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Found 6 results

  1. Celiac.com 01/02/2017 - New research shows that a group of proteins in wheat, called ATIs, may be responsible for activating inflammation in such disorders as celiac disease, multiple sclerosis, asthma, and rheumatoid arthritis. Scientists also believe that the proteins may promote the development of non-celiac gluten sensitivity. The findings were presented at UEG Week 2016 in Vienna in Vienna, Austria, a meeting organized by United European Gastroenterology for specialists to communicate the latest research in digestive and liver diseases. One group of proteins found in wheat - amylase-trypsin inhibitors (ATIs) - has been shown to trigger an immune response in the gut that can spread to other tissues in the body. ATIs are plant-derived proteins that inhibit enzymes of common parasites - such as mealworms and mealybugs - in wheat. Interestingly, ATIs also have an important role in metabolic processes that occur during seed development. The finding that ATIs may promote inflammation in the and beyond the gut, is a major step forward in understanding the mechanics of celiac disease and/or gluten-intolerance. Stay tuned for more news on this and other breaking stories in celiac disease research. Read more at MedicalNewsToday.com.
  2. Celiac.com 02/28/2008 - A study published in the Leukemia Research Journal (Volume 30, issue 12, Pages 1585-1586 - December 2006) looked at samples of serum from multiple myeloma patients. In 35% of the samples the myeloma monoclonal proteins had antigliadin activity, and migrated just like celiac anti-gliadin antibodies when subjected to electrophoresis. Monoclonal gammopathy (MGUS) is a precursor stage to multiple myeloma, with the same or very similar sort of monoclonal proteins as in multiple myeloma, and converts to it at the rate of about 1.5% per year. Therefore if one lives for 20 years after diagnosis with MGUS, one has a 30% chance of ending up with deadly, so far incurable, multiple myeloma, which is a cancer of the bone marrow and blood. For those diagnosed with MGUS it seems like a time bomb ticking, and each time one goes for the monitoring blood tests, there is some degree of anxiety. It was postulated by the researchers that multiple myeloma may actually be an end result of untreated celiac disease. This is why there has been a large reaction about this on the various MGUS web forums.Thirty-five percent is very high! At least one of our ChooseHope.com MGUS forum members was recently tested and found to have Celiac Disease and there are numerous other persons on the various MGUS forums alleging that they have this combination of conditions. In another publication from the database at PubMed.gov (Gut. 1976 Sep;17(9):735-9.), a study that showed that when a patient with MGUS and Celiac Disease was put on a gluten-free diet the monoclonal proteins entirely disappeared by the end of 3 years! Hence you can imagine what big news this is to all the MGUS patients, on the various online MGUS forums. Here is the suggestion that Celiacs might avoid becoming MGUS patients, that MGUS patients might perhaps avoid progression to multiple myeloma, and that multiple myeloma patients might have halted or slower progression of their disease, simply by being on a gluten-free diet! This is indeed big news! The ramifications of this are that everyone with Celiac Disease really should undergo testing for MGUS/Myeloma which can be associated with various autoimmune diseases, increased rate of osteoporosis, and neuropathy, or no symptoms at all! Likewise all MGUS patients should be tested for celiac disease, which again can be associated with various autoimmune diseases, increased rate of osteoporosis, and neuropathy, or no symptoms at all! Do you see the similarities? I am currently working on a letter to Blue Cross Blue Shield, informing them of the results of these studies and suggesting that their policy of reimbursing for celiac DNA testing of first degree relatives of known celiacs should be expanded to also include all persons having serum monoclonal proteins. This would include not just MGUS and multiple myeloma, but also Waldenstrom's macroglobulinemia. I would also like to call for intensified research on the link between celiac disease and paraproteinemia.
  3. Celiac.com 12/29/2014 - While the immune response to gluten proteins in celiac disease has been well researched, and is pretty well understood, researchers really don’t know much about the immune response to non-gluten proteins in wheat. A team of researchers recently set out to determine the level and molecular specificity of antibody response to wheat non-gluten proteins in celiac disease. The research team included Sina Huebener, Charlene K. Tanaka, Melanie Uhde, John J. Zone, William H. Vensel, Donald D. Kasarda §, Leilani Beams, Chiara Briani, Peter H. R. Green, Susan B. Altenbach, and Armin Alaedini. They are variously affiliated with the Department of Medicine at Columbia University in New York, New York, USA, the Celiac Disease Center at Columbia University in New York, New York, USA, the Western Regional Research Center, Agricultural Research Service of the United States Department of Agriculture in Albany, California, USA, the Department of Dermatology at the University of Utah in Salt Lake City, Utah, USA, the Department of Neurosciences at the University of Padova, in Padova, Italy, and the Institute of Human Nutrition at Columbia University in New York, New York, USA. Together, the team screened blood samples from celiac patients and control subjects for IgG and IgA antibody reactivity to a non-gluten protein extract taken from the wheat cultivar Triticum aestivum Butte 86. They also analyzed the antibodies for reactivity to specific non-gluten proteins by two-dimensional gel electrophoresis and immunoblotting. They used tandem mass spectrometry to identify any immuno-reactive molecules. They found that, compared with healthy control subjects, celiac patients showed significantly higher levels of antibody reactivity to non-gluten proteins. The main immuno-reactive non-gluten antibody culprit proteins were serpins, purinins, α-amylase/protease inhibitors, globulins, and farinins. Assessment of reactivity toward purified recombinant proteins further confirmed the presence of antibody response to specific antigens. These results show that, in addition to the well-understood immune reaction to gluten, people with celiac disease experience reactions to a number of non-gluten proteins of wheat. The short take away is that the bodies of people with celiac disease show clear immune responses, not just to gluten proteins in wheat, but to non-gluten proteins, as well. Source: J. Proteome Res., DOI: 10.1021/pr500809b
  4. 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.
  5. Proteins ingested by mother can appear in the breast milk. There is well known disease in breast fed babies called eosinophilic colitis, which causes eosinophilic infiltration in the large intestine of the babies and clinically presents as rectal bleeding. The therapy is very simple: the mother stops ingesting cow milk and cow milk products and the babies do not have bleeding and they are completely well. Based on this clinical syndrome, the same possibility exists for the presence of gluten peptides in Human milk. Studies on this have been done by Dr. Reichelt.
  6. AU- Baudon JJ; Mougenot JF; Didry JR CS- Unite de Gastroenterologie Pediatrique, Hopital Trousseau, Paris, France. JN- J Pediatr Gastroenterol Nutr; 6 (2) p244-51 PY- Mar-Apr 1987 AB- The lymphoblastic stimulation test (LST) with cows milk proteins was performed in 114 infants. In 42 infants, digestive intolerance to cows milk proteins (CMI) was suspected; withdrawal/re-challenge test confirmed intolerance in 34, and disproved it in the other eight patients. Of the other patients, 17 had acute gastroenteritis, 11 had postgastroenteritis sub-acute diarrhea, 12 had gluten intolerance, 14 had intractable diarrhea, and 18 had no digestive disorders. Of the 34 infants with CMI, 27 (79%) had a positive LST to one or more cows milk proteins. Of the 34 positive LST patients, 12 also had Soya intolerance; nine of these 12 infants (75%) had positive LST to Soya. Of the eight infants who had a negative cows milk re-challenge test, five (62%) had a positive LST. In the other groups, results were also positive in 12-27% of those having diarrhea of infectious origin or gluten intolerance, and in none of the infants without digestive disorders. Of the 14 cases of severe intractable diarrhea, 12 (86%) were also LST-positive, but CMI could not be excluded. LST was positive, particularly in diarrhea of neonatal origin. Lymphoblastic stimulation was induced more frequently by casein than by beta lactoglobulin, and least frequently by alpha lactalbumin. In conclusion, LST is frequently positive in CMI, but is not sufficiently specific to be a reliable diagnostic examination.
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