still on my journey to figure out what's going on with me! I've had a positive gliadin IgG test, negative gliadin IgG, Negative tissue transglutaminase IgG/IgA... Negative biopsy, it showed inflammation and lymphocytes infiltrating the epithilium but no issues with the villi... After I went gluten free for a month and felt great... Reintroduced and all my aches pains and respiratory issues came back I didn't think I had any GI issues but when I reintroduced I realized it made me constipated.... Now I had the genetic testing done and my HLA-DQB1*02 and HLA-DQB1*03:02 were negative but HLA-DQA1*05 is positive. Report says this is rarely observed in individuals with celiac and that it is only mildly supportive of a clinical diagnosis of celiac disease..... I know I should just go gluten free cause it makes me feel better... But I would have really loved a yes you have this or a no you don't
  13. Celiac.com 10/07/2013 - People with non-celiac gluten-sensitivity often report gut and non-gut symptoms shortly after eating gluten; symptoms disappear on gluten-free diets, although these patients have no serologic markers of celiac disease, and no intestinal damage. However, there is no evidence to suggest any changes to blood or mucosa in those individuals. To better understand non-celiac gluten sensitivity, a research team recently assessed immunologic responses of duodenal mucosa samples and peripheral blood basophils, isolated from NCGS patients, after exposure to gliadin. The research team included Cristina Bucci, Fabiana Zingone, Ilaria Russo, Ivonne Morra, Raffaella Tortora, Norberto Pogna, Giulia Scalia, Paola Iovino, and Carolina Ciacci. They are affiliated with CEINGE in Naples, Italy; the Consiglio per la Ricerca e la Sperimentazione in Agricoltura in Rome, Italy; the Gastrointestinal Unit of the Department of Medicine and Surgery at the University of Salerno in Salerno, Italy; and with the Gastrointestinal Unit at the Department of Clinical and Experimental Medicine of Federico II University of Naples. Between January 2010 and July 2011, the research team gathered mucosa samples from 34 celiac disease patients who followed gluten-free diets for at least 6 months, 35 patients with untreated celiac disease, 16 patients with non-celiac gluten sensitivity (NCGS) and 34 healthy control subjects. The team diagnosed non-celiac gluten sensitivity based on patient symptoms and current diagnositic guidelines. For each of the 119 patients, the team conducted a complete clinical evaluation to exclude celiac disease while on a gluten-containing diet, a skin prick test to exclude wheat allergy, and upper endoscopy at 2 tertiary medical centers in Italy. After incubating each biopsy sample with gliadin, the team measured inflammatory markers, including anti-phosphotyrosine-monoclonal antibody (PY99), HLA-DR, intercellular cell adhesion molecule-1 (ICAM-1), CD3, CD25 and CD69. After incubation with gliadin, mucosa samples from the 69 patients with celiac disease showed increased immunofluorescence intensity for early and delayed markers of inflammation. They also found low levels of some of these markers in three patients with non-celiac gluten sensitivity and three controls. The team found normal mucosal architecture in 56.3% of patients with non-celiac gluten sensitivity. The remaining seven patients showed increased intraepithelial infiltration, but without eosinophils. They found no villous atrophy in patients with non-celiac gluten sensitivity, and no significant increases in the levels of CD63 and CD203c. The team did find that one patient each in the NCGS and control groups, whose results indicated only weak PY99 and ICAM-1 positivity, also had Helicobacter pylori infection. Unlike mucosa from patients with celiac disease, once incubated with gliadin, mucosa from patients with NCGS does not express markers of inflammation, nor does the gliadin activate their basophils. The in vitro gliadin challenge therefore should not be used to diagnose NCGS. This study does suggest that wheat components, other than proteins, might be associated with GI symptoms in patients with IBS, and should be assessed for a possible role in the pathogenesis of NCGS. Source: Clinical Gastroenterology and Hepatology. Volume 11, Issue 10 , Pages 1294-1299.e1, October 2013
  14. Celiac.com 06/10/2013 - Researchers have known for some time that immunoglobulin G antibodies against deamidated gliadin peptides are about as accurate as tissue transglutaminase and endomysium autoantibodies in diagnosing celiac disease in adults. However, not much is known about their predictive value in infants with a suspected gluten enteropathy. A team of researchers recently set out to determine if antibodies to deamidated gliadin peptides could be an accurate predictor of celiac disease in infants. The research team included S. Amarri, P. Alvisi, R. De Giorgio, M.C. Gelli, R. Cicola, F. Tovoli, R. Sassatelli, G. Caio, and U. Volta. They are affiliated with the Pediatric Unit, IRCCS - Arcispedale Santa Maria Nuova, Reggio Emilia, Italy. To test whether deamidated gliadin immunoglobulin G antibodies are more reliable than traditional tests for screening celiac disease in infants, the researchers tested 65 children under 2 years of age for deamidated gliadin immunoglobulin G, tissue transglutaminase and endomysium immunoglobulin A, and gliadin immunoglobulins A and G. The group included 42 infants with malabsorption, along with 23 infants as control subjects. Thirty-seven of the 42 children with malabsorption had deamidated gliadin antibodies, associated with tissue transglutaminase and endomysial antibodies in 33, and with gliadin immunoglobulins A and G in 21 and 29, respectively. The team conducted intestinal biopsy in 34 of the 37 children who tested positive for deamidated gliadin antibodies. Thirty-two of the 34 showed villous atrophy consistent with celiac disease, while one of the remaining two had a Marsh 1 and the other showed normal mucosa. The control group showed only gliadin immunoglobulins A (4.3 %) and G (39.1 %). The results showed that deamidated gliadin, tissue transglutaminase and endomysial antibodies were significantly more sensitive for celiac disease than gliadin immunoglobulins G and A. High levels of deamidated gliadin antibodies correlated with severe intestinal damage. For infants, deamidated gliadin antibodies showed a higher diagnostic accuracy for celiac disease than gliadin antibodies. High levels of deamidated gliadin antibodies are good predictors of severe gluten-dependent duodenal damage. Source: J Clin Immunol. 2013 Apr 5.
  15. Hi My blood values are coming down, but while the anti-deaminated gliadin IGG has come down to normal values, the TTG IGA is still lagging behind at 12 (should be <7). TTG IGA was 15 in January. Why is it that the anti-deaminated gliadin comes down before the TTG?
  16. I've been reading all about these test results and I don't understand what I have. There seems to be different wording for some of the tests and I don't understand my results. I know one is high, but does that mean I've got Celiac Disease, or just a gluten intolerance Do I need to get the biopsy done? I've been gluten-free for 3 months now, would I need to go back to eating gluten before I get the biopsy done? Here are my test results: Immunoglobulin A: 427 (normal range 68-378) Tissue Transglutaminase Antibody, lgA: 5 (normal range 0-19) Gliadin lgA Antibodies: 5 (normal range 0-19) thanks in advance for any assistance!
  17. Celiac.com 12/31/2012 - In people with celiac disease, eating wheat, barley, or rye triggers inflammation in the small intestine. Left unchecked, this inflammation causes the gut damage that is associated with untreated celiac disease. Specifically, the storage proteins in these grains (gluten) trigger an adaptive Th1-mediated immune response in individuals carrying HLA-DQ2 or HLA-DQ8 as major genetic predisposition. Researchers actually have a pretty good understanding of this aspect of celiac disease, part of a process called adaptive immunity. However, there has been some research that suggests that gluten proteins might trigger an immune response in people who do not have celiac disease, and who do not carry the HLA-DQ2 or HLA-DQ8 genetic markers that predispose them to developing celiac disease. Such a response is part of a process called innate immunity, and is far less understood than the adaptive immunity process. The innate immune system provides an early response to many microbial and chemical stimuli and is critical for successful priming of adaptive immunity. To better understand the relationship between adaptive immunity and innate immunity in celiac disease, a research team recently set out to determine if gliadin digests might induce innate immune responses in celiac and non-celiac individuals. Specifically, they wanted to know if wheat amylase trypsin inhibitors drive intestinal inflammation, and if so, by what receptor mechanism. The research team included Yvonne Junker, Sebastian Zeissig, Seong-Jun Kim, Donatella Barisani, Herbert Wieser, Daniel A. Leffler, Victor Zevallos, Towia A. Libermann, Simon Dillon, Tobias L. Freitag, Ciaran P. Kelly, and Detlef Schuppan. They are affiliated variously with the Division of Gastroenterology and the Proteomics and Genomics Center at Beth Israel Deaconess Medical Center at Harvard Medical School in Boston, with the Department of General Pediatrics and the Department of Internal Medicine I at the University Medical Center Schleswig-Holstein Kiel in Kiel, Germany, the Department of Experimental Medicine at the University of Milano-Bicocca in Milan, Italy, the German Research Center for Food Chemistry in Garching, Germany, the Hans-Dieter-Belitz-Institute for Cereal Grain Research in Freising, Germany, the Division of Molecular and Translational Medicine in the Department of Medicine I at Johannes Gutenberg University in Mainz, Germany, and with the Department of Bacteriology and Immunology at the Haartman Institute at the University of Helsinki in Finland. A number of earlier studies (Molberg et al., 1998; Anderson et al., 2000; Shan et al., 2002) have found HLA-DQ2– and HLA-DQ8–restricted gluten peptides that trigger the adaptive immune response in people with celiac disease. However, only 2–5% of individuals who show these HLAs develop celiac disease, which means that other factors, especially innate immune activation, are at play in the generation of celiac disease. Responsive innate cells are primarily macrophages, monocytes, DCs, and polymorphonuclear leukocytes that by means of their pattern-recognition receptors, such as TLRs, trigger the release of proinflammatory cytokines and chemokines, resulting in recruitment and activation of additional inflammatory cells (Medzhitov, 2007). Earlier studies (Maiuri et al., 2003) showed that peptides p31-43 or p31-49 from α-gliadin, that lack adaptive stimulatory capacity, triggered innate immune reactions by inducing IL-15 and Cox-2 expression in patient biopsies, and MHC class I polypeptide–related sequence A (MICA) on intestinal epithelial cells (Hüe et al., 2004). However, these studies have proven difficult to reproduce in cell culture, and researchers could not identify any specific receptor responsible for the observed effects. In a subsequent study, gliadin, in cell culture, reportedly triggered increased expression of co-stimulatory molecules and the production of proinflammatory cytokines in monocytes and DCs (Nikulina et al., 2004; Cinova et al., 2007). Two other studies (Thomas et al., 2006; Lammers et al., 2008) implicated the chemokine receptor CXCR3 in increased intestinal epithelial permeability upon gliadin challenge in a MyD88-dependent manner. However, those studies failed to reproducibly identify a specific gliadin peptide as the trigger. So far, no clear picture of the role of the innate immune system in celiac disease has emerged. In this study, the researchers show that members of the non-gluten α-amylase/trypsin inhibitors (ATIs), CM3 and 0.19, pest resistance molecules in wheat and related cereals, are strong triggers of innate immune responses in human and murine macrophages, monocytes, and dendritic cells. Their results show that ATIs activate the TLR4–MD2–CD14 complex and lead to up-regulation of maturation markers and elicit release of proinflammatory cytokines in cells from celiac and nonceliac patients and in celiac patients’ biopsies. They also show that mice deficient in TLR4 or TLR4 signaling are protected from intestinal and systemic immune responses upon oral challenge with ATIs. These findings define cereal ATIs as novel contributors to celiac disease. Moreover, ATIs may fuel inflammation and immune reactions in other intestinal and nonintestinal immune disorders. The findings of this study mean that the proteins in wheat may trigger immune reactions not just in people with celiac disease, but in people without celiac disease, and that these reactions may be actively contributing to the development of numerous other intestinal and non-intestinal immune disorders. That's a pretty big deal. Stay tuned to see how future studies elaborate these findings. Read the entire study in the Journal of Experimental Medicine. Source: J Exp Med. 2012 Dec 17;209(13):2395-408. doi: 10.1084/jem.20102660
  18. Celiac.com 12/12/2012 - In duodenal biopsy samples from people with active celiac disease, the transferrin receptor, CD71, is up-regulated, and promotes retro-transport of secretory immunoglobulin A (SIgA)-gliadin complexes. To better understand how interactions between SIgA and CD71 promote transepithelial transport of gliadin peptides, a team of researchers set out to determine if interactions among secretory immunoglobulin A, CD71, and transglutaminase-2 affect permeability of intestinal epithelial cells to gliadin peptides. The research team included C. Lebreton, S. Ménard, J. Abed, I.C. Moura, R. Coppo, C. Dugave, R.C. Monteiro, A. Fricot, M.G. Traore, M. Griffin, C. Cellier, G. Malamut, N. Cerf-Bensussan, and M. Heyman. They are affiliated with the Mixed Research Unit 989 of the National Institute of Health and Medical Research (INSERM UMR989) in Paris, France. For their study, the team evaluated duodenal biopsy specimens from 8 adults and 1 child with active celiac disease. The team used fluorescence-labeled small interfering RNAs against CD71 to transfect Caco-2 and HT29-19A epithelial cell lines. They used flow cytometry, immunoprecipitation, and confocal microscopy to assess interactions among IgA, CD71, and transglutaminase 2 (Tgase2). They then assessed transcytosis of SIgA-CD71 complexes and intestinal permeability to the gliadin 3H-p31-49 peptide in polarized monolayers of Caco-2 cells. To assess physical interplay between SIgA and CD71 or CD71 and Tgase2 at the apical surface of enterocytes in biopsy samples and monolayers of Caco-2 cells, the team used fluorescence resonance energy transfer and in situ proximity ligation assays. They co-precipitated CD71 and Tgase2 with SIgA, bound to the surface of Caco-2 cells. They found that SIgA-CD71 complexes were internalized and localized in early endosomes and recycling compartments, but not in lysosomes. In the presence of celiac IgA or SIgA against p31-49, transport of intact 3H-p31-49 increased significantly across Caco-2 monolayers, while soluble CD71 or Tgase2 inhibitors interfered with transport. Once it binds to apical CD71, SIgA (with or without gliadin peptides) enters a recycling pathway and avoids lysosomal degradation; this process allows apical-basal transcytosis of bound peptides. This mechanism is assisted by Tgase2 and might be involved in the pathogenesis of celiac disease. Source: Gastroenterology. 2012 Sep;143(3):698-707.e1-4. doi: 10.1053/j.gastro.2012.05.051.
  19. Celiac.com 10/24/2012 - Doctors can face challenges when attempting to diagnose celiac disease in patients who have already begun a gluten-free diet, and/or when the results of tests are inconsistent. To better understand this problem, a group of researchers set out to assess the benefits of an in vitro gliadin challenge. The research team included Raffaella Tortora, MD, Ilaria Russo, PhD, Giovanni D. De Palma, MD, Alessandro Luciani, PhD, Antonio Rispo, MD, Fabiana Zingone, MD, Paola Iovino, MD, Pietro Capone, MD and Carolina Ciacci, MD. The study cohort included 57 patients without celiac disease, 166 patients with untreated celiac disease, 55 patients with celiac disease on a gluten-free diet, and 59 patients with challenging diagnosis. The team provided all patients with endoscopy for collection of duodenal samples, which served for the diagnosis of celiac disease and for the in vitro evaluation of the gliadin-induced mucosal expression of seven inflammatory markers: PY99, ICAM-1 (intercellular cell adhesion molecule), HLA-DR, CD3, CD25, CD69, and transglutaminase 2 IgA. Diagnostic work-up for celiac disease included the search of specific serum antibodies. Researchers asked patients in the challenging diagnosis group to stop gluten-free diet to facilitate the search for these antibodies under untreated conditions. They used the area under the receptor-operated curve (ROC) for statistical analyses on accuracy. For patients with and without celiac disease (not including those on a gluten-free diet) HLA-DR offered the best accuracy for diagnosing celiac disease (area under ROC = 0.99). Combining the data from the HLA-DR with data of other markers did not increase test accuracy. The team found similar results in the 39 patients of the difficult diagnosis group undergoing the search celiac disease-speciï¬c antibodies under untreated conditions. In vitro testing of mucosal HLA-DR to gliadin is an accurate tool for the diagnosing celiac disease, and also works in patients who are hard to diagnose. Source: Am J Gastroenterol 2012; 107:111–117; doi:10.1038/ajg.2011.311; published online 27 September 2011
  20. Celiac.com 08/16/2012 - Tests for blood antibodies against native gliadin (anti-nGli) are still often assumed to perform better in the diagnosis of celiac disease in young children than tests for antibodies to deamidated gliadin (anti-dGli), tissue transglutaminase (anti-tTG), and endomysium (EmA). A team of researchers recently set out to determine whether testing IgG and IgA antibodies Against native gliadin was best for diagnosing celiac disease in children under 2-years old. Specifically they wanted to compare the performance of assays for anti-nGli, anti-dGli, anti-tTG, and EmA in this age group. The research team included T. Richter, X. Bossuyt, P. Vermeersch, H.H. Uhlig, M. Stern, A. Hauer, K.P. Zimmer, L. Mearin, J.H. Roo, C. Dähnrich, and T. Mothes. They are affiliated with the University Children's Hospital, the Children's Hospital of the Clinical Centre, "Sankt Georg," and the Institute of Laboratory Medicine, Clinical Chemistry and Molecular Diagnostics at University Hospital in Leipzig, Germany; with the Department Laboratory Medicine of University Hospital in Leuven, Belgium, the University Children's Hospital in Tübingen, Germany, the University Children's Hospital in Graz, Austria, the University Children's Hospital in Giessen, Germany, the Department of Paediatrics at Leiden University Medical Centre in Leiden, The Netherlands, and with EUROIMMUN Medizinische Labordiagnostika GmbH in Lübeck, Germany. For their study, they conducted a retrospective analysis of 184 children. The study group included 42 children with celiac disease under normal diet, and a control group of 142 children up to 2 years of age. The team measured immunoglobulin (Ig) A- and IgG-anti-dGli, IgA- and IgG-anti-nGli, IgA- and IgG-anti-tTG, and IgA-EmA in blood samples. They calculated areas under receiver operating characteristics curves, sensitivities, specificities, positive and negative predictive values, positive and negative likelihood ratios, as well as diagnostic odds ratios. When all the data was complete, they found that only tests for IgG-anti-dGli, IgA-anti-tTG, and IgA-EmA had high specificity (≥0.96) connected with high sensitivity (≥0.86), with high positive predictive values (≥0.52 and ≥0.69 at pretest probabilities of 0.05 and 0.1, respectively) and negative predictive values (≥0.99 and ≥0.98 at pretest probabilities of 0.05 and 0.1, respectively). These tests also showed high positive likelihood ratio (≥24) at low negative likelihood ratio (≤0.15) and high diagnostic odds ratios (≥136). From their data, the team concluded that using anti-nGli tests to diagnose celiac disease in young children was not helpful. They maintain that IgA-anti-tTG, IgA-EmA, and IgG-anti-dGli provided much more reliable results than anti-nGli in diagnosing celiac disease in young children. Source: J Pediatr Gastroenterol Nutr. 2012 Jul;55(1):21-25.
  21. Celiac.com 03/28/2012 - A clinical research team wanted to determine if adding ascorbate (vitamin C) to gliadin-stimulated biopsy culture could reduce the mucosal immune response to gliadin in people with celiac disease. The research team included D. Bernardo, B. Martínez-Abad, S. Vallejo-Diez, E. Montalvillo, V. Benito, B. Anta, L. Fernández-Salazar, A. Blanco-Quirós, J. A. Garrote, and E. Arranz. They are affiliated with the Mucosal Immunology Lab of the Department of Paediatrics & Immunology at Spain's Universidad de Valladolid-CSIC. Their quest was fueled by the understanding that the IL-15/NF-κB axis plays a key role in celiac disease. Because ascorbate is known to inhibit effects on NF-κB, the IL-15/NFκB axis looks like a good possible molecular target for reducing gliadin-induced inflammation in celiac disease. For their study, the team conducted in vitro gliadin challenges (100 μg/ml) on duodenal biopsy explants from treated patients with celiac disease. Challenges were conducted with and without 20mM ascorbate. As an internal control, the team used an extra tissue explant in basal culture. The team then measured secretion levels of nitrites (3h), and IFNγ, TNFα, IFNα, IL-17, IL-13, and IL-6 (24h) on the supernatants. They measured IL-15 using western-blot on whole protein duodenal explants. When the team added ascorbate to in vitro culture gliadin-challenged biopsies, they found that the ascorbate blocked secretion of nitrites (p=0.013), IFNγ (p=0.0207), TNFα (p=0.0099), IFNα (p=0.0375), and IL-6 (p=0.0036), as compared with samples from culture that received no ascorbate. They also found that the addition of ascorbate reduced cytokine secretion to levels even lower than those observed in basal cultures (IFNγ: p=0.0312; TNFα: p=0.0312; IFNα: p=0.0312; and IL-6: p=0.0078). Moreover, the gliadin-challenge triggered IL-15 production in biopsies from treated celiac disease patients, while IL-15 was completely blocked in the cultures that received ascorbate. Interestingly, ascorbate completely blocked IL-15 production even in the only treated celiac disease-patient who showed basal IL-15 production. From these results, the team concludes that ascorbate reduces the mucosal inflammatory response to gluten in an in vitro biopsy culture. As such, ascorbate might offer supplementary benefits in future celiac disease therapy. Source: Allergol Immunopathol (Madr). 2012 Jan-Feb;40(1):3-8.
  22. Celiac.com 03/09/2011 - A team of researchers recently identified a novel immunomodulatory gliadin peptide that triggers interleukin-8 release in a chemokine receptor CXCR3-dependent manner only in patients with celiac disease. The research team included Karen M. Lammers; Sunaina Khandelwal; Fatima Chaudhry; Debby Kryszak; Elaine L. Puppa; Vincenzo Casolaro; and Alessio Fasano. The same research team had previously reported that the chemokine receptor CXCR3 serves as a receptor for specific gliadin peptides that trigger zonulin release and increase in intestinal permeability. This mechanism plays an important role in the adverse immune reaction to gluten-containing grains that is central to the classic celiac disease response. To examine the role of CXCR3 in the immune response to gliadin, the researchers incubated peripheral blood mononuclear cells of both celiac patients and healthy controls with either pepsin-trypsin-digested gliadin or 11 α-gliadin synthetic peptides in the presence or absence of a blocking anti-CXCR3 monoclonal antibody. The team then analyzed supernatants for interleukin-6 (IL-6), IL-8, IL-10, IL-13, IP-10 (CXCL10), tumour necrosis factor-α and interferon-γ. Gliadin triggered cytokine production regardless of clinical condition. However, only small number of individuals showed IL-8 production. In those individuals, cells originating from white blood cells were the main source of IL-8 production. The team used one of a comprehensive panel of synthetic α-gliadin peptides to reproduce the induction of IL-8. They were able to cease the process by blocking CXCR3 before stimulation with either gliadin or this peptide in the celiac group, but not in the control group. This suggests that gliadin-induced IL-8 production is CXCR3-dependent only in people with celiac disease. Source: Immunology, Volume 132, Number 3, March 2011 , pp. 432-440(9)
  23. Celiac.com 10/20/2010 - U.S. doctors and patients looking for accurate early diagnosis of celiac disease now have a state of the art celiac disease assay with a high level of sensitivity and specificity. The US Food and Drug Administration (FDA) has given 510(k) clearance for the first two fully automated gliadin tests featuring deamidated peptides for celiac disease. Manufactured by Phadia US, the tests, EliA GliadinDP IgA and EliA GliadinDP IgG, are designed to be used in conjunct with other laboratory and clinical findings in the early diagnosis of celiac disease. According to Gabi Gross, autoimmune franchise leader for Phadia US, "EliA GliadinDP IgA and EliA GliadinDP IgG will offer physicians who suspect a possible case of celiac disease, antibody tests with the lowest number of false positive results." This means less "unnecessary endoscopies and biopsies," she adds. EliA GliadinDP IgA and EliA GliadinDP IgG will offer antibody tests with the lowest number of false positive results for doctors who suspect a patient has celiac disease. The assays are optional on Laboratory Systems Phadia 100Є and Phadia 250 instruments with features like quick turnaround, monthly calibration, onboard instrument dilution, and a discrete single-well, random-access, nonmicrotiter plate format. Phadia also manufactures other approved CLIA moderately complex assays in the EliA autoimmune product line, including anticardiolipin IgG/IgM, anti-B2-glycoprotein 1 IgG/IgM, cyclic citrullinated peptide, tissue transglutaminase IgA/ IgG, gliadin IgA/IgG, dsDNA, antinuclear antibody screen, and ENA antibodies to the following antigens: Sm, U1RNP, RNP70, Ro, La, Scl-70, CENP, and Jo-1. Source: Medscape
  24. Celiac.com 03/25/2010 - A team of researchers recently set out to compare the diagnostic performance of IgG anti-deamidated gliadin peptide antibody assays against IgA anti-tTG in celiac disease. The team included P. Vermeersch, K. Geboes, G. Mariën, I. Hoffman, M. Hiele, X. Bossuyt, all associated with the department of Laboratory Medicine, Immunology of University Hospitals at the Catholic University of Leuven, Belgium. Using IgG anti-deamidated gliadin peptide antibody assays to test for celiac disease is more sensitive and more specific for celiac disease than detection of IgG antibodies against native gliadin. The team compared assessed the technical performance and accuracy (sensitivity and specificity) of commercial IgG anti-DGP assays from Euroimmun, Inova, Phadia and The Binding Site against other serologic assays for celiac disease, such as 3IgA and 2IgG anti-tTG assays, 1IgA and 1IgG anti-gliadin assay, 1IgA anti-DGP assay. For the study, they tested 86 patients with clinically proven celiac disease and 741 healthy control subjects. Technical performance of IgG anti-DGP assays as gauged by linearity, interference and imprecision, was within acceptable levels. IgG anti-DGP assay sensitivity ranged between 76.7% and 83.7% at the manufacturer's recommended cut-off, and between 74.4% and 84.9% at a cut-off that corresponded to a 98% specificity level. Specificity ranged between 97.3% and 99.3%. The diagnostic accuracy of the IgG anti-DGP assays was comparable to the diagnostic accuracy of the IgA anti-tTG assays. IgG anti-DGP assays showed significantly better than sensitivity than the IgG anti-tTG assays (p<0.05) and and significantly better specificity than IgA and IgG anti-gliadin assays (p<0.05). The four IgG anti-DGP assays all performed within acceptable limits, and diagnosed celiac disease with comparable accuracy as did the three IgA anti-tTG assays. Source: Clin Chim Acta. 2010 Feb 19.
  25. Celiac.com 03/10/2010 - A team of researchers recently observed that monocytes differentiated with IL-15 support Th17 and Th1 responses to wheat gliadin. They discuss the implications of this discovery for celiac disease in a recent article in Clinical Immunology. The research team included K. M. Harris, A. Fasano, and D. L. Mann of the Pathology Department at the University of Maryland School of Medicine. It is understood that interleukin (IL)-15 contributes to the immuno-pathogenesis of celiac disease. However, the effect of IL-15 on APC that shape adaptive immune responses to gliadin is not well understood. Using PBMC from healthy individuals, the team demonstrated that monocytes differentiated with IL-15 (IL15-DC) produced IL-1beta, IL-6, IL-15, IL-23, TNFalpha and CCL20 in response to pepsin-trypsin digested gliadin (PTG) and activated contact-dependent Th17 and Th1 responses from autologous CD4(+) T cells. Compared with control subjects, PBMC from celiac disease patients showed lower concentrations of IL-15 augmented IFNgamma responses to PTG. So, by generating IL15-DC, IL-15 supports Th17 and Th1 responses to a dietary antigen that produces no such responses in healthy individuals.The team notes that IL-15 hypersensitivity may cause these potentially pathogenic immune responses to develop in celiac patients, but not in healthy individuals. They conclude that the pathogenesis of celiac disease is likely due in part to genetic and/or environmental factors that control IL-15 expression and responsiveness in the gut. Source: Clin Immunol. 2010 Feb 10.