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    Jefferson Adams earned his B.A. and M.F.A. at Arizona State University, and has authored more than 2,000 articles on celiac disease. His coursework includes studies in biology, anatomy, medicine, and science. He previously served as Health News Examiner for Examiner.com, and provided health and medical content for Sharecare.com.

    Jefferson has spoken about celiac disease to the media, including an appearance on the KQED radio show Forum, and is the editor of the book Dangerous Grains by James Braly, MD and Ron Hoggan, MA.

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    Jefferson Adams
    Celiac.com 05/27/2008 - People with celiac disease know all too well that the only effective treatment at present is faithfully following a gluten-free diet. There’s been a lot of talk about various therapies and enzyme treatments that would allow people with celiac disease to return to a normal diet. Talk to anyone who suffers from celiac disease and they’ll likely have a personal horror story about a time when they had an unhappy episode of cross-contamination.
    So, the idea of a drug that would prevent such symptoms is appealing, and the goal, desirable. The chief cause of recurring symptoms in celiac disease is accidental gluten exposure, usually through cross-contamination. Cross-contamination doesn’t always mean food. Gluten is a common ingredient in many medicines and vitamins, and exposure in celiacs can cause diarrhea, weight loss, abdominal pain, anemia and oral ulcerations in the short-term, and myriad other problems in the long-run.
    The drug AT-1001 is a good example of how the realities are playing out on the front-lines of science. AT-1001 is an enzyme therapy that has promised some degree of protection from gluten exposure in people with celiac disease.
    A team of researches recently set out to assess the effectiveness of AT-1001 in preventing gluten from crossing the gut barrier by reversing the defective barrier mechanism. This required evaluating intestinal permeability between those exposed to gluten after taking AT-1001, those exposed without AT-1001, and control groups. The of intestinal function is done by gauging the absorption rates of various sugars.
    Early testing of AT-1001 showed some progress and a significant rate of protection of celiac patients exposed to wheat proteins. The research team looked at 86 subjects with celiac disease. The patients were divided into three groups. The first group was given placebo AT-1011 and challenged with gluten, the second group was given either active or placebo AT-1001, while the third group was given gluten and active AT-1001.
    After the first week, all subjects showed improvement, possibly due to closer adherence to a gluten-free diet. At three weeks, those given AT-1001 showed substantial improvement over the group given gluten and placebo AT-1001, including reduced intestinal permeability and fewer symptoms of gluten toxicity.
    The problem is that while AT-1001 shows a degree of promise, the results are so far underwhelming. The research team noted that the degree of improvement did not match the primary study. The results are, however, strong enough to encourage researchers to conduct a larger trial of AT-1001, which is currently underway.
    It’s important to remember that celiac disease is an immune disorder and no immune disorder has ever been fully cured. So, the idea of people with celiac disease being able to take a pill and head out for a night of pizza and beer without the standard celiac-related reactions is far-fetched at best. At best, such drugs would likely help to prevent cross-contamination, rather than conveying immunity to gluten proteins.
    Until then, stay tuned…best of luck with the gluten-free diet!
    Presented by Dr. Leffler at the 2009 Digestive Disease Week on Tuesday, May 20 at 10:45 a.m. Pacific Time in room 10, San Diego Convention Center.


    Jefferson Adams
    Celiac.com 11/15/2008 - Managing celiac disease can be challenging in the best of circumstances, so imagine the frustration of experiencing on-going gastro-intestinal symptoms even while following a gluten free diet. Such frustration is increasingly common among people with celiac disease.
    With increasing frequency, doctors worldwide are finding persistent villous atrophy in celiac patients who are following a gluten-free diet. Results of a study published recently in the Scandinavian Journal of Gastroenterology indicate that persistent intestinal villous atrophy in celiac disease patients on a gluten-free diet is associated with gastrointestinal symptoms considered 'atypical' for celiac disease and which are different from those present at the original celiac disease diagnosis.
    A team of doctors based in Italy recently set out to assess a possible connection between persistent damage of the villi and 'atypical' gastrointestinal symptoms in celiac disease patients on a gluten-free diet. The team assembled a study group of 69 patients with celiac disease, all of whom were following a gluten-free diet. They then isolated 42 patients with gastrointestinal symptoms that warranted esophagogastroduodenoscopies (group I), while the remaining 27 control patients were asymptomatic at the time of the study, and served as a control group.
    Group I showed higher numbers of persistent endoscopic lesions compared with the control group. In fact, 35 patients (85%) from group I showed villous atrophy compared to just 9 (33%) of the control group.
    The team noted that the gastrointestinal symptoms experienced by group I differed from those present at the time of their celiac disease diagnosis. 6 patients from group I experienced anemia/diarrhea/weight loss, while 12 experienced symptoms similar to gastroesophageal reflux disease, and 24 patients experienced abdominal pain and/or constipation.
    Among the patients from group I, there was no difference in gender distribution, age and duration of gluten-free diet between those with normal villi and those with persistent partial villous atrophy, though the patients with persistent symptoms showed higher intraepithelial eosinophil counts than the asymptomatic patients.
    These findings speak to the importance of developing protocols to monitor the progress of celiac patients over the long term. Until such protocols are developed, it is important that people with celiac disease pay close attention to any symptoms that may be celiac-related, and report those symptoms to their health care professionals at the earliest signs of trouble.
    Scandinavian Journal of Gastroenterology; 2008: 43(11): 1315-21

    Jefferson Adams
    For the first time, researchers at the University of Chicago Celiac Disease Center will use mouse model research to explore root causes of celiac disease, test new therapies, and explore new targets for treatment.
    Celiac disease is the most common genetic autoimmune disease in the world. Celiac disease affects approximately three million Americans, but only three out of every one hundred people with celiac disease have been diagnosed.
    At least ninety-seven percent of people with celiac disease undiagnosed. Untreated celiac disease can lead to osteoporosis, infertility, neurological conditions, and cancer. Moreover, people with celiac disease have a substantially higher risk of developing other autoimmune diseases, especially Type-1 diabetes.
    Bana Jabri, M.D., Ph.D., Associate Professor, University of Chicago Medical Center, and a leading celiac disease researcher, will create the new mouse model with the goal of identifying new remedies and preventive treatments targeted at children of families with a history of celiac disease. The studies will also investigate events that contribute to the development of Type-1 diabetes.
    “There is a critical need to provide the proper resources to those who suffer from celiac disease,” said Stefano Guandalini, M.D., professor of pediatrics at the University of Chicago Medical Center, founder and medical director of the Celiac Disease Center. “This commitment from University of Chicago Celiac Advisory Board reaffirms the Celiac Disease Center’s mission to bring cutting edge research, education and encouragement to those affected by the disease”.
    Dr. Jabri believes that mouse models are central to understanding the underlying causes of celiac disease, its connection to other autoimmune diseases.
    The University of Chicago Celiac Disease Center is a 501-c3 non-profit organization, completely funded by donor contributions, and committed to improving the care, diagnosis and awareness of celiac disease. The University of Chicago Celiac Disease Center also provides necessary infrastructure and support for cutting-edge celiac research, including investigations into structure of gluten peptides and the mechanisms by which gluten modifies self molecules.
    Mouse model studies show promise in helping researchers to better and more quickly unlock the secrets of celiac disease.

    For more information please visit: www.celiacdisease.net 

    Jefferson Adams
    Celiac.com 06/20/2014 - Celiac disease is a T cell–mediated disease triggered by the protein in wheat gluten. More than 9 out of 10 of people with celiac disease carry human leukocyte antigen (HLA)-DQ2 locus.
    A team of researchers recently set out to determine if T-cell receptor recognition of HLA-DQ2–gliadin complexes was connected with celiac disease.
    The researchers included Jan Petersen, Veronica Montserrat, Jorge R Mujico, Khai Lee Loh, Dennis X Beringer, Menno van Lummel, Allan Thompson, M Luisa Mearin, Joachim Schweizer, Yvonne Kooy-Winkelaar, Jeroen van Bergen, Jan W Drijfhout, Wan-Ting Kan, Nicole L La Gruta, Robert P Anderson, Hugh H Reid, Frits Koning, and Jamie Ross.
    They are variously affiliated with the Department of Biochemistry and Molecular Biology at the School of Biomedical Sciences, and the Australian Research Council Centre of Excellence in Advanced Molecular Imaging at Monash University in Clayton, Victoria, Australia, the Department of Pediatrics, and the Department of Immunohematology and Blood Transfusion at Leiden University Medical Center in Leiden, The Netherlands, the Department of Microbiology and Immunology, Peter Doherty Institute for Infection and Immunity, at the University of Melbourne in Parkville, Victoria, Australia, ImmusanT, Inc., in Cambridge, Massachusetts, USA, and the Institute of Infection and Immunity at Cardiff University School of Medicine in Heath Park, Cardiff, UK.
    The team first determined T-cell receptor (TCR) usage and fine specificity of patient-derived T-cell clones specific for two epitopes from wheat gliadin, DQ2.5-glia-α1a and DQ2.5-glia-α2.
    They also determined the ternary structures of four distinct biased TCRs specific for those epitopes. They were able to establish a basis for the biased TCR usage through mutagenesis and affinity measurements, together with the fact that all three TCRs specific for DQ2.5-glia-α2 docked centrally above HLA-DQ2. They found that a non–germline–encoded arginine residue within the CDR3β loop served as key of this common docking footprint.
    Although the TCRs specific for DQ2.5-glia-α1a and DQ2.5-glia-α2 docked similarly, their interactions with the respective gliadin determinants differed markedly, thereby providing a basis for epitope specificity.
    This is the first time a research team has determined that T-cell receptor recognition of HLA-DQ2–gliadin complexes was connected with celiac disease. Further study is needed to better understand the nature of their relationship.
    Source:
    NATURE STRUCTURAL & MOLECULAR BIOLOGY

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