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Found 8 results

  1. Celiac.com 01/11/2006 - For many years, biopsy of the small bowel demonstrating villous atrophy has been fundamental to the diagnosis of celiac disease. Older celiacs will remember, fondly or otherwise, the Crosby suction biopsy device which was swallowed attached to a long tube and made its way down to the small bowel where, position confirmed by x-rays, it guillotined a small portion of tissue. The procedure was tedious and technical failures common—only identified when the device was hauled up after several hours. Later it became clear that biopsies from the duodenum obtained during endoscopy were just as good, and the biopsy process became a five minute job with no need for X-rays. Nevertheless, many celiacs are reluctant to undergo biopsy and its necessity is increasingly questioned, particularly now that blood tests for celiac-related antibodies are highly sensitive and specific. There are a number of reasons why, in my own practice, biopsies continue to be helpful in celiacs diagnosed in adulthood. Biopsies are necessary when blood tests are negative. While endomysial (EmA) and tissue transglutaminase (TTGA) antibodies are detectable in most cases where villous atrophy is present, 5-10% of patients lack these antibodies1. In this situation, where the story is suggestive of celiac, perhaps with a family history or strongly suggestive symptoms, biopsy is the only way to make the diagnosis. Increasingly, physicians recognize that many patients with gluten sensitivity do not have villous atrophy (Grade III of the Marsh classification) of "classic" celiac disease, but have milder abnormalities such as crypt hyperplasia (Marsh II) or an excess of the inflammatory cells called lymphocytes (Marsh I). Patients in these categories are less likely to have positive serology2. Biopsies are necessary where false positive blood tests may occur. TTGA, particularly where levels are low, may be associated with diseases other than celiac: ulcerative colitis, Crohns disease, arthritis and liver diseases without any evidence of celiac disease have been linked3. Newer TTGA tests have steadily improved in this regard but I still would be reluctant to diagnose celiac on a TTGA test alone. "False positive" EmA is a different issue which I will return to. Biopsies give a baseline for comparison. Suppose a patient starts a gluten-free diet without biopsy—we dont know whether she or he had Marsh I, II or III or even normal histology. A year later, same patient develops new symptoms of diarrhea, weight loss, whatever. Well get a duodenal biopsy as part of the workup, but its going to be difficult to interpret without knowing what things were like before going gluten-free. Specifically, a baseline to look back at tells us whether the small bowel is better, worse or no different, and helps us decide whether we need to focus on celiac disease as the most likely cause of new problems or explore other possibilities involving the rest of the gut. The biggest diagnostic disaster of all, of course, is the gluten-free diet started without any sort of baseline investigation including antibodies, raising the specter of the infamous gluten challenge if a definitive diagnosis is needed. Biopsies provide a "gold standard" assessment of the state of the bowel. There has been much excitement recently about capsule endoscopy, a wireless device the size of a large pill (not to be confused with the Crosby capsule!) which makes its own way down the small bowel taking pictures as it goes. Characteristic abnormalities can be seen in celiac disease, raising the possibility that this device might be useful in diagnosis. If experience with conventional endoscopes is any guide, however, these abnormalities are missing in a sizeable minority of celiacs particularly with mild disease4 (Capsule endoscopy in its present state of development can not take biopsies). Certainly the capsule allows assessment of the bowel beyond the reach of conventional "anaconda-style" endoscopes, but I am not convinced at present that it can replace biopsy. A follow-up biopsy gives an indicator of progress. I offer my patients a repeat biopsy after two years gluten-free and perhaps surprisingly most take up the offer and are keen to hear how things have improved. Ive increased the biopsy interval from one to two years because only 40% of people had complete recovery after 12 months gluten-free5. EmA and TTGA disappearance is only a marker of how successful gluten exclusion has been and is not a reliable indicator of bowel recovery. Does persisting villous atrophy matter if the patient is doing well on a gluten-free diet? Intuitively, one might like to keep a closer eye on the patient with persistently flat biopsies, who could be at greater risk of complications in the future6. The endoscopy not only allows examination and biopsy of the duodenum but also a look at the esophagus and stomach. Sad fact of the ageing process is that you start to collect diseases like trading cards, and just because youre celiac doesnt mean you cant have something else. Its important to have a good look for bleeding lesions in the upper gut even if the blood work for a seventy year old with anemia says celiac (and check out the colon too, but thats a topic for another day). On the other hand, we recognize that biopsies are not always the final arbiter in diagnosis. While the jury is still out on what a TTGA positive, biopsy negative result means with regard to gluten sensitivity, there is plenty of evidence that a positive EmA generally does mean that biopsy abnormalities will follow: My own follow-up of EmA positive, biopsy negative patients indicates that they will develop abnormal histology if not treated7. So it makes sense to start EmA positive people on gluten-free without waiting for significant bowel damage—and as already stated, even a normal baseline biopsy will provide a reference for any problems that might arise in the future. Sometimes I meet a patient with bad gut symptoms but completely normal blood work up and biopsies and when all else fails I will run a trial of gluten-free. It often works, particularly if there is a family history of celiac. But then again, if it doesnt, we have a baseline normal biopsy to say there is no need to persevere. I guess in the future diagnosis of gluten sensitivity will rely on totting up various factors, none individually essential: blood tests, biopsies, family history, genetic testing for the HLA celiac genes. Some researchers are making a case for dropping the biopsy requirement if the antibody blood work checks out in children8, for whom (and for the parents) endoscopy and biopsy is a major issue. In adults however it is quick, straightforward and safe and will remain a key part of my celiac workup. William Dickey is a gastroenterologist at Altnagelvin Hospital, Londonderry, Northern Ireland, with over 400 celiac patients attending his clinics. His interest in celiac disease goes back some fourteen years and he has published extensively on the subject. He is an associate member of Coeliac UKs Medical Advisory Council. References: Dickey W, McMillan SA, Hughes DF. Sensitivity of serum tissue transglutaminase antibodies for endomysial antibody positive and negative coeliac disease. Scand J Gastroenterol 2001; 36: 511-4. Wahab PJ, Crusius JBA, Meijer JWR, Mulder CJJ. Gluten challenge in borderline gluten-sensitive enteropathy. Am J Gastroenterol 2001; 96: 1464-69. Di Tola M, Sabbatella L, Anania MC, Viscido A, Caprilli R, Pica R, Paoluzi P, Picarelli A. Anti-tissue transglutaminase antibodies in inflammatory bowel disease: new evidence. Clin Chem Lab Med. 2004;42(10):1092-7. Oxentenko AS, Grisolano SW, Murray JA, Burgart LJ, Dierkhising RA, Alexander JA. The insensitivity of endoscopic markers in celiac disease. Am J Gastroenterol. 2002 Apr;97(4):933-8. Dickey W, Hughes DF, McMillan SA. Disappearance of endomysial antibodies in treated celiac disease does not indicate histological recovery. Am J Gastroenterol 2000; 95: 712-4. Meijer JWR, Wahab PJ, Mulder CJJ. Histologic follow-up of people with celiac disease on a gluten-free diet: slow and incomplete recovery. Am J Clin Pathol 118(3):459-63, 2002 Sep. Dickey W, Hughes DF, McMillan SA. Patients with serum IgA endomysial antibodies and intact duodenal villi: clinical characteristics and management options. Scand J Gastroenterol 2005: in press Barker CC, Mitton C, Jevon G, Mock T.Can tissue transglutaminase antibody titers replace small-bowel biopsy to diagnose celiac disease in select pediatric populations? Pediatrics. 2005 May;115(5):1341-6
  2. Celiac.com 05/09/2017 - For years, industry observers, health experts and even food companies have questioned the staying power of gluten-free food. With more people than ever embracing gluten-free products and gluten-free diets, including a majority of folks who do not have celiac disease, gluten-free food has never been more popular. There have also never been more gluten-free products hitting store shelves. Couple that with the fact that U.S. sales of gluten-free products are projected to exceed $2 billion by 2019, and the market for gluten-free products looks as solid as ever. But, do hidden caveats await potential investors, especially on the retail end? Maybe. There's a great article over at Fooddive.com about the challenges of succeeding in the gluten-free grocery business especially on the retail end. The article interviews a number of major gluten-free retailers, and notes that the higher margins and intense customer loyalty that come with gluten-free products also come with warning signs that may portend a looming downturn. Far from being doom-and-gloom, the article includes some interesting insights on the strategies and tactics being used by retailers to bolster their gluten-free sales. Read more at Fooddive.com.
  3. Celiac.com 02/15/2013 - If you think the FDA has dropped the ball on gluten-free food labeling, you are not alone. In 2004, the Food Allergen Labeling and Consumer Protection Act (FALCP) gave the FDA four years to create and implement final rules for gluten-free food labeling. The FALCP requires manufacturers to identify these allergens by their common names (i.e. wheat, milk, or soy) on labels so that consumers can easily identify them. In 2007, the FDA followed FALCP's mandate by issuing a proposed rule "Food Labeling: Gluten-Free Labeling of Foods." The proposed rule states that a food is gluten-free if the food does not contain any of the following: an ingredient that is any type of wheat, rye, barley, or crossbreeds of these grains; an ingredient derived from these grains and that has not been processed to remove gluten; an ingredient derived from these grains and that has been processed to remove gluten, if it results in the food containing 20 or more parts per million (ppm) gluten; or 20 ppm or more gluten. -- "Food Labeling; Gluten-Free Labeling of Foods," 72 Fed. Reg. 2795 (proposed January 23, 2007) (to be codified at 21 CFR Part 101). The FDA's proposed rule was based on the fact that currently-adopted analytical methods can reliably detect gluten at or above 20 parts per million in most foods. Also, under that rule, food manufacturers looking to market products as 'gluten-free' would voluntarily test those products prior to labeling. However, the FDA allowed the comment period for the proposed rule to pass with no action, and issued no final rule for gluten-free labeling. In 2011, the FDA announced a second comment period for their proposed rule, but that comment period also closed with the FDA taking no action. A full year and a half later, on Dec. 14, 2012, the FDA issued a new proposed rule titled "Request for Comments and Information on Initiating a Risk Assessment for Establishing Food Allergen Thresholds; Establishment of a Docket." They opened comment period on this proposed rule until Feb. 12, 2013, and scheduled an advisory committee meeting of the FDA for March 7, 2013 from 8 a.m. to 5 p.m. It has been eight years, since FALCP mandated the FDA to devise standards for gluten-free labeling, and five years since the legal deadline for final gluten-free rule, and the FDA has yet to accurately define the term "major food allergen," establish safe gluten thresholds for food products, and meet its statutory mandate to create and implement final rules for gluten-free food labeling. Until the FDA formally adopts a final rule for gluten-free labeling, there is no legal definition for what makes food "gluten-free" in the United States, and people with celiac disease will no clear assurance that when a product claims to be gluten-free, it is safe to consume. Please go to the Federal Register and comment on the FDA's latest ofrmulation of their rule (Docket No. FDA-2012-N-0711) regarding gluten-food.
  4. Celiac.com 04/06/2012 - The first step in diagnosing celiac is serological testing, looking for the presence of anti-tTg antibodies. But in adults at least a duodenal biopsy is still the gold standard of diagnosis, partially because of the risk of false positive anti-tTg results. Yet serum anti-tTg levels positively correlate with the severity of small intestinal histopathology. This prompted researchers in Italy to wonder if those patients with the highest ant-tTg levels could be spared an endoscopy, and if so, how high their anti-tTg levels had to be. They conclude, in their words, that "tissue-transglutaminase antibody level 5-folds the upper limit of normal is 100% specific for duodenal atrophy and using this cut-off biopsy could by avoided in 1/3 of patients. Diagnostic criteria of celiac disease in adults need revision." They retrospectively looked at 945 patients who came to their center because of suspected celiac disease. Three different commercially available methods were used to assess anti-tTg levels, which were then correlated with duodenal histology. By all serological methods used, anti-tTg levels increased in parallel with increasing severity of intestinal damage. As noted above, a cut off of five times the upper limit of normal ant-tTg included all of the patients with significant levels of villous atrophy. Celiac disease was confirmed in these patients by the presence of antiendomysial antibodies (EMS) and by their positive response to a gluten free diet. The use of serological results alone had previously been suggested as diagnostic guidelines for children, but these authors suggest that many adults could be spared an endoscopy as well. They also note this strategy is already being implemented in primary care, with people adopting a gluten free diet solely on the basis of blood work; this study is valuable in that it validates that approach. Source: Zanini B, Magni A, Caselani F, Lanzarotto F, Carabellese N, Villanacci V, Ricci C, Lanzini A. High tissue-transglutaminase antibody level predicts small intestinal villous atrophy in adult patients at high risk of celiac disease. Dig Liver Dis. 2012 Apr; 44(4):280-5. Epub 2011 Nov 25.
  5. Dr. Vikki Petersen D.C, C.C.N

    Gluten-Free But Still Feeling Ill

    This article originally appeared in the Spring 2010 edition of Celiac.com's Journal of Gluten-Sensitivity. Celiac.com 10/22/2010 - More and more we’re hearing from frustrated patients who, despite being vigilant about their gluten-free diet, continue to suffer health problems. I have been involved in the field of celiac and gluten sensitivity for over 15 years and am delighted by much of the recent increased awareness and attention given to the area. But I’m also concerned about the lack of assistance given to many patients who have been definitively diagnosed with either celiac disease or gluten sensitivity. While being correctly given the advice to not eat gluten, they are not provided with a follow-up program to address and treat the secondary effects of gluten sensitivity. This oversight condemns many to ongoing ill health. The focus of this article is on the types of conditions we see clinically with our patients, some of the recent research that corroborates our findings, and steps you can take to address the underlying root cause of these problems. Leaky GutAlso known as increased intestinal permeability, a leaky gut refers to a loss of integrity of the lining of the small intestine. Recall that the small intestine is approximately 23 feet in length and has the surface area of a tennis court.Gluten, in the sensitive individual, is a known cause of leaky gut, but in a perfect world the elimination of gluten would allow healing to occur resulting in an intact, healthy intestinal lining. Alas, we do not live in a perfect world and other factors contribute to the health of the gut. Infections in the form of parasites, amoebas, bacteria, and the like, can certainly contribute to continued increased permeability. Likewise, other food reactions, chief among them dairy, can cause persistent irritation and thereby prevent healing. Imbalance of the beneficial bacteria or microbes that comprise the microbiota of the intestine, as well as nutritional and pancreatic enzyme deficiencies, are also suspected to limit healing. Let’s take a look at each of these individually: InfectionsWhether one has celiac disease or is gluten sensitive, one thing is for sure, one’s immune system has been overtaxed due to the presence of gluten in the diet. Depending on the age at diagnosis, it is often several decades of stress that the immune system has undergone.Such an overburdened immune system is unable to be as vigilant as a healthy one and as a result it allows such organisms as parasites, amoebas or bacteria to infiltrate the body. Some estimates suggest that the digestive tract is normally exposed to a pathogenic organism every 10 minutes. A healthy intestinal immune system is able to identify and eradicate those organisms as part of its normal activities. An unhealthy immune system often “misses” such organisms and they happily take up residence in the small intestine. Interestingly, some of these organisms create crypt hyperplasia and villous atrophy that appears the same as that caused by gluten. Imagine the frustration of a patient who is being told by their doctor that they are not following their diet when indeed they are. What’s being missed? The presence of an infectious agent. In the 2003 American Journal of Gastroenterology, researchers reported a large percentage of small intestinal bowel overgrowth (SIBO) in celiac patients with persistent GI symptoms despite adherence to a gluten-free diet. These patients were off gluten, as instructed, but were still having diarrhea due inhospitable organisms in their intestines. This segues nicely into the next area I want to discuss – dysbiosis or imbalance of the friendly bacteria in the small intestine. DysbiosisThe population of organisms found in the intestines of celiac patients (treated with a gluten-free diet or not) is different from that found in healthy control groups. The ratio of good bacteria to bad was found to be reduced in celiac patietnts regardless of whether their celiac disease was active or inactive. Because the “bad” bacteria are pro-inflammatory in nature, they can be responsible for creating some of the initial problems with celiac disease, as well as helping to perpetuate them despite following a gluten-free diet.In the August 2009 Scientific American, Dr Fasano made a very interesting statement regarding these microbes or probiotics as relates to the age of initiation of celiac disease. He stated: “Apparently they [probiotics] can also influence which genes in their hosts are active at any given time. Hence, a person whose immune system has managed to tolerate gluten for many years might suddenly lose tolerance if the microbiome changes in a way that causes formerly quiet susceptibility genes to become active. If this idea is correct, celiac disease might one day be prevented or treated by ingestion of selected helpful microbes.” Isn’t this fascinating? If you haven’t read the complete article I encourage you to do so, but it is sufficient to say there is scientific discussion that entertains the notion that a healthy microbiome or probiotic population is not only anti-inflammatory (a good thing to help prevent many diseases) but may actually act as a “switch” that turns on and off the expression of certain genes. Therefore, part of our program is to examine the population of the microbiome through laboratory testing, and supplement as needed, to support a healthy anti-inflammatory population. In the past we typically prescribed probiotics only for a few short months following the eradication of a pathogenic organism. But in the last several years it has become clear that our patients’ clinical profile is much more stable with continued probiotic supplementation. Dairy SensitivityIt can be difficult to confront major changes in one’s diet. Removing gluten is definitely a big challenge and sometimes my patients look at me forlornly when I simultaneously recommend the elimination of dairy products. I try to encourage them by promising that organic butter is allowed and by quickly recommending my favorite coconut ice cream, as well as cheese and milk substitutes.Contrary to the passing thought that I wish to be cruel, there is excellent documentation to back up what we’ve seen clinically for years - gluten and dairy are truly not our friends. The majority of the world’s people are lactose intolerant. Populations such as Asians, African Blacks, those of Jewish descent, Mediterraneans, Mexicans and North American Blacks all exceed 70% intolerance to lactose. Note that many drugs and supplements may contain lactose as well, so be vigilant. Estimates suggest that we retain the enzyme to digest our human mother’s milk for 2 to 5 years and after that milk from any mammal is likely toxic because it’s too high in protein and phosphorus, making proper digestion impossible. Human milk is very low in protein but rich in essential fatty acids. Casein, a protein from milk, is strongly associated with allergic reactions. Therefore putting lactose and casein together presents double jeopardy to the body. In this country, milk contains more toxins per gram than any other food, so you can see that there’s great cause for concern. Earlier we spoke of leaky gut. Dairy stops the formation of glucosamine in the intestine making it one of the primary causes of leaky gut. I could expand on this further but perhaps we’ll save that for a future article. Nutritional DeficienciesWhen we eat, the ultimate goal is that the food will be broken down into components that can be assimilated into the bloodstream and delivered as fuel to all our trillions of cells. Discovering that one is sensitive to gluten and eliminating it goes a long way toward achieving this goal. However, some vitamins and minerals should be tested to ensure that their levels are normalizing on a gluten-free diet. Otherwise good health may be a fleeting target.Folic acid, vitamin B12, Iron and Vitamin D levels are all very important to measure. Supplementation is often needed to optimize the levels of these substances. Follow-up testing ensures that this objective has been achieved or maintained and should be part of a comprehensive program. Discovering that you’re gluten sensitive and following the diet should be rewarded with dramatically improved health. If that is not the result, other problematic factors need to be isolated and treated. Such a program is not difficult and is well worth the effort. Please let me know if I can answer any further questions. To your good health!
  6. Celiac.com 04/15/2010 - Ten years ago, I embarked on a life that came with a warning about the Specific Carbohydrate Diet from my naturopathic practitioner, "it is a great diet, but a hard one." Those were fighting words to someone who has made a lifetime of "cosmetic" dieting with tendencies to yo yo back and forth into the obesity zone. The Specific Carbohydrate Diet diet was chosen to relieve pain. Starting a new weight-loss diet had always been inviting and exciting. The magic of the initial water weight-loss, the restrictive ruthless regimentation, calorie counting, portion control and forced water consumption were as exciting as hair shirts and beds of nails for religious fanatics. Dieting was my religion, food was like the duplicitous friend who is an enemy at the same time. The years marched on and my "stuff and starve" lifestyle beat a destructive highway to digestive hell in the form of celiac disease, an illness that could have been caused by any number of things, age, a compromised immune system, a recent illness or maybe even the evil eye. That was ten years ago. It has turned out that the Specific Carbohydrate Diet is no transient companion to my fork, knife and spoon. It blossomed into a creative and motivating experience, a learning opportunity, a template for sharing, writing and creating recipes and a sometimes tiresome topic at social gatherings (although as we age, health chat is pretty popular). I have made more friends through the Specific Carbohydrate Diet than at the dog park and have been given the opportunity to help strangers. Food at the good restaurants pales in comparison to the ever innovative pure, tasty, quality meals and dishes I create from the Specific Carbohydrate Diet palette of foods. Excluded are refined sugars, starches and gluten and they are not much missed. After eight years on the Specific Carbohydrate Diet, I tried occasional servings of rice and potatoes and some dark chocolate just to see if I had healed. Sometimes I tolerated these well, sometimes not and mainly lost interest. As for grain, it can remain on that plain in Spain. I want no part of it. The Specific Carbohydrate Diet has not cured me, and I doubt that it will, but it is an effective dietary management program. Yes I still get the bloat, the night time rashes, and the irritated bowel and sometimes I still have a very touchy immune system. It depends on the load at a given time. One thing that is really helpful then is a few days back on the initial introductory portion of the Specific Carbohydrate Diet. It calms the "Gut Devils" and clears the "Digestive Decks." If people deal the "pity card" as I describe being on a gastric diet, I ignore it as my diet deals aces and also the "Get Out of Pain Jail" card and of course, to this old dieter, the permanent thrill of the drill.
  7. Celiac.com 03/16/2009 - Current treatment for celiac disease consists of a lifetime gluten-free diet. However, once the diagnosis is made, most people don’t really receive regular follow-up or monitoring of their treatment unless they have some obvious complaint. That’s beginning to change, and more doctors are beginning to advocate long-term celiac care, which includes regular tests to assess dietary compliance. To accomplish this goal, doctors are working to determine the best program of follow-up treatment. A team of Austrian researchers recently set out to determine which noninvasive test for celiac disease is best for assessing mucosal status in people with celiac disease. The research team was made up of doctors Andreas K. W. Vécsei, Ulrike B. Graf, and H. Vogelsang, associated with St. Anna Children's Hospital, Vienna, Austria and the Department of Gastroenterology and Hepatology, Clinic of Internal Medicine III, Medical University of Vienna, Vienna, Austria. The research team set out to clarify which noninvasive follow-up methods for testing blood serum or intestinal permeability (IPT) – best match the patient’s histology, and whether the accuracy of these tests is affected by the interval between diagnosis and follow-up affects. The team mined a computer database to compile information from adult patients, diagnosed with celiac disease between December 1989 and July 2006, who underwent follow up via biopsy, IPT, and serological testing via IgG anti-gliadin antibodies (AGA-IgG), AGA-IgA, and endomysial antibodies (EMA). They measured effectiveness of noninvasive test results based on the presence of villous atrophy upon biopsy. The team divided patients into two groups. The first, group A, comprised patients followed up within 24 months of diagnosis, and group B, comprising patients followed up after 24 months. In all, the team was able to evaluate forty-seven patients. The tests showed the following results: Lactulose/mannitol (L/M) ratio showed a sensitivity of 85% and a specificity of 46.2% for mucosal atrophy, while saccharose excretion showed a sensitivity of 60% and a specificity of 52.6%. AGA-IgA and AGA-IgG showed 15% and 20%, respectively, and both showed specificity of 100%. AGA was of limited usefulness due to low number of positive results. EMA assay was 50% sensitive and 77.8% specific. In group A (n = 23) L/M ratio performed best in terms of sensitivity (88.9%), whereas EMA achieved a higher specificity (71.4%). In group B, the sensitivity of the L/M ratio decreased to 85.7%, while the specificity of EMA increased to 91.7%. The team concluded that these results show that none of the non-invasive tests was an accurate replacement for follow-up biopsy in detecting severe mucosal damage. Until an accurate test is developed, long-term follow-up monitoring of gluten-free status in people with celiac disease will remain difficult to do reliably without biopsy. Endoscopy 2009; 41: 123-128
  8. Gastroenterology. 2003 Aug;125(2):337-344. Celiac.com 08/07/2003 - This studys aim was to determine the feasibility of altering gluten proteins to make them harmless to those with celiac disease. Unfortunately the altered protein still produced a toxic T-cell reaction in almost half of the patients studied. Here is the abstract: Intestinal T-cell responses to high-molecular-weight glutenins in celiac disease. Molberg O, Solheim Flaete N, Jensen T, Lundin KE, Arentz-Hansen H, Anderson OD, Kjersti Uhlen A, Sollid LM. BACKGROUND & AIMS: The chronic, small intestinal inflammation that defines celiac disease is initiated by a HLA-DQ2 restricted T-cell response to ingested gluten peptides after their in vivo examination by tissue transglutaminase (TG2). To date, celiac disease can only be treated by a lifelong abstinence from foods that contain wheat, rye, or barley; better therapeutic options are hence needed. An attractive target would be to identify nontoxic wheat cultivars or components thereof with intact baking qualities. Because these qualities are mainly determined by the high molecular weight (HMW) glutenin proteins of gluten, it is critical to know if these proteins are toxic or, more specifically, if they will trigger the activation of T cells in the celiac lesion. METHODS: Different, highly purified HMW glutenins were isolated from wheat cultivars or expressed as recombinant proteins. The proteins were first tested for recognition by a large panel of gluten-specific T-cell lines established from celiac lesions and then applied during ex vivo challenges of celiac biopsies to allow for a direct identification of HMW specific T cells. RESULTS: Intestinal T-cell responses to TG2-deamidated HMW glutenins but not the corresponding native proteins were detectable in 9 of the 22 adult and childhood celiac disease patients tested. CONCLUSIONS: T cells within celiac lesions frequently recognize deamidated HMW glutenin proteins. This finding questions the possibility of implementing these proteins in novel food items destined to be nontoxic for celiac disease patients.
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