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Found 52 results

  1. Celiac.com 11/28/2018 - Patients with gluten ataxia without enteropathy have lower levels of antigliadin antibodies (AGA) compared to patients with celiac disease. Magnetic Resonance Spectroscopy (NAA/Cr area ratio) of the cerebellum improves in patients with gluten ataxia following a strict gluten-free diet, and is associated with an improvement in symptoms. A team of researchers recently set out to present their experience of the effect of a gluten-free diet in patients with ataxia and low levels of AGA antibodies measured by a commercial assay. The research team included Marios Hadjivassiliou, Richard A Grünewald, David S Sanders, Panagiotis Zis, Iain Croall, Priya D Shanmugarajah, Ptolemaios G Sarrigiannis, Nick Trott, Graeme Wild, and Nigel Hoggard. They are variously affiliated with the Academic Departments of Neurosciences and Neuroradiology; the Departments of Gastroenterology, the Departments of Dietetics; the Departments of Immunology, Sheffield Teaching Hospitals NHS Trust, in Sheffield, UK. The team conducted MR spectroscopy on 21 consecutive patients with ataxia and serum AGA levels below the positive cut-off for celiac disease, but above a re-defined cut-off in the context of gluten ataxia, at baseline and after a gluten-free diet. Of the 21 included patients with gluten ataxia, the team found that ten were on a strict gluten-free diet with elimination of AGA, 5 were on a gluten-free diet, but continued to have AGA, while 6 patients did not follow a gluten-free diet. The NAA/Cr area ratio from the cerebellar vermis increased in all patients on a strict gluten-free diet, increased in only 1 out of 5 patients on a gluten-free diet with persisting circulating AGA, and decreased in all patients who did not follow a gluten-free diet. From these results, the team concludes that patients with ataxia and low levels of AGA benefit from a strict gluten-free diet. The results suggest an urgent need to redefine the serological cut-off for circulating AGA in the diagnosis of gluten ataxia. Read more in Nutrients 2018, 10(10), 1444; doi:10.3390/nu10101444
  2. So aside from the title, I’ve still been experiencing diarrhea, and severe abdominal pain. The gi said she thinks I have ibs d. I’m worried it might be refractory celiacs. I’ve gone 100% gluten-free for these 7 months as I feel like s$#& and want to be well. I’ve changed my kitchen tools, pots, pans etc. I have also changed all my beauty products to gluten-free ones, including lotion, makeup, shampoo etc. I don’t eat gluten and I don’t even eat out or at others houses. I don’t understand why I still have the antibodies. My ONLY idea is maybe a course of antibiotics I took for mouth surgery (military isn’t very nice about my celiacs and wouldn’t change my medicine even if it said “contains wheat” on it so I didn’t Nima test it. Although that was 7 days and I felt the same dying the period I was on those as I did these last 7 months. I have been glutened early into my time so I know how that feels for me so I really don’t think it was the antibiotics. Either way I still feel like crap and was wondering if anyone has some insight. At this point I’m like dang I should just eat gluten it wouldn’t be any different ( I def wouldn’t but I laugh about how it wouldn’t change things for me)
  3. Celiac.com 11/11/2017 - (NOTE: This article is from 2012 and is being made available as Celiac.com rolls our past issues of Journal of Gluten Sensitivity) It's just like being a little kid with a super sore throat and your mom taking you to the doctor to get a test for strep throat. The doctor swabs your throat with two sticks to find out what nasty bacteria is camping out. In just moments you've got a diagnosis of strep throat and can start antibiotics to miraculously make the pain go away. You go home with a prescription, get in bed and eat mom's homemade chicken rice soup until you feel better in a couple of days. How cool would it be if getting diagnosed with celiac disease was this easy? The wonderful news is that we're getting closer to having a test that will diagnose celiac disease with just a simple prick of a finger and a 10-minute wait. The CeliacSure Test Kit measures (anti-tTG) IGA antibodies from a fingertip blood sample. It works by taking a small drop of blood, mixing it with a buffer and applying the mixture onto a test cartridge. Within moments two red lines appear if the test is positive, while only one line appears if the result is negative. And, you can take the test at home without ever getting out of your pajamas! "The test kit is a point-of-care, at-home test that's very similar to reading results of a pregnancy test," said Dr. Daniel Leffler of the Celiac Disease Center at Beth Israel Deaconess Medical Center in Boston. Dr. Leffler, a gastroenterologist by training with a background in nutrition, has a long-standing interest in celiac disease. Several years ago he teamed up with Dr. Ciaran Kelly and Dietitian Melinda Dennis to found the Celiac Disease Center at Beth Israel Deaconess Medical Center where they focus not only on providing top notch patient care, but also on high level disease research. The latest project: studying the efficacy of the CeliacSure test for celiac disease diagnosis. Dr. Leffler said his team got involved with the finger prick test study because they feel it's important to take down barriers to patients getting diagnosed with celiac disease. "We do a lot with educating other medical providers about offering in-clinic testing, but I think it's really important to put a tool in the hands of the people." "We've teamed up with the [marketers] of the test kit at GlutenPro/Biocard CeliacSure Test to see how effective this test is in the USA. We're providing 2 kits per family to use on first-degree relatives of people with celiac disease. To qualify, participants in the study must not be on a gluten-free diet. We send them the test kit to take as well as a survey about their ability to use and understand the test. The goal is that this small study comes out favorable [sic] so we can move on to large scale studies that will compare the finger prick test to the gold standard laboratory serology testing." Dr. Leffler says he's really excited about the potential of this point-of-care test because it will "allow us to reach a population that might not otherwise come in to get tested, mainly first degree relatives of patients already diagnosed with celiac disease." It's important to note that right now the CeliacSure test is only for research purposes, not actual diagnosis. It is available in Canada and other countries, but it's still under evaluation here in the United States. And, while the strep throat analogy is a great way to think about how this test will work, it's extremely important to understand that if you get a positive result with the CeliacSure test, do not start a gluten-free diet until you have followed up with a doctor to confirm the diagnosis. As with all medical studies there's some fine print you need to know about. Participants in the study must meet all of the following criteria: 1. Over the age of 18 2. A first or second degree relative with celiac disease 3. Not previously diagnosed with celiac disease 4. Not on a gluten-free diet or low-gluten diet within the past 3 months 5. Able and willing to self administer the test, complete a short survey form and return both in the envelope provided 6. Willingness to have follow up medical evaluation in the event of a positive test 7. A resident of the United States Listen to a full interview with Dr. Leffler about the CeliacSure study on the Hold the Gluten Podcast (http://traffic.libsyn.com/holdthegluten/050_HoldTheGluten-05Apr2012.mp3) with Vanessa Maltin Weisbrod and Maureen Stanley now! And, if you would like to participate in the study, please contact Dr. Toufic Kabbani at celiac@bidmc.harvard.edu or by phone at 617-667-0528.
  4. I recently took a blood test and went over the results with my GI doctor who will be performing and endoscopy and colonoscopy on me soon. I can't remember exactly what she said, but I believe she was talking about my IGA-TTG levels. She said the normal range was under 10 but mine was 639. I think she was talking about IGA-TTG but I'm not sure. For people who have done this test what were your high levels? Thanks! Female, 16
  5. I recently found out I have the DQ8 hetero gene. Because my life was being affected so drastically, I discontinues eating gluten and have started to feel myself. about 90% of my symptoms have resolved during the past 2 weeks of eating gluten-free. Now, I need to decide whether I should continue with a gluten challenge and test for antibodies and do the endoscopy/biopsy. I am one that would be unsettled not knowing whether or not I have Celiac. Does anyone have advice on whether or not I should do a gluten challenge and do further testing to pursue a diagnosis?
  6. Celiac.com 10/13/2017 - Tissue transglutaminase (tTG) immunoglobulin A (IgA) testing is a sensitive adjunct to the diagnosis of coeliac disease. The threshold for positivity was developed for diagnosis, with negative results reported as below the reference value (<4 U/mL). A team of researchers recently set out to investigate if an undetectable tissue transglutaminase IgA antibodies (tTG IgA<1.2 U/mL) is more predictive of healing compared to patients with negative but detectable serology (1.2-3.9 U/mL). The research team included H. Fang, K. S. King, J. J. Larson, M. R. Snyder, T. T. Wu, M. J. Gandhi, and J. A. Murray. They are variously affiliated with the Department of Medicine, the Division of Gastroenterology and Hepatology, the Division of Anatomic Pathology, the Division of Clinical Biochemistry and Immunology, the Division of Biomedical Statistics and Informatics, and the Division of Transfusion Medicine at the Mayo Clinic, Rochester, MN, USA. The research team conducted a retrospective study of 402 treated coeliac disease patients seen at the Mayo Clinic with negative tTG IgA values drawn within 1 month of duodenal biopsy between January 2009 and December 2015. The team used Corazza-Villanacci scores to assess mucosal healing, and logistic regression to assess the relationship of clinical variables with a normal biopsy. They also noted the presence of gastrointestinal symptoms. Their results showed that patients with undetectable test levels more frequently had normal duodenal histology, as compared with patients with detectable tTG IgA levels. Asymptomatic patients more often showed normal duodenal histology as compared to symptomatic patients. Patients with undetectable blood levels, and who followed a gluten-free diet for ≥2 years were more likely to have no villous atrophy, as compared to patients with detectable blood levels. Follow-up biopsies revealed that people recovering from celiac disease with negative tTG IgA serology showed that undetectable test levels are associated with normal histology. Source: AP&T
  7. Celiac.com 10/12/2015 - There's been a good deal of attention devoted to gluten sensitivity in people without celiac disease, but researchers still don't know much about potential risks associated with the condition. A research team recently looked at the prevalence of autoimmune diseases among patients with non-celiac wheat sensitivity (NCWS), and investigated whether they carry antinuclear antibodies (ANA). The research team included A. Carroccio, A. D'Alcamo, F. Cavataio, M. Soresi, A. Seidita, C. Sciumè, G. Geraci, G. Iacono, and P. Mansueto. They are variously affiliated with the DiBiMIS University of Palermo, Palermo, Italy; the department of Internal Medicine at Giovanni Paolo II Hospital in Sciacca, Italy; the DiBiMIS University of Palermo, in Palermo, Italy; the department of Pediatric Gastroenterology in ARNAS Di Cristina Hospital, Palermo, Italy; and the Surgery Department at the University of Palermo in Palermo, Italy. The research team conducted a retrospective study of 131 patients diagnosed with NCWS, 121 of whom were female. The average patient age was 29.1 years, and the study was conducted at 2 hospitals in Italy from January 2001 through June 2011. The team also collected data from 151 patients with celiac disease or irritable bowel syndrome, who served as control subjects. They reviewed patient medical records to identify those with autoimmune diseases. They then conducted a prospective study of 42 patients, 38 of whom were female, with an average age of 34 years, who had been diagnosed with NCWS from July 2011 through March 2014 at 3 hospitals in Italy. For the prospective study, one hundred age- and sex-matched subjects with celiac disease or IBS served as control subjects. The team collected serum samples from all subjects and measured ANA levels using immunofluorescence analysis. Participants completed a questionnaire and the team reviewed patient medical records to identify those with autoimmune diseases. In the retrospective analysis, about 30% of patients with either NCWS or celiac disease developed autoimmune diseases; mainly Hashimoto's thyroiditis, of which there were 29 cases. Compare this with about 4% of IBS who developed an autoimmune disease (P < .001). In the prospective study, 24% of patients with NCWS, 20% of patients with celiac disease, and 2% of patients with IBS developed autoimmune diseases (P < .001). In the retrospective study, serum samples tested positive for ANA in 46% of subjects with NCWS (median titer, 1:80), 24% of subjects with celiac disease (P < .001), and just 2% of subjects IBS (P < .001). In the prospective study, serum samples were positive for ANA in 28% of subjects with NCWS, 7.5% of subjects with celiac disease (P = .02), and 6% of subjects with IBS (P = .005 vs patients with NCWS). From these results, they conclude that positive ANA results are associated with the presence of the HLA DQ2/DQ8 haplotypes (P < .001). Source: Gastroenterology. 2015 Sep;149(3):596-603.e1. doi: 10.1053/j.gastro.2015.05.040.
  8. Celiac.com 06/05/2017 - Doctors diagnose celiac disease by confirming various clinical, genetic, serologic, and duodenal morphology features. Based on retrospective data, recent pediatric guidelines propose eliminating biopsy for patients with IgA-TTG levels more than 10-times the upper limit of normal (ULN), along with a few other criteria. One retrospective study showed that researchers using levels of IgA-TTG and total IgA, or IgA-TTG and IgG against deamidated gliadin (IgG-DGL) could identify patients both with and without celiac disease. A team of researchers recently set out to validate the positive and negative predictive values (PPV and NPV) of these diagnostic procedures. The research team included Johannes Wolf, David Petroff, Thomas Richter, Marcus KH. Auth, Holm H. Uhlig, Martin W. Laass, Peter Lauenstein, Andreas Krahl, Norman Händel, Jan de Laffolie, Almuthe C. Hauer, Thomas Kehler, Gunter Flemming, Frank Schmidt, Astor Rodriques, Dirk Hasenclever, and Thomas Mothes. Their team conducted a prospective study of 898 children undergoing duodenal biopsy analysis to confirm or rule out celiac disease at 13 centers in Europe. They then compared results from antibody tests with results from biopsies, follow-up data, and diagnoses made by the pediatric gastroenterologists. In all cases, diagnosis was made for celiac disease, no celiac disease, or no final diagnosis. Blinded researchers measured levels of IgA-TTG, IgG-DGL, and endomysium antibodies, while tissue sections were analyzed by local and blinded reference pathologists. The team validated two procedures for diagnosis: total-IgA and IgA-TTG, as well as IgG-DGL with IgA-TTG. Patients whose antibody concentrations for all tests were below 1-fold the ULN were assigned to the no celiac disease category. Those whose antibody concentrations for at least one test were above 10-fold the ULN were assigned to the celiac disease category. All other cases were considered to require biopsy analysis. The team calculated the ULN values using the cut-off levels suggested by the test kit manufacturers. They conducted HLA-typing for 449 participants. To extrapolate the PPV and NPV to populations with lower rates of celiac disease, they used models that accounted for how specificity values change with prevalence. In all, the team found 592 patients with celiac disease, 345 who did not have celiac disease, and 24 with no final diagnosis. The TTG-IgA procedure identified celiac disease patients with a PPV of 0.988 and an NPV of 0.934. The TTG-DGL procedure identified celiac disease patients with a PPV of 0.988 and an NPV of 0.958. Their extrapolation model estimated that PPV and NPV would remain above 0.95 even at a disease prevalence as low as 4%. Meanwhile, tests for endomysium antibodies and HLA type did not increase the PPV of samples with levels of IgA-TTG 10-fold or more above the ULN. Interestingly, the pathologists disagreed in their analyses of duodenal morphology about 4.2% of the time, a rate comparable to the error rate for serologic tests. This study validates the use of the TTG-IgA procedure and the TTG-DGL procedure in lieu of biopsy to diagnose pediatric patients with or without celiac disease. Source: Gastroenterology. DOI: http://dx.doi.org/10.1053/j.gastro.2017.04.023 The researchers are variously affiliated with the Institute of Laboratory Medicine, Clinical Chemistry and Molecular Diagnostics, Medical Faculty of the University and University Hospital, Leipzig, Germany, the Institute for Medical Informatics, Statistics & Epidemiology (IMISE), University of Leipzig, Germany, the Department of Paediatrics, University of Oxford, Oxford, United Kingdom, the Translational Gastroenterology Unit, Nuffield Department of Medicine, University of Oxford, John Radcliffe Hospital, Oxford, United Kingdom, the, University Children's Hospital Halle, Germany, the Medical School, Hannover, Germany, Helios Hospital, Department of Paediatrics, Plauen, Germany, the Children's Hospital Prinzessin Margaret, Darmstadt, Germany, the University Children's Hospital Graz, Austria, the Children's Hospital, Justus Liebig University Giessen, Germany, the University Children's Hospital Leipzig, Germany, the Children's Hospital of the Clinical Centre Sankt Georg Leipzig, Germany, the Clinical Trial Centre, University of Leipzig, Germany, the DKD Helios Children's Hospital, German Clinic for Diagnostics, Wiesbaden, Germany, the University Children's Hospital, Technical University Dresden, Germany, and the Alder Hey Children's National Health Service Foundation Trust, Liverpool, United Kingdom.
  9. Celiac.com 04/07/2014 - Histologically non-responsive celiac disease (NRCD) is a potentially serious condition found in celiac disease patients who suffer persistent villous atrophy despite following a gluten-free diet (GFD). Currently, the only way to monitor patient progress rely on invasive and costly serial duodenal biopsies. Looking for better options, a team of researchers recently set out to identify antibody biomarkers for celiac disease patients that do not respond to traditional therapy. The research team included B. N. Spatola, K. Kaukinen, P. Collin, M. Mäki, M. F. Kagnoff, and P. S. Daugherty. They are affiliated with the Department of Chemical Engineering, University of California, Santa Barbara in California, the Department of Gastroenterology and Alimentary Tract Surgery and the Center for Child Health Research at the University of Tampere and Tampere University Hospital in Tampere, Finland, with the Department of Medicine at Seinäjoki Central Hospital in Seinäjoki, Finland, and with the Laboratory of Mucosal Immunology in the Departments of Medicine and Pediatrics at the University of California San Diego in La Jolla, California. Using flow cytometry to screen bacterial display peptide libraries, the team was able to identify the epitopes specifically recognized by antibodies from patients with NRCD, but not by antibodies from responsive celiac disease patients. By comparing ELISA results for sera from 15 NRCD patients and 45 patients with responsive celiac disease, all on a strict GFD for at least 1 year, the team confirmed that deamidated gliadin was the antigen mimicked by library peptides. They identified the dominant consensus epitope sequence by unbiased library screening QPxx(A/P)FP(E/D). The epitope sequence was highly similar to reported deamidated gliadin peptide (dGP) B-cell epitopes. They also found that anti-dGP IgG measurement by ELISA discriminated between NRCD and responsive celiac disease patients with 87% sensitivity and 89% specificity. Most importantly, they found that dGP antibody levels correlated with the severity of mucosal damage, meaning that IgG dGP levels may be useful in monitoring small intestinal mucosal recovery on a GFD in NCRD patients. The team found that celiac patients with NRCD can be spotted by their increased levels of anti-dGP IgG antibodies even when the patients are following strict gluten-free diets Lastly, they feel that anti-dGP IgG assays may be useful for monitoring mucosal damage and histological improvement in celiac disease patients on a strict GFD. Source: Aliment Pharmacol Ther. 2014;39(4):407-417.
  10. Celiac.com 05/26/2017 - Can a gluten-free diet help improve symptoms in people suffering from IBS? A new study says yes, some of them, at least. More than 60% of patients with IBS suffer from bloating and abdominal pain after eating certain foods. In some patients, who do not have celiac disease or wheat allergy, these symptoms may be due to an adverse reaction to wheat and gluten. Several studies have suggested that anti-gliadin antibodies can be a useful benchmark for predicting which patients with irritable bowel syndrome will benefit from a gluten-free diet. However, the idea remained untested until recently, when researchers conducted a prospective study in IBS patients. An update on their research was presented at Digestive Disease Week. The research was conducted by María Inés Pinto Sanchez, MD, and colleagues at the department of medicine at McMaster University and the Farncombe Institute in Ontario, Canada. To better understand the usefulness of these predictors, the research team looked at 44 patients with IBS and 23 healthy volunteers, both before and after 1 month of adhering to a gluten-free diet. They assessed GI transit, GI symptoms, anxiety, depression, somatization and dietary habits. The team tested each subject for anti-gliadin antibodies, then stratified the patients based on the results. Patients with celiac disease were not included in the study. The investigators found that just over half (53%) of the IBS patients, and 25% of the healthy volunteers, tested positive for IgA or IgC anti-gliadin antibodies. Additionally, HLA DQ2/DQ8 genetic predisposition was comparable for both groups. IBS patients who tested positive for antigliadin antibodies, and who followed a gluten-free diet, showed overall improvement in symptoms, especially constipation (P = 0.01), diarrhea (P = 0.001) and abdominal pain (P < 0.001) while IBS patients who tested negative only experienced improvements in abdominal pain (P = 0.01). Compared with patients who tested negative, gluten-free IBS patients who tested positive saw more normalization in GI transit (OR = 1.75 95% CI, 1.06 - 3.06). Regardless of antibody status, all IBS patients saw comparable improvements in anxiety, somatization and well-being, but only patients who tested positive saw reduced depression scores. A gluten-free diet in patients who tested positive for anti-gliadin antibodies was associated with symptomatic improvement (OR = 8.54; 95% CI, 1.41-48.21), while other factors like changes in motility, dietary adherence or genetic risk were not. Their data led the team to conclude that anti-gliadin antibodies can be used to determine which IBS patients are more likely to see an improvement in symptoms, and in functionality. Interestingly, strict compliance with the gluten-free diet did not predict improvement, which indicates that gluten restriction, rather than gluten avoidance, may help to manage symptoms in these IBS patients. That means that patients might be able to get better by cutting back on gluten, instead of cutting it out of their diet entirely. Read more at Healio.com.
  11. Celiac.com 04/08/2017 - "Do not fear to be eccentric in opinion, for every opinion now accepted was once eccentric" – Bertrand Russell. I would like to introduce the term "zero" when we talk about eliminating gluten. Precise language leads to precise action. Zero means none, not some. Yes, my recommendation is to change the gluten-language that we have been using. The meaning of the phrase 'gluten-free' has been diluted, so it almost has the connotation of 'not-much-gluten'. It suggests that 'a-little-gluten-does-not-matter' or 'you-are-free-to-give-up-gluten-if-you-want-to'. A much stronger expression is needed. I am changing the term 'gluten-free diet' to 'gluten-zero-diet'. This should change how people think about gluten. I am a paediatrician, so I see lots of sick children, and many of them are gluten-affected. Happily, they get better much more quickly, after going off gluten, than gluten-affected adults. I am a strong believer in putting these children on a gluten-free diet well before they end up with substantial gluten-related harm, and to spare them from years or even decades of gluten- induced symptoms. This means making an early diagnosis. It also means putting them on a gluten-zero-diet before they get the severe gut damage of celiac disease. The big question for the children, their parents, and me is "how gluten-free does he need to be?" and "for how long does he have to be gluten-free?" If you read my early books, I talk about eating gluten to tolerance. But I have completely changed my mind about that. My stance now is firmly zero-gluten. This might seem a radical position to take in the face of the FDA and other groups talking about 20 ppm as the okay level of gluten contamination. So, how can I justify my gluten-zero-diet opinion? I'll explain a little background information first. Do I have to go gluten-free? I am often asked if a gluten-free diet is the only way to manage celiac disease. Many of my families are initially resistant to the idea. This is no surprise because gluten-foods are all they know about. Actually, all they know about gluten is that they are just living like everyone else, mostly on wheat-derived foods. They have a food habit. They do not think much about what they are eating. They just eat what is cheap and convenient - that means wheat. But the simplistic answer to this question is "Yes! a zero-gluten diet is the answer." However, this is a complex question. So to broaden the question I have included all gluten-related disorders. I repeat, "Yes! A gluten-free diet is the central management strategy for celiac disease and gluten-related disorders." But what does a 'gluten-free diet' mean? How free-of-gluten do you have to be? To me, a gluten-free diet means zero-gluten for life – with no exemptions. Certainly there are many who suggest that people can eat gluten to tolerance. (I used to say this as well.) But now I strongly disagree. Any gluten has the potential to cause you harm. Get your gluten antibodies down Going on a gluten-free diet is more than just the eradication of gluten from your diet. Surprisingly, it is also about reducing the gluten antibodies that your immune system is churning out. Gluten can harm you in more ways than by a direct, or an immune effect, in your gut. Did you know that gluten can also cause you harm through the gluten antibodies that your body produces? (See the chapter on neurological harm.) There is growing evidence that the gluten antibodies (AGA – anti-gluten-antibody) are damaging to us, particularly to our neurological system. The research work done by Hadjivassiliou (2012) needs to be heeded. Think about why you get vaccinated. Vaccination is to keep you protected from bacteria and virus throughout your life. For this purpose, once you have stimulated antibody production by your immune system, whenever your body comes in contact with the identical stimulant again, your immune system begins to produce much more of this same antibody again. Most people get vaccinated against illnesses. For instance, most people have had their tetanus shot. This comprises a tiny amount of tetanus protein (the allergen), which stimulates your body to produce antibodies against the tetanus bacteria. This then protects you from tetanus infection for years to come. The vaccine is intended to stimulate your body to produce the anti-tetanus-antibodies, lifelong. To ensure this happens you will need to get a couple of booster shots during your lifetime. This also happens in gluten sensitization. So when you think about gluten, and the antibodies against gluten that your body is continually making, you can now understand that every time you eat gluten, by error or design, this will stimulate more gluten antibody production. And that is a very bad thing for you. It is crucial to reduce gluten antibody levels. Even a tiny amount of gluten is enough to stimulate ongoing antibody production, which is potentially harmful for your nerves and brain. The goal should be to get and keep your gluten antibodies down. Antibody reduction rather than just the elimination of gluten Hadjivassiliou, in his 1998, paper says, "These results strengthen our contention that eliminating these antibodies through strict adherence to a gluten-free diet may have important therapeutic implications for patients with gluten ataxia." Here the focus is on antibody reduction rather than just the elimination of gluten. Surely there is a strong case for investigating for gluten-sensitivity in all people with the likelihood of gluten-related disorders. Is 20 ppm really okay? Does a gluten-zero-diet literally mean no-gluten-at-all? Definitely, "Yes!" But the question everyone is asking is, "what does a gluten-zero-diet mean in terms of every-day practicality?" There is ongoing debate about how many parts per million (ppm) of gluten is acceptable in food. Pragmatically, because it is so difficult to get rid of cross-contamination in food production and processing, the number of 20 ppm is now surfacing as a 'reasonable' level of gluten to be consumed (some countries have 200 ppm, and the FDA is recommending 20 ppm). When you first hear about this number, it seems to be a negligible amount. However, there are still concerns for some people who seem to be exquisitely sensitive to gluten. For me, a gluten-zero-diet means 'no-gluten-at-all'. This can be achieved if you eat fresh fruits and vegetables, unprocessed meat and fish, uncontaminated rice, corn and other alternate grains, eggs, nuts and unprocessed dairy foods. This means no packet or processed foods – I have called this the no-packet-food-diet. Gluten-free is more than removing gluten It is a lot more than 'just' going gluten-free. Yes, there are many more things to do when healing someone with celiac disease/ gluten-related disorders. The longer you have had gluten-symptoms, the worse your body will be. More healing will be required. You may need additional minerals, vitamins and probiotics. There are many routine health checks to take. You should also ensure that your gut has healed (via blood test and, maybe, a repeat endoscopy). Advocating ZERO gluten Yes! I am a zero-gluten man. I advocate a gluten-zero-diet. This is based on the concern that tiny amounts of gluten in your food are enough to stimulate your immune system. Even if you are not feeling unwell from this apparently trivial exposure, your body could be getting sick. What seems trivial to you may not be trivial to your highly tuned and sensitized immune system. By definition, 'zero gluten' means ZERO! In other words – it is undetectable gluten (say less than 1 ppm – gluten detection is now getting down to these very low levels). Consequently, any food in which gluten can be detected (between 5–20 ppm should not be labeled gluten-free. This is because it is NOT gluten-free. It does contain (an apparently) trivial amount of gluten. These foods that contain 5–20 ppm need to be labelled 'contains gluten at levels 5–20 ppm'. We need to know exactly what is in our food. We need this information to make informed, healthy food choices. The main opposition to zero-gluten labeling comes from the food manufacturing and processing industries – not from the gluten-free community. Food companies say it is not practical or economic to make zero-gluten products. They claim that a 20 ppm is a realistic compromise. They say that 20 ppm is close enough. But this is not what the gluten-free community want: we demand "no-gluten-at-all". That is zero-gluten. The gluten-contaminated food chain needs to be entirely cleaned up. The zero-gluten market is growing. The gluten-free community does not want any gluten traces in their food. Gluten labeling: a two-tier approach In New Zealand, "Coeliac New Zealand" runs a gluten-logo program to give "consumers a quick reference point when shopping and faced with uncertainty about the genuine gluten-free status of a product." They have, very sensibly, adopted a two-tier system of certification (http://www.coeliac.org.nz/crossed_grain). Products carrying the 'Crossed-Grain-symbol' in addition to the words 'GLUTEN-FREE' adhere to the FSANZ standard of "No detectable gluten". Products carrying the Crossed-Grain-symbol without any other words (that is, not displaying the wording 'GLUTEN-FREE') adhere to the international Codex standard for 'gluten-free tested' and they have gluten levels of less than 20 ppm ( which is considered suitable as per the Codex standard for gluten content). This two-tier system: undetectable-gluten; and less-that-20-ppm-gluten, is simple. We know just what we are getting. How hard is this? Everyone is satisfied. So why does the FDA just want a single definition? If we, the gluten-free consumers, refuse to buy gluten-contaminated products, then food makers will have to change – or some may decide not to chase the gluten-free market. Refractory celiacs still gluten contaminated Another argument for zero-gluten is that not all celiac sufferers heal on an apparently gluten-free diet. Celiac disease does not heal when you are constantly exposed to gluten. Dewar and co-workers investigated 100 patients who had non-responsive celiac disease. They found the following: 45 (45%) of these patients were not adequately adhering to a strict gluten-free diet, of whom 24 (53%) were inadvertently ingesting gluten, and the remaining 21 (47%) admitted non-compliance. http://www.ncbi.nlm.nih.gov/pubmed/22493548. Cross-contamination I suggest that you look at the "Gluten-Free Certification Organization (GFCO)" website for detailed information on testing for gluten and gluten cross-contamination. http://gfco.org The GFCO is a program of The "Gluten Intolerance Group" (GIG). GFCO inspects products specifically for gluten. They say "Unless food is grown in your own garden in an airtight bubble, it is impossible to guarantee a 100% pure product." Measuring gluten contamination is difficult as there are so many factors to consider. For example: the raw materials and the possibility they were cross-contaminated; the process used in production (such as the movement of raw materials and equipment) that could increase cross contamination; cleaning and packaging processes. Also their testing procedures need to be robust but affordable. They have to take into account: what is being tested (raw materials, equipment or finished products); the type of laboratory technology that is appropriate; the appropriate frequency for testing samples. Companies rely on "their Good Manufacturing Practices (GMP), Hazard Analysis Critical Control Point (HACCP) programs, and standard operating processes and procedures to determine a corrective action plan." Living with cross contamination Terri says about cross contamination at school, "We have to be so careful. So we go with home lunches, because food preparation can be an issue. Just one spoon in the wrong dish, and then back again, contaminates everything … and have you ever seen the cloud of flour that emits when you turn on a food mixer? We deal with celiac disease for my girls and for me. It is just not worth the risk of cross contamination. We prepare homemade gluten-free pasta salads, make homemade gluten-free "Lunchables" with far healthier ingredients, homemade minestrone, gluten-free sandwiches, chili, and a thousand other foods. We make gluten-free granola and trail mix for snacks. It gets easier. The best thing you can do is to find some awesome recipes and make sure whoever has celiac disease learns how to cook! My daughters are 7 and 9, and both know how to read labels and search for hidden gluten. They can prepare several easy foods and snacks, and do not feel like they are missing out. It really does get better!" How much easier it would be if there was no gluten in the food chain! Yes, cross contamination is the big on-going issue that few gluten-outsiders understand. At a recent hotel breakfast, I asked if they offered gluten-free options. She said, "yes, we have gluten-free bread". This was sitting among the ordinary gluten-breads, and shared the same toaster – covered in crumbs. The staff had no understanding of the concept of cross contamination. Should the whole family go gluten-free? Yes, there is a huge benefit for the entire household when all adopt a gluten-free lifestyle. But there is always resistance due to the cost and the "inconvenience" – and dads who do not want not give up their beer. However, if there is gluten in the house, there will be cross-contamination. Also, it is poor role modelling when the parents eat gluten (a forbidden food for the child) but their child is denied foods that (from their child's perspective) might seem like a punishment or an arbitrary rule. (Children often do not understand the reason they were put onto a gluten-free diet.) Having said that, at least having their child on a gluten-free diet is a great start, and many children seem to manage with low levels of cross-contamination. By the way, the parents can eat gluten outside the house if they are prepared to play gluten-roulette. However, for their own health they should adopt the gluten-zero policy. If gluten is in the house, there is cross-contamination. A Day in the Life: Living in a Mixed House If you want to know how to avoid cross contamination on a day-to day basis, I recommend that you read this article by Al Klapperich (GIG, East Central WI). http://www.gigofecw.org/news/files/living_in_a_mixed_house.php Al says "This document draws upon my knowledge and experience I have acquired since going gluten-free in 2003. I have given you, the reader, a glimpse into how I personally carry out a gluten-free diet in a mixed house. I am not suggesting this is the only way or the best way; it's simply my way. My only intent is to help others that may be struggling with the gluten-free lifestyle. Not only do we have to be concerned about gluten ingredients that make up our food – we also have to be concerned about any gluten that may come into contact with our gluten-free food." Do you put gluten on your skin? Cosmetics, should they be gluten-free? Nancy asks: "Doctors in the USA state there is no need to avoid gluten-containing cosmetics & topical medications for those with celiac. What is your viewpoint on this?" This is a great question. I tell my patients to avoid any gluten on their skin. However, the answer depends upon where your focus is. If your focus is only on gut damage (that is, celiac disease), then the tiny amounts of gluten in these skin products is trivial and not enough to cause intestinal damage. But, if your focus is on the person and symptoms, then gluten on the skin often causes itch and irritability. For example, people complain of itchy hair if using a gluten-containing shampoo. Children using play-dough can develop a contact rash and become irritable. Swallowing gluten in lipstick causes some people a sore tummy. I recommend gluten-free cosmetics and topical medications. Gluten-free food not always healthy There is a not-so-subtle message promoted by many food-manufacturers, that gluten-free foods are, as of by right, healthy foods. This is definitely not true. Have you seen all those advertisements for gluten-free cookies and sweet treats? They are empty calories, full of fat and sugar, and lacking micronutrients. I was recently sent a message that was advertising the gluten-free benefits of a "Natural alternative healthy energy drink". This was misleading and dishonest. This drink was just a sugar (sucrose) water, with a few added vitamins. It is a terrible product. It cannot even be called a food. It would be much healthier to eat fruit and vegetables than drink this. It would be much better value to buy and eat healthy whole foods and drink water. Carrying the label "gluten-free" does not automatically mean that the product is either healthy or good for you. Often it is not. For example, Coca-Cola is both gluten-free and fat-free, however, few health professionals would recommend it. Lots of specialized gluten-free products are full of sugar and fat. They might taste great, and they are okay for a treat, but should not be eaten as a regular every-day food. When first confronted with the need to go on a gluten-free diet, most people feel overwhelmed. They also want to reject the whole notion of being gluten-free. They might be angry. They feel as though they are giving up a cherished food, and they certainly are. They have been used to eating gluten-foods for their whole lives. Suddenly, they have to start paying attention to what they are eating. This is very difficult. No wonder there is resistance to a gluten-free diet from so many people. Is gluten-free food safe to eat for everyone? Anna asks me by email: "Hi Dr Ford, I would like to know if people who are not gluten-free should eat gluten-free food? Can you provide any information of this topic please for me as to the pro's and con's of this? Many thanks." This is an interesting question, as it insinuates that gluten-free foods could be unhealthy for some people. Except for the gluten-grains of wheat rye and barley, all foods are naturally gluten-free. Gluten free foods are naturally healthy. It is only over the last 100 years that wheat has been added to more and more of our foods. There is nothing harmful about eating gluten-free foods. Can you live without gluten? Arthur wrote: "Your article about gluten causing nerve problems has touched a nerve, as you could see from the general round of applause and approval it received. Bravo! I have consulted dozens of doctors over 30 years (in USA and France) but not one had ever suggested gluten could be the culprit for my problems. Now, I wonder if more education is needed in the medical community on this problem. I've been gluten-free for nearly three months now, and all my symptoms have disappeared and I feel great." My question is 'Can humans get along without gluten?' and what role does gluten play in nutrition. Thanks. Best wishes, Art." Who needs gluten? Here is the dilemma. The world still needs gluten grains to feed the population. But this is creating ill health in at least 10% of the population. If so many people are getting ill from the foods that they are eating, then surely it would be better to shift to other food types to improve the health of the population. It turns out that gluten is not a necessary protein. The gluten grains are convenient and demanded - but they are not biologically essential. In fact, for perhaps a third of the population, gluten is biologically undesirable. (This is a controversial statement and needs a lot more research to back it up.) Are there risks when going gluten-free? It is my experience that for most families who go gluten-free, the quality of their diet actually improves. As they no longer rely on the easy-filling cheap breads, they are forced to branch out into vegetables, fruits, meats and other non-gluten grains. This greatly enhances their food variety, which, in turn, improves their health. Gluten is unnecessary for a well-rounded diet. Is the gluten habit easy to kick? Unfortunately, gluten has an addictive quality because one of its breakdown products has a morphine-like activity. As you know, foods crammed with gluten such as cakes, dumplings, steamed puddings and big hunks of bread are often referred to as "comfort foods". For some, this comfort is derived from this morphine-like sedation of gluten on the brain. Consequently, when gluten is suddenly removed from the diet, some people experience a withdrawal effect. This is one of the reasons a gluten-free diet is viewed as a horror story by so many people. Indeed, withdrawal effects from gluten during the first week of a gluten-free diet are not uncommon. Although this usually passes after a week or so, it can be difficult for children during the first few days. It is sensible to gradually go gluten-free over a week or so to avoid this reaction. To sum up, yes! You can you live a healthy life without gluten! Absolutely! Overall, your diet without gluten is a much more healthy, wholesome and packed with goodness. This will be good news to people who have embarked on their gluten-free journey. High-fat high-sugar. When deprived of gluten, people often feel that they deserve something to replace it. This yearning for some sort of compensation for being on a strict gluten-free diet leads to people over-indulging in these high-fat, high-sugar gluten-free specialty products. Although these foods are gluten-free, they are not disease-free. They have a high glycemic index, and you can eat too much. They are unhealthy. Weight gain, obesity and insulin resistance may catch up to you. Many people are also addicted to gluten. Therefore, as they go through the withdrawal phase, the pleasure of eating sweet-food can provide some compensation to them for being denied gluten. Going gluten-free is not an easy thing for most people. Gluten-free reluctance You would think that being diagnosed with celiac disease would be a big motivation factor to go onto a gluten-zero-diet. But a study in England (2011) found that over 40% of patients with celiac disease were dissatisfied with a gluten-free diet (http://www.jgld.ro/2011/1/6.pdf). They said that they were keen to go back onto gluten if they could get some sort of vaccine or pill to change the way their gut processes gluten. They were willing to make unknown changes to their immune system just so that they could go on eating a toxic food. To me this shows: the massive ignorance of these people about the seriously harmful nature of gluten. the low level of family and community support for these people. Going gluten-free should be easy, healthy and enjoyable. Gluten-free does need assistance initially. the lack of knowledge about the neurological and autoimmune harm caused by gluten. This is a chapter from Dr Rodney Ford's new book "Gluten: ZERO Global" which is available as an ebook at http://www.glutenZEROglobal.com
  12. Two years ago I suffered from a bout of diarrhea and abdominal pain for 7 days. During this time period I ate HEAVY amounts of gluten. Sometimes two sandwiches w/ wheat bread 2 times a day, pasta for dinner, and honey wheat smacks at night. I went to doctor and eventually GI. The tests they ran came in as follows: Total IGA - Normal EMA IGA - Negative tTG IGA - Negative Gliadin DP IgA - Negative Gliadin DP IgG - POSITIVE; Score of 43 U/mL Gene Test: LOW RISK DQ2.2 Heterozygous By the time I saw the GI my symptoms had subsided. He told me not to worry and that Celiac is highly unlikely. Said biopsy wasn't necessary given my genetic markers and lack of symptoms. I wasn't convinced so I monitored my body closely. As 2015 went on symptoms would reoccur but were mild. I'd have abdominal pain and lose stools for one day. Eventually these attacks disappeared even though I continued eating gluten. In 2016 I had my next physical. No flags and no signs of malabsorbtion. Numbers were literally perfect. If I have Celiac, symptoms are EXTREMELY MILD. At least two times a month I get a minor headache. I had a few canker sores last summer. Sometimes I have minor bloating. Had a loose stool last month. But overall, I am very healthy. I run 2-3 miles a day, have a very physically intensive job, and feel great. So obviously I'm getting some mixed signals here. These symptoms appear in healthy people as well! Also there is no consistency in symptoms! I can still eat a big mac and feel fine! I am in the process of getting 2nd opinion. On one hand I fear that I'm in the early stages of Celiac. But at the same time I don't want to follow a highly restrictive diet unless its necessary. On the other hand, I've read studies how high gluten intake can lead to something called leaky gut (even in healthy people). So it is possible I inflamed my gut temporarily and then healed after a few months. Either way I need an answer. Even though I feel good now I don't want to wake up with cancer in ten years! What is your assessment of my situation? Also, do some of you also have VERY MILD symptoms? What did your labs look like and did you have any signs of malabsorbtion? Finally, do any of you have this low risk 2.2 Heterozygous gene? Like I said I'm getting another opinion shortly. But I'd like some peace of mind either way.
  13. Please if anyone can help me. I just got my blood work back. I have been having bad diarrhea for months now. I went through an extremely stresful situation and was diagnosed with PTSD which brought on a ton of health problems. I have a dull pain in my stomach and the gastro diagnosed me with gastritis. Then my blood work came back. i have elevated liver enzymes and the following blood panel testing for celiac disease Antiliadin Abs, IgA (Deamidated Gliadin Abs, IgA. 12 . NEGATIVE Antiliadin Abs, IgG (Deamidated Gliadin Abs, IgG. 5 . NEGATIVE tTG IgA 4. WEAK POSITIVE tTG IgG 11. POSITIVE EMA ENDOYSIAL ANTIBODY IgA . NEGATIVE The doctor said she is confident I have celiac disease which is so odd to me because I have never felt any intolerances to food and before my PTSD had perfect health and perfect blood work. I am waiting for the biopsy results after I had my colonoscopy / endoscopy. It is confirmed that i do have gastritis so I am taking PPI's to reduce the inflammation. i am such a food lover. I am so sad that this is going to change my life forever. Does this blood work confirm celiac or maybe just gluten intolerance?
  14. Celiac.com 06/29/2012 - A group of researchers recently set out to study cases of positive tissue transglutaminase antibodies with negative endomysial antibodies to determine whether or not such cases amount to celiac disease. The team included Thomas Hornung; Pavel Gordins; Clare Parker; and Nicholas Thompson. They are variously affiliated with the departments of Gastroenterology, and Immunology at the Northern Deanery of Newcastle upon Tyne, and with the department of Gastroenterology at Freeman Hospital in Newcastle upon Tyne in the UK. The most sensitive and specific blood tests for diagnosing celiac disease are those that detect immunoglobulin A (IgA) antibodies against human tissue transglutaminase (tTGA) enzyme, and those that measure aspects of connective tissue covering individual smooth muscle fibers, endomysial antibodies (EMA). Because of the high sensitivity (up to 98%) and high specificity (around 96%) reported for the tTGA assay, detection of tTGA is currently the primary blood test used in screening for celiac disease. The tTGA test also has a high negative predictive value approaching 100%, which makes it an excellent test for excluding celiac disease in both high and low risk groups. In contrast, positive predictive value of the tTGA test is rather poor with values between 28.6% and 60.2% being reported in several studies. EMA, on the other hand, has extremely high specificity values close to 100% and positive predictive value values approaching 80%.[5 10] However, compared with tTGA, EMA has lower sensitivity, usually under 90%. This being the case, the present standard celiac disease screening strategy is to first use tTGA, and then confirm positive results using EMA. However, doing it this way, doctors often end up with a group of patients who show divergent test results. For their study, the researchers wanted to gauge the percentage of patients with positive tTGA and negative EMA, but who were confirmed with celiac disease upon biopsy, and to identify factors in these patients that may help to increase diagnostic accuracy in such patients. The research team identified 125 consecutive patients with positive tTGA and negative EMA, who subsequently underwent endoscopy with at least two biopsies from the second part of the duodenum. The team charted any tTGA result over 15 U/ml as positive. They excluded any patients with known celiac disease at the time of testing. They then reviewed patient notes to assess indications for celiac disease serological screening, including the presence of iron deficiency anaemia, and symptoms such as diarrhea or weight loss, and family history of celiac disease. They defined diarrhea as a bowel frequency of more than three times a day. They then assessed histological evidence of celiac disease based on subsequent duodenal biopsies, plus Marsh grading. In cases where patient histology was unclear, they relied on the clinical assessment of a consulting gastroenterologist. Unclear histology included minimal/mild increase in intraepithelial lymphocytes of not more than 30 per 100 enterocytes and without villous atrophy, plus mild villous blunting with no increase in intraepithelial lymphocytes. They then categorized patients as either celiac disease negative, or celiac disease positive. Patients with no histological evidence of celiac disease on duodenal biopsies or equivocal histology plus overall clinical impression of celiac disease absence were categorized as celiac disease negative. Patients with histological evidence of celiac disease on duodenal biopsies or equivocal histology plus overall clinical impression of celiac disease presence were categorized as celiac disease positive. To measure IgA anti-tTGA antibody the team used a commercially available enzyme linked immunosorbent assay called Aeskulisa, manufactured by Aesku Diagnostics GmbH in Wendelsheim, Germany. To detect IgA anti-EMA with the standard immunofluorescent method, they used commercial slides of monkey oesophagus sections (Euroimmun, Euroimmun AG, Lübeck, Germany). They used conjugated sheep antihuman IgA as a secondary antibody, relying on a test manufactured by Instrumentation Laboratory UK Ltd., in Warrington, UK. Overall, the team categorized 113 patients (90.4%) as celiac disease negative. Of these, 102 patients had no histological features of celiac disease, while 11 patients had unclear histology plus an overall clinical impression of not having celiac disease. They categorized twelve patients (9.6%) as celiac disease positive. Of these, 10 patients had positive histology, and two patients had unclear histology plus an overall clinical impression of having celiac disease. Of those with positive histology, 17% were Marsh grade I, 8% were Marsh grade II, 33% were Marsh grade IIIa, 17% were Marsh grade IIIb and 25% were Marsh grade IIIc. Those with celiac disease were more likely to be older and to have a higher tTGA level. The groups showed no difference in any clinical parameter. Source: Frontline Gastroenterol. 2012;3(2):81-83.
  15. Celiac.com 12/08/2008 - Celiac disease is a life-long autoimmune enteropathy that results in damage to the small intestinal mucosa. When people with celiac disease eat the gluten proteins found in wheat, rye and barley, they damage the cells that line the small intestine, which interferes with normal digestion and absorption of nutrients. Recent studies have shown that most people present with a silent, non-diarrheal form of the disease, and show no obvious symptoms. People with celiac disease face rates of autoimmune disease that are10 times higher than the general population. People with untreated celiac disease have higher rates of thyroid problems, which generally improve with the adoption of a gluten-free diet. A connection between the span of gluten consumption and autoimmune diseases has been observed in people with celiac disease. Tissue transglutaminase (TGase) is a ubiquitous enzyme and manifests in all tissues, with both intra- and extracellular localization. A team of researchers recently set out determine if tissue transglutaminase-2 IgA antibodies (anti-TGase II) present in blood samples from celiac disease patients react with thyroid tissue and possibly contribute to thyroid disease. The research team made up of doctors Afzal J. Naiyer, Jayesh Shah, Lincoln Hernandez, Soo-Youl Kim, Edward J. Ciaccio, Jianfeng Cheng, Sanil Manavalan, Govind Bhagat, and Peter H.R.Green. The team took blood samples from 40 people with active celiac disease, but not following a gluten free diet, samples from 46 celiac patients on a gluten-free diet (celiac disease), 40 normal controls (NC), and 25 with Crohn’s disease. They screened all samples for anti-thyroperoxidase antibodies (TPO-AB) and thyroglobulin antibodies (TG-AB), and conducted indirect immunofluorescence on primate thyroid tissue sections using TPO-AB– and TG-AB–negative blood samples. The team performed indirect immunofluorescence on thyroid seronegative, anti-TGase II–positive celiac disease+ blood samples (n1/423) and observed staining patterns on thyroid follicular cells and extracellular matrices that was identical with monoclonal anti-human TGase II antibody. Signs of TGase II as the antigen in thyroid tissue were reinforced by elimination of the IIF pattern when sera were depleted of anti-TGase II by pretreatment with human recombinant TGase II. The team saw no such staining of thyroid tissue in blood samples from celiac disease patients who were negative for TGase II antibodies, or samples from the non-celiac control group. Thyroid antibodies were found in 43% of celiac disease+ patients, substantially higher than NC and CROHN patients ( p < 0.0001). Moreover, a positive correlation was observed between anti-TGase II and TPO-AB titers (p1/40.0001; r1/40.63). The results show that anti-TGase II antibodies bind to TGase II in thyroid follicles and extracellular matrix, and that titers correlate with TPO antibody titers. This indicates that anti-TGase II antibodies might contribute to the development of thyroid disease in people with celiac disease. Thyroid Volume 18, Number 11, 2008
  16. Celiac.com 11/04/2016 - Patients in the earliest stages of celiac disease have TG2-autoantibodies present in serum and small-intestinal mucosa. Many suffer abdominal symptoms long before the development of villus atrophy. The classic small-bowel mucosal damage that marks celiac disease develops over time and in stages; from normal villi to inflammation and finally to villus atrophy with crypt hyperplasia. Previously, researchers have shown that intraperitoneal injections of sera from celiac patients or of purified immunoglobulin fraction into mice trigger a condition mimics early-stage celiac disease. Those same researchers recently set out to show whether re-combinantly produced, patient-derived TG2-targeted autoantibodies are alone sufficient to trigger such condition in immune-compromised mice. The research team included Suvi Kalliokoski, Victoria Ortín Piqueras, Rafael Frías, Ana-Marija Sulic, Juha A. E. Määttä, Niklas Kähkönen, Keijo Viiri, Heini Huhtala, Arja Pasternack, Kaija Laurila, Daniele Sblattero, Ilma R. Korponay-Szabó, Markku Mäki, Sergio Caja, Katri Kaukinen, Katri Lindfors. They are various affiliated with the Tampere Center for Child Health Research, the Tampere School of Health Sciences, the Department of Internal Medicine, with BioMediTech at Tampere University Hospital and School of Medicine at the University of Tampere in Tampere, Finland, with the Department of Equine and Small Animal Medicine, Faculty of Veterinary Medicine, and Department of Bacteriology and Immunology at the University of Helsinki in Helsinki, Finland, with the Central Animal Laboratory at the University of Turku in Turku, Finland, with the Comparative Medicine Karolinska Institutet in Stockholm, Sweden, with the Department of Life Sciences at the University of Trieste in Trieste, Italy, and with the Celiac Disease Center, Medical and Health Science Center, Heim Pál Children’s Hospital and Department of Pediatrics at the University of Debrecen in Debrecen, Hungary. Interestingly, mice injected with celiac patient TG2-antibodies showed changes to small-intestinal mucosa, increased lamina propria cellular infiltration and disease-specific autoantibodies in the small bowel, but did not show any clinical signs of celiac disease. Thus, celiac patient-derived TG2-specific autoantibodies seem to be enough to trigger small-bowel mucosal changes in mice, but probably not enough to trigger clinical features on their own. Triggering clinical celiac features likely requires other factors, such as other antibody populations implicated in celiac disease. Source: Amino Acids, pp 1–12. DOI: 10.1007/s00726-016-2306-0
  17. Celiac.com 09/19/2016 - At the time of diagnosis, some celiac patients suffer also from what is called celiac hepatitis, which is liver damage in patients with celiac disease that resolves after a gluten-free diet. A team of researchers recently set out to evaluate predictive factors of celiac hepatitis at the celiac disease diagnosis stage. To do so, they conducted a retrospective study that included 46 adult patients with clinically diagnosed celiac disease. The research team included Andreia Albuquerque, Susana Rodriguesa, and Guilherme Macedoa of the Department of Gastroenterology at Centro Hospitalar São João, in Porto, Portugal. Of the 46 patients, eighty-seven percent were women, with an average age of 33 ± 11 years, 87% showed Marsh 3, and 21 patients (46%) had celiac hepatitis. At the time of diagnosis, these patients had average Immunoglobulin A anti-tissue transglutaminase antibody (TTG-IgA) levels of 208.0 U/ml (p25–p75: 89–1316 U/ml), a mean aspartate aminotransferase of 42 ± 24 U/L, alanine aminotransferase 50 ± 28 U/L, alkaline phosphatase 111 ± 64 U/L. One year after diagnosis, the median average TTG-IgA was 9U/ml (p25–p75: 4.5–30.5 U/ml) and one-third of the patients had normal values. At diagnosis, patients without celiac hepatitis had an average TTG-IgA of 77U/ml (p25–p75: 24–288 U/ml), average aspartate aminotransferase of 23 ± 4 U/L, alanine aminotransferase 20 ± 6 U/L, alkaline phosphatase 69 ± 17 U/L. One year after diagnosis, median TTG-IgA was 6 U/ml (p25–p75: 3–19 U/ml) and nearly half of the patients showed normal values. At diagnosis, patients with celiac hepatitis had higher values of TTG-IgA (p = 0.007). Also, at diagnosis, there was a statistically significant positive correlation between TTG-IgA and alanine aminotransferase (r = 0.324, p = 0.028). For patients with a TTG-IgA level higher than 310 U/ml (OR = 4.8, 95%CI = 1.213–18.781, p = 0.025), the risk of having celiac hepatitis was nearly 5-times higher. From this, the team concludes that higher TTG-IgA levels can help predict celiac hepatitis in adult patients with celiac disease at diagnosis. Source: Scandinavian Journal of Gastroenterology. DOI:10.1080/00365521.2016.1203017
  18. Celiac.com 02/01/2016 - Among celiac researchers, there's been a good deal of professional curiosity about the clinical and immunological relevance of anti-neuronal antibodies in celiac disease with neurological manifestations. At present, doctors don't know very much about the clinical and immunological features in celiac disease patients with neurological problems, and many of them want to know more. Researchers estimate that about 10% of celiac disease patients have neurological issues, with the majority of those suffering from anti-neuronal antibodies (NA) to central nervous system (CNS) and/or anti-neuronal antibodies to the enteric nervous system (ENS). With that in mind, the question of the importance of such antibodies in celiac patients with neurological problems becomes important. To get a better picture of the issue, a team of researchers in Italy recently set out to assess rates of anti-neuronal antibodies, and to assess their correlation with neurological disorders and bowel habits in people with celiac disease. The research team included G. Caio, R. De Giorgio, A.Venturi, F. Giancola, R. Latorre E. Boschetti, M. Serra, E. Ruggeri, and U.Volta. They are all associated with the Department of Medical and Surgical Sciences, University of Bologna and St. Orsola-Malpighi Hospital, Bologna, Italy. For their study, the team investigated anti-neuronal antibodies to central nervous system and enteric nervous system in 106 celiac disease patients and in 60 controls with autoimmune disorders, using indirect immunofluorescence on rat and/or primate cerebellar cortex and intestinal (small and large bowel) sections. Their results showed that 21% of celiac patients were positive for IgG NA to central nervous system (titer 1:50 - 1:400); nearly half of those patients showed neurological dysfunction, compared with just 8% without. (P< 0.0001). Of the 26 celiacs (24%) with IgG anti-neuronal antibodies to enteric nervous system, 11 out of 12 with an antibody titer greater than 1:200 had severe constipation. Only one patient with cerebellar ataxia and intestinal sub-occlusion was positive for anti-neuronal antibodies to central nervous system and enteric nervous system. Anti-neuronal antibodies to central nervous system and enteric nervous system were found in 7% and 5% of controls, respectively. These results confirm that the presence of anti-neuronal antibodies to central nervous system can be regarded as a marker of neurological manifestations for people with celiac disease. High titer anti-neuronal antibodies to enteric nervous system are associated with severe constipation. The presence of anti-neuronal antibodies to central nervous system and enteric nervous system is a big red flag for an immune-mediated disease path that leads to central neural impairment, and gut dysfunction with associated constipation. Source: Gastroenterol Hepatol Bed Bench. 2015 Spring;8(2):146-52.
  19. Hi everyone. I was wondering if an accidental glutening made one's antibody levels higher? And by this I mean high enough to show up on a blood test. I am fairly certain that I was glutened about 4-5 weeks ago, judging by the symptoms (I have no idea by what though). Being relatively new to this whole glutening thing, I thought I'd go and get my antibodies checked to see if it was indeed a glutening. However, my antibody levels haven't gotten any higher (Transglutaminase IgA at 11.6 whereas it was at 18.6 in June and higher before that - have had slowly decreasing levels ever since diagnosis 20 months ago). Since I have read that one must be on a gluten diet containing a fairly high level of gluten for the diagnosis-purpose blood tests to actually work, I was just wondering if it was possible that I had been glutened, but that it didn't show up in my blood work. Does anybody have any experience with this? Any help is appreciated. Thanks.
  20. Celiac.com 08/26/2015 - People with IgA antibodies to tissue transglutaminase (anti-tTg) likely have a higher risk for celiac disease. Some clinicians and researchers have suggested that common multiples of the upper limit of normal (ULN) be useful tool in improving diagnostic pathways, as well as continuity between tests. However, a new study suggests that both sensitivity and specificity of tests for IgA antibodies to tissue transglutaminase vary widely by individual kit, and that their test values are not easily commutable using common multiples of the ULN to correct for inter-assay variations. Commutability just means the ability to make sure that two different tests really are equal. If results of different tests are commutable, it means that they are equal. In this case, the term applies to test results for various representative samples from healthy and diseased individuals. For the study, the research team recently looked at the use of immunoassays for the detection of IgA antibodies to tissue transglutaminase, and also sought to better understand of the significance of multiples of the upper limit of normal and inter-assay correlations. The research team included B.B. Suh-Lailam, K.W. Davis, and A.E. Tebo. Using indirect immunofluorescence assay (IFA) as reference, the team assessed characteristics of four anti-tTG IgA assays relative to endomysial IgA (EMA). They also assessed commutability between anti-tTG immunoassays and/or EMA based on manufacturer's recommended cut-off values and three common multiples of ULN (3×, 5× and 10×). To do this, they analyzed samples from 200 patients and 100 healthy individuals. They found that, at manufacturer's cut-off, the sensitivities for the tTG assays ranged from 72.5% to 98.6% and specificities from 60.3% to 99.2%. The percent positive agreements between any anti-tTG and EMA or any two anti-tTG immunoassays varied from 56.7% to 98.0% and 46.7% to 100.0%, respectively. At 3×, 5× or 10× ULNs, the inter-rater reliability as measured by Cohen κ between any two anti-tTG assays were quite variable and ranged from 0.28 to 0.96, 0.26 to 0.89 or 0.13 to 0.78, respectively. Furthermore, the percent positive agreements between any two anti-tTg IgA immunoassays ranged from 83.1% to 98.2%, 92.0% to 100%, or 100%, at 3×, 5× or 10×, respectively. Hence, the team's basic takeaway that result parameters for tTG IgA immunoassays or tTG IgA and EMA vary by kit, and thus common multiples of the ULN are not enough to correct for variation between tests. Source: Clin Chem Lab Med. 2015 Jul 14. doi: 10.1515/cclm-2015-0348.
  21. 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.
  22. Celiac.com 04/22/2014 - Blood tests are highly valuable for diagnosing celiac disease. However, their role in gauging mucosal healing in celiac children who have adopted gluten-free diets is unclear. A team of researchers recently set out to compare the performance of antibody tests in predicting small-intestinal mucosal status in diagnosis and follow-up of pediatric celiac disease. The research team included Edith Vécsei, Stephanie Steinwendner, Hubert Kogler, Albina Innerhofer, Karin Hammer, Oskar A Haas, Gabriele Amann, Andreas Chott, Harald Vogelsang, Regine Schoenlechner, Wolfgang Huf, and Andreas Vécsei. They are variously affiliated with the Clinical Department of Pathology and the Department of Internal Medicine III of the Division for Gastroenterology and Hepatology, the Center for Medical Physics and Biomedical Engineering, the Department of Pediatrics and Pediatric Gastroenterology of St. Anna Children's Hospital, all at Medical University Vienna, and with the Institute of Pathology and Microbiology, Wilhelminenspital in Vienna, and with the Department of Food Science and Technology, Institute of Food Technology, University of Natural Resources and Life Sciences in Vienna, Austria. The team conducted a prospective cohort study at a tertiary-care center, where 148 children received biopsies either for symptoms ± positive celiac disease antibodies (group A; n = 95) or following up celiac disease diagnosed ≥ 1 year before study enrollment (group B; n = 53). Using biopsy (Marsh ≥ 2) as the criterion standard, they calculated areas under ROC curves (AUCs) and likelihood-ratios to gauge the performance of antibody tests against tissue transglutaminase (TG2), deamidated gliadin peptide (DGP) and endomysium (EMA). They found that AUC values were higher when tests were used for celiac disease diagnosis compared with follow-up: 1 vs. 0.86 (P = 0.100) for TG2-IgA, 0.85 vs. 0.74 (P = 0.421) for TG2-IgG, 0.97 vs. 0.61 (P = 0.004) for DPG-IgA, and 0.99 vs. 0.88 (P = 0.053) for DPG-IgG, respectively. Empirical power was 85% for the DPG-IgA comparison, and on average 33% (range 13–43) for the non-significant comparisons. A total of 88.7% of group B children showed mucosal healing, at an average of 2.2 years after primary diagnosis. Only the negative likelihood-ratio of EMA was low enough (0.097) to effectively rule out persistent mucosal injury. However, out of 12 EMA-positive children with mucosal healing, 9 subsequently tested EMA-negative. Among the celiac disease antibodies examined, negative EMA most reliably predict mucosal healing. In general, however, antibody tests, especially DPG-IgA, are of limited value in predicting the mucosal status in the early years after celiac diagnosis, though they may do better over a longer time. Source: BMC Gastroenterology 2014, 14:28. doi:10.1186/1471-230X-14-28
  23. Hello everyone, I just have a question because I have seen some conflicting information online. So I was wondering, is it possible to have negative antibody tests and a positive biopsy? That is of course prior to going Gluten Free, as it would certainly be possible at that point. I am just confused because I read that Antibody tests can only confirm you do not have Celiac Disease, which indicates that false negatives are not possible? But I read elsewhere and always thought that false negatives were possible? Are false negatives only possible if you've gone gluten free before testing or are false negatives also possible if you are still consuming gluten? My doctor told me if the test came back false that it doesn't mean I don't have it, but according to this article http://www.uchospitals.edu/pdf/uch_007935.pdf a negative blood test confirms that you do not have Celiac. I am so confused. Any information to enlighten me would be a big help. Thanks! ~ Thursday
  24. Celiac.com 04/22/2013 - A recent study of celiac screening methods shows that testing for antireticulin antibodies (ARA) in patients with celiac disease is obsolete. The study includes a review of the medical literature, and recommendations for improved celiac blood screening. Researchers S. L. Nandiwada, and A. E. Tebo are affiliated with the Department of Pathology of the University of Utah, and ARUP Laboratories in Salt Lake City, Utah. Citing advances in celiac disease-specific serologic testing, Nandiwada and Tebo are calling for the elimination of ARA as a test for diagnosing celiac disease. People with celiac disease nearly always carry HLA-DQ2 and/or -DQ8 haplotypes, suffer from any of a range of diverse clinical presentations, including gluten-sensitive enteropathy. Celiac disease patients typically produce several autoantibodies, of which endomysial, tissue transglutaminase, and deamidated gliadin peptide antibodies are considered specific indicators of celiac disease. Although antireticulin antibodies (ARA) have traditionally been used to screen for celiac disease, these tests do not provide the best sensitivities and specificities for celiac screening. This review highlights recent advances in celiac-specific blood testing and supports the elimination of ARA from celiac disease screening and diagnosis. Source: Clin Vaccine Immunol. 2013 Apr;20(4):447-51. doi: 10.1128/CVI.00568-12. Epub 2013 Jan 30.
  25. So I recently went to see a gastrointestinal doctor thinking I had IBS or Celiac disease and he put me on an IBS diet and ordered a blood test and Celiac disease was negative but I was low on the antibodies which attach to the antigens that basically are Celiac disease. My doctor told me that because of that I may actually have Celiac disease. The IBS diet really made a difference so my doctor recommended that I stay with it for a month and then visit him. I can feel weird feelings in my gut and bloating still though. I think my possible Celiac disease and definite IBS may be symptoms of a larger problem;Thyroid disease. I noticed getting cold all the time, moodiness,irregular periods,insomnia ( almost 4 am). Does anybody here think it's worth checking on? I feel like I may be just over reacting?
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