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    Using Non-Inflammatory Gluten Peptide Analogs as Biomarkers for Celiac Disease


    Jefferson Adams

    Celiac.com 09/30/2009 - Are non-inflammatory gluten peptide analogs effective as biomarkers for celiac disease? Recent research indicates that they just might represent an effective new tool in the management of celiac disease.

    In the August 28th issue of Chemical Biology, a team of researchers from Stanford University's Department of Biochemistry issues a call for new tools to manage celiac disease, a lifelong immune disease of the small intestine. Non-inflammatory gluten peptide analogs may be one of the important new tools in that effort.

    The research team is made up of M. T. Bethune, M. Crespo-Bosque, E. Bergseng, K. Mazumdar, L. Doyle, K. Sestak, L. M. Sollid, and C. Khosla.

    They note that current drug trials are sparking a researchers to seek non-invasive biomarkers of gluten-induced intestinal change.  They note also that they have synthesized and characterized non-inflammatory gluten peptide analogs in which Asn or His replace key Gln residues.

    As with their pro-inflammatory associates, these genetic markers resist gastrointestinal proteases, are susceptible to glutenases, and permeable across enterocyte barriers.

    In contrast with gluten peptides, however, the markers are not commonly acknowledged by transglutaminase, HLA-DQ2, or disease-specific T cells.

    In vitro and animal tests prove that the biomarkers can reveal shifts in intestinal permeability as well as glutenase-catalyzed gastric detoxification of gluten.

    As a result, they call for controlled clinical studies to assess the use of these peptides as markers for abnormal intestinal permeability in celiac patients and for the effectiveness of glutenase in clinical trial and treatment of celiac disease.

    Chem Biol. 2009 Aug 28;16(8):868-81.

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  • About Me

    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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    Scott Adams
    The following excerpt was taken from the November 24, 1996 edition of the The Sprue-nik Press, which is published by the Tri-County Celiac Sprue Support Group (TCCSSG), a local chapter of CSA/USA located in southeast Michigan.
    Dr. Joseph Murray, of the Mayo Clinic Rochester, MN, is a gastroenterologist who specializes in treating Celiac disease. Dr. Murray gave us the standard definition of celiac disease: celiac disease is a permanent intolerance to gluten that results in damage to the intestine and is reversible with avoidance of dietary gluten. There are some important parts in this definition:
    Permanent: The effects of celiac disease may change from time to time. You may be sicker at one phase of your life than at another. For example, you may be sicker at age two, may seem to get better during the teenage years, may be sick again in your 20s (but with different symptoms), and then present with bone problems when you are in your 50s. So there may be different phases, but it is a PERMANENT intolerance. You do NOT outgrow it; you do not go through phases where you dont have it anymore. (That used to be what was thought and TAUGHT in medical schools.).
    Damage to the intestine: There is definitely intestinal damage; without it you cannot define . For some people the damage is severe, for others it is not so severe. It is the cases which are not so severe that can be difficult to diagnose. If the damage is mild then the person interpreting the biopsy might not even think of celiac disease as being a possible cause of the damage.
    Reversible: The damage should be reversible. Dr. Murray says there are about 5% of people with what he believes is celiac disease in whom at one point in their lives the damage becomes irreversible. In these cases there is intestinal damage that does not completely recover. It may partially heal, but not completely. One can infer that they have the same condition as celiacs that do recover, based on their history. There may be something different about that group of patients in their immune systems that makes them different, but that is an area that is still being actively researched.

    Jefferson Adams
    Celiac.com 10/07/2009 - A team of Maltese researchers, led by genetics specialist Christian Scerri, has discovered that a previously unassociated gene contributes to the development of celiac disease. The association of the gene, a variant of a gene called CD59, is the result of three years of research at a University of Malta lab.
    The research team made the discovery after examining the DNA of six people who suffered from gluten intolerance, together with 9 close relatives.
    Armed with about $35,000 in research funds provided by the Malta Council for Science and Technology, the research team set out to examine the DNA of each family member along with their different genes.
    "If you have a grandmother, a mother and a son who all suffer from a particular disease, we will look for the part of DNA that is common in all three," Scerri said.
    Once the researchers isolated the matching parts of the DNA, the researchers begging combing through all the different genes in that section of the DNA.
    Several prior studies have shown that only people with a certain type of the molecule human leukocyte antigen, called HLA-DQ2/DQ8, were pre-disposed to celiac disease. HLA-DQ2/DQ8 is found in about 30 per cent of the worldwide population.
    Although HLA-DQ2/DQ8 does not cause gluten intolerance on its own, it can combine with a number of genes to cause celiac disease. According to Dr. Scerri, the results showed that "all those patients who suffered from celiac disease had both HLA-DQ2/DQ8 and a variant of CD59."
    The study also confirmed that people who had HLA-DQ2/DQ8 or CD59 alone did not suffer from celiac disease, providing strong evidence that the two combine to cause gluten intolerance.
    The gene variant was also rare in Malta and was not found among another 99 families who have members with celiac disease. "This seems to be the only family in Malta which has this gene," Dr Scerri says of the 17-strong family that was tested.
    Though the gene is quite rare, the research is crucial, as it will likely lead to further study to discover how specific genes bring about particular conditions.
    Dr Scerri hopes to have additional staff in place to begin research by the end of next year when a $7 million restructuring of the University's molecular genetics lab would be finalized.
    Source:
    Times of Malta


    Jefferson Adams
    Rifaximin Does Not Relieve Persistent Celiac Disease Symptoms
    Celiac.com 12/27/2011 - Non-controlled studies suggest that Rifaximin may improve celiacdisease symptoms in such cases. However, up to now, no controlledtrials have been conducted.
    A team of researchers used a double-blind clinical trial to assess the effectiveness of rifaximin in relieving gastrointestinal symptoms in patients with poorly responsive celiac disease. They also assessed the effects of rifaximin on lactulose-hydrogen breath tests in those patients.
    The research team included Matthew S. Chang, Maria T. Minaya, Jianfeng Cheng, Bradley A. Connor, Suzanne K. Lewis, and Peter H. R. Green.
    Small intestinal bacterial overgrowth (SIBO) is one of the main reasons that certain people with celiac disease fail to respond well to a gluten-free diet, and why they often suffer persistent symptoms.
    To make their assessment, the team designed a single-center, double-blind, randomized, controlled trial of patients with biopsy-proven celiac disease and persistent gastrointestinal symptoms despite following a gluten-free diet.
    For the trial, the team 25 randomly assigned patients received a placebo, while the other 25 received rifaximin (n = 25) 1,200 mg daily for 10 days.
    For each patient, the team then used the Gastrointestinal Symptom Rating Scale (GSRS) and administered lactulose-hydrogen breath tests at weeks 0, 2, and 12.
    The team defined an abnormal breath test as showing either: (1) a rise in hydrogen of C20 parts per million (ppm) within 100 min, or (2) two peaks C20 ppm over baseline.
    They found that rifaximin had no effect on GSRS scores, regardless of baseline breath tests.
    Using a multivariable regression model, they found that the length of a patient's gastrointestinal symptoms significantly predicted overall GSRS scores (estimate 0.029, p.006).
    According to criteria 1 and 2, respectively, SIBO was present in 55 and 8% of patients at baseline, intermittently present in 28 and 20% given placebo, and 28 and 12% given rifaximin.
    Results showed no difference SIBO rates between placebo and treatment groups at weeks 2 and 12.
    From their study, the team concludes that rifaximin does not improve gastrointestinal symptoms, and that hydrogen breath tests do not reliably show which patients will respond favorably to antibiotic therapy.
    Source:

    Dig Dis Sci (2011) 56:2939–2946

    Jefferson Adams
    Celiac.com 10/23/2013 - Celiac disease remains seriously under diagnosed in adults and, in many places, often takes years and even decades to diagnose.
    A team of researchers recently evaluated the usefulness of an on-site rapid fingertip whole blood point-of-care test (POCT) that would help primary workers to spot patients who might benefit from further diagnostic tests for celiac disease.
    The research team included Alina Popp, Mariana Jinga, Ciprian Jurcut, Vasile Balaban, Catalina Bardas, Kaija Laurila, Florina Vasilescu, Adina Ene, Ioana Anca and Markku Mäki. They are affiliated with the University of Medicine and Pharmacy “Carol Davila,” the Institute for Mother and Child Care “Alfred Rusescu,” Central University Emergency Military Hospital “Dr. Carol Davila,” Str. Mircea Vulcanescu, in Bucharest, Romania and with theTampere Center for Child Health Research, University of Tampere and Tampere University Hospital, in Tampere, Finland.
    Because celiac disease often runs in families, the team tested 148 healthy relatives of 70 Romanian index cases with biopsy-proven celiac disease, for a total of 87% of all first-degree family members, with a median age 36 years, for the presence of circulating autoantibodies.
    In addition to using the POCT to measures blood erythrocyte self-TG2-autoantibody complexes on site, the team took blood samples for later evaluation of serum IgA-class endomysial antibodies (EMA).
    The then tested all EMA-positive samples for transglutaminase 2 antibodies (TG2-IgA). They conducted blind analysis of all serological parameters in a centralized laboratory with no knowledge of the on site POCT result. The team recommended endoscopic small intestinal biopsies for all POCT- or EMA-test positive subjects.
    Overall, 12 of 148 (8%) first-degree relatives showed positive results for the POCT, and all twelve tested serum EMA-positive. Only one other test subject showed a positive EMA test result.
    All remaining 135 healthy first-degree relatives showed negative results for both POCT and EMA.
    Four subjects who tested positive for both POCT and EMA were negative for TG2-IgA. Ten out of thirteen of the antibody-positive subjects consented to endoscopy.
    In all, eight out of nine first-degree relatives with celiac-type mucosal lesions of grade Marsh 2 (n = 3) or Marsh 3 (n = 6) showed positive results with the POCT.
    The three POCT-positive subjects refused endoscopy tested positive for both EMA and TG2-IgA.
    The fingertip whole blood rapid POCT could be a simple and cheap way to spot biomarkers and promote further testing for faster diagnosis of celiac disease.
    The team is calling for further studies in adult case-finding in specialized outpatient clinics and in primary care.
    Source:
    BMC Gastroenterology 2013, 13:115. doi:10.1186/1471-230X-13-115

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