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Found 5 results

  1. Celiac.com 04/18/2012 - Biopharmaceutical development company, BioLineRx, has announced results from pre-clinical trials which show that their compound, BL-7010, an orally available treatment for celiac disease, reduces the toxic effects of gluten in patients with celiac disease. The findings, which appear in the February issue of Gastroenterology, show that BL-7010, which was previously labeled P(HEMA-co-SS, lowers gluten toxicity by reducing the body's digestion of wheat gluten. The findings also show that BL-7010 also improves the immune response to gluten in rodents, as well as preventing gluten-induced pathological damage to the small intestine. Furthermore, they note that BL-7010 is not absorbed systemically, indicating that its gluten-neutralizing effects are likely safe. These data demonstrate BL-7010's therapeutic potential for reducing or blocking gluten-induced disorders in humans with celiac disease. Because it can be difficult to maintain a life-long, strict, gluten-free diet, the fact that BL-7010 may attenuate the immune response to gluten and reduce subsequent damage to the small intestine, suggests that this drug, or others like it may be useful in improving quality of life for millions of celiac disease patients. Source: http://www.news-medical.net/news/20120222/BioLineRx-BL-7010-may-reduce-gluten-toxicity-in-patients-with-celiac-disease.aspx
  2. Celiac.com 02/21/2011 - After reading this new book by celiac nurse specialist Shelly Stuart, RN, what shines through above all is her true understanding of the complex nature of gluten-related illnesses, and her heartfelt compassion for patients who suffer from them. Her book is extremely well researched and documented. As a registered nurse and celiac herself, Ms. Stuart is able to use her strong patient teaching experience to clearly educate the reader about even very complicated subjects. She provides excellent explanations of leaky gut and the pathophysiology of celiac disease, and she is one of the first clinicians to write in-depth about non-celiac gluten intolerance. Importantly, she makes the point that immune mediated reactions can and do occur in non-celiac gluten intolerance, and backs this up by citing clinical evidence. Another important point made concerns pancreatic insufficiency, which can accompany celiac disease, but few know that this condition can persist even after diagnosis and transition to a gluten-free diet. Her discussion of the many, varied health disorders associated with celiac disease is very comprehensive. One of the most compelling aspects to “Gluten Toxicity” is the many important questions asked regarding the future of clinical research. Ms. Stuart makes it crystal clear that we need to know much more about the physical and mental health effects of gluten-related illness. This can only come about by increasing awareness both within the medical and research communities, and throughout each of our communities. We must all become advocates for greater testing and more accurate diagnosis. Shelly’s personal story, woven throughout the book, adds interest and a personal appeal, but never attempts to substitute anecdote for the hard science she relies on throughout the book. In fact, at first glance, the book seemed rather technical to me, and I thought it would be best-suited for clinicians, but after reading through to the end, I changed my mind. This is an excellent resource, offering really insightful and accurate explanations for anyone suffering from or attempting to treat gluten related illness. Some of you may be familiar with Cleo Libonati, RN, and the book “Recognizing Celiac Disease”, which was one of the first books to comprehensively make connections between a vast array of medical conditions and celiac disease, and back them up with clinical research citations. Shelly Stuart’s book goes quite a bit farther, to discuss the pathophysiology, symptoms, and diagnosis of a huge number of health conditions associated with celiac disease and also non-celiac gluten intolerance.
  3. Celiac.com 10/16/2009 - A team of researchers recently set out to investigate the ability of a polymeric binder to reverse the toxic effects induced by gliadin in human intestinal cells and gliadin-sensitive HCD4-DQ8 mice. The team was made up of Maud Pinier, Elena F. Verdu, Mohamad Nasser–Eddine, Chella S. David, Anne Vézina, Nathalie Rivard, and Jean–Christophe Leroux. The team neutralized gliadin through complexation to a linear copolymer of hydroxyethylmethacrylate (HEMA) and sodium 4-styrene sulfonate (SS). They then examined the ability of the polymeric binder to mitigate the damaging effect of gliadin on cell-cell contact in IEC-6, Caco-2/15, and primary cultured differentiated enterocytes. They used gliadin-sensitive HLA-HCD4/DQ8 transgenic mice to measure the effectiveness of the polymeric binder in averting gliadin-triggered intestinal barrier dysfunction. They found that Poly(hydroxyethylmethacrylate-co-styrene sulfonate) [P(HEMA-co-SS)] complexed with gliadin in a fairly precise manner. Exposing intestinal cells to gliadin caused major changes in both cell structure and cell to cell contacts. By complexing the gliadin with P(HEMA-co-SS) the researchers were able to prevent these undesirable changes. More importantly, the P(HEMA-co-SS) inhibited gliadin digestion by gastrointestinal enzymes, which minimized the development of peptides that trigger immune adverse immune reactions. By co-administering P(HEMA-co-SS) with gliadin to HLA-HCD4/DQ8 mice, researchers were able to eliminate gliadin-triggered changes in the gut barrier and lower intraepithelial lymphocyte and macrophage cell counts. From these results, the team concludes that polymeric binders can prevent in vitro gliadin-induced epithelial toxicity and intestinal barrier dysfunction in HCD4/DQ8 mice. Such polymeric binders might play a significant role in the treating people with gluten-induced disorders. Source: GASTROENTEROLOGY 2009;136:288–298
  4. Gastroenterology, Oct 2003, Vol 125, No 4, p1105-13 Celiac.com 10/30/2003 – It has long been known that celiac disease is caused by T-cell responses to wheat gluten-derived peptides, but the toxicity of other widely consumed grains has not been well studied. The researchers who conducted this study were aimed at determining the toxic T-cell stimulatory properties of barley hordeins, rye secalins, and oat avenins. Except for one instance, they found that there were no identical T-cell stimulatory gluten peptide matches in these grains. There were, however, similar responses found in "11 homologous sequences in hordeins, secalins, and avenins located in regions similar to those in the original gluten proteins," and seven of the 11 peptides were recognized by gluten-specific T-cell lines and/or clones from patients with celiac disease. The team discovered that key amino acids can be substituted, which will either partially or totally stop the T-cell stimulation by the gluten peptides, and that "single nucleotide substitutions in gluten genes will suffice to induce these effects." The researchers conclude: "These results show that the disease-inducing properties of barley and rye can in part be explained by T-cell cross-reactivity against gluten-, secalin-, and hordein-derived peptides. Moreover, the results provide a first step toward a rational strategy for gluten detoxification via targeted mutagenesis at the genetic level."
  5. Author: Auricchio S; De Ritis G; De Vincenzi M; Silano V. Source: J Pediatr Gastroenterol Nutr, 1985 Dec, 4:6, 923-30. This paper is a critical appraisal of current theories on the mechanisms of toxicity of wheat and other cereals in celiac disease and some related enteropathies. The peptidase deficiency, primary immune defect, and gluten-lectin theories on celiac disease are examined and critically discussed on the basis of the relevant data available in 88 references. Special attention has been paid in this review to the nature of the cereal components triggering the appearance of toxic symptoms and signs in celiac disease as well as to underlying action mechanisms. The gluten-lectin theory is the one best able to explain celiac disease. It also explains some secondary intolerance that may occur in temporarily predisposed individuals as a consequence to viral hepatitis and intestinal infections, as well as the occurrence of intestinal lesions in healthy subjects that are administered very high amounts of gluten.
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