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  • Jefferson Adams
    Jefferson Adams

    How Are Gluten Immunogenic Peptides Like Santa Claus?

    Celiac.com 12/21/2015 - For people with celiac disease, gluten immunogenic peptides might reveal whether you've been bad or good on your gluten-free diet, and whether or not you have gut damage.

    Photo: CC-- Sam HowzitIn fact, the best way to spot transgressions in the gluten-free diet and incomplete mucosal healing in people with celiac disease might just be to check for gluten immunogenic peptides in their urine.

    For people with celiac disease, the presence of gluten immunogenic peptides in the urine indicates a break in the gluten-free diet, along with incomplete mucosal healing.

    How do we know this? Because available methods to determine gluten-free diet adherence couldn't detect occasional gluten ingestion that may cause gut mucosal damage, a team of researchers recently set out to develop a method to assess gluten intake, monitor gluten-free diet compliance in celiac patients, and to correlate those results with mucosal damage.

    The research team included María de Lourdes Moreno, Ángel Cebolla, Alba Muñoz-Suano, Carolina Carrillo-Carrion, Isabel Comino, Ángeles Pizarro, Francisco León, Alfonso Rodríguez-Herrera, and Carolina Sousa. They are variously affiliated with the Facultad de Farmacia, Departamento de Microbiología y Parasitología, Universidad de Sevilla, Sevilla, Spain, with Biomedal S.L., Sevilla, Spain, with Unidad Clínica de Aparato Digestivo, Hospital Universitario Virgen del Rocío in Sevilla, Spain, with Celimmune, Bethesda, Maryland, USA, and with Unidad de Gastroenterología y Nutrición, Instituto Hispalense de Pediatría, Sevilla, Spain.

    For their study, the research team collected urine samples of 76 healthy subjects and 58 patients with celiac disease subjected to different gluten dietary conditions. To quantify gluten immunogenic peptides (GIP) in solid-phase extracted urines, the team used a lateral flow test (LFT) with the highly sensitive and specific G12 monoclonal antibody for the most dominant GIP, along with an LFT reader.

    They found that, in healthy individuals previously subjected to a gluten-free diet, GIP were detectable in concentrated urines as early as 4–6 hours after single gluten intake, and remained detectable for 1–2 days. The urine assay revealed deviation from a gluten-free diet in about 50% of the patients.

    Analysis of duodenal biopsies showed that nearly 90% of celiac patients with no villous atrophy had no detectable GIP in urine, while all patients with measurable GIP in urine showed incomplete intestinal mucosa recovery.

    GIP are easily detected in urine after gluten consumption, enabling a new and non-invasive method to monitor gluten-free diet compliance and deviation. The method was sensitive, specific and simple enough to be convenient for clinical monitoring of celiac patients, as well as for basic and clinical research applications, including drug development.

    Such tests could be very useful for both doctors and patients looking to monitor gluten-free dietary progress and gut healing in people with celiac disease, to say nothing of research and treatment development.

    Source:


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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, science, and advanced research, and scientific methods. He previously served as Health News Examiner for Examiner.com, and devised 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 "Cereal Killers" by Scott Adams and Ron Hoggan, Ed.D.

  • Related Articles

    Jefferson Adams
    Celiac.com 08/19/2015 - For the first time since it was described and named by 1st century Greek physician Aretaeus of Cappadocia, first linked to wheat in the 1940's, and specifically linked to gluten in 1952, scientists have discovered the cause of celiac disease.
    Professor Ludvig Sollid, and his team at the Centre for Immune Regulation at University of Oslo, have discovered that people with celiac disease suffer from one of two defective human leukocyte antigens (HLAs), which cause the immune system to see gluten molecules as dangerous, triggering the immune response that causes classic celiac-associated inflammation and other symptoms.
    To be true, the team was not working in the dark. They were armed with a complete map of the genes, an understanding that two types of HLA (HLA-DQ2 and HLA-DQ8) predispose a person for celiac disease, and the very crucial recent discovery by a team of German colleagues that celiac patients have antibodies for a very precise enzyme: transglutaminase 2.
    "We also found that the bits of gluten that were presented to the T-cells have some changes caused by an enzyme in the body – transglutaminase 2", says Sollid. HLAs are proteins which act as markers, binding to fragments of other proteins, and telling T-cells how to treat them.
    So it wasn't much of a stretch for Professor Sollid's team to determine that the defective HLAs bind to fragments of gluten, causing the T-cells to treat them as bacteria or viruses.
    Basically, two HLA types present gluten remnants to the T-cells, causing the T-cells to regard the gluten as dangerous, and to trigger immune reactions that cause inflammation in the intestines, and this is what causes celiac disease.
    "We think that this is huge," Sollid said. "We understand the immune cells that are activated and why they are activated."
    At present, Professor Sollid and his group are investigating how antibodies against transglutaminase are formed.
    This is a simple, but huge moment in the annals of medicine and in the annals of celiac disease. It's a discovery that will help researchers develop new approaches to treatment, and/or a cure for celiac disease in the future.
    Source:
    Med.uio.no

    Jefferson Adams
    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.

    Jefferson Adams
    Celiac.com 11/09/2015 - Can mass screening for celiac disease help enough people, and improve enough lives to justify the cost and effort?
    While celiac disease fulfills several WHO criteria for mass screening, such as high prevalence, available treatment and difficult clinical detection, it remains unproven that treatment of asymptomatic celiac disease can lower the risk of severe complications and improve quality of life, or that it is cost-effective.
    A research team recently set out to review the literature on screening for celiac disease in relation to the current World Health Organization (WHO) criteria for mass screening.
    The team included Jonas F Ludvigsson, Timothy R Card, Katri Kaukinen, Julio Bai, Fabiana Zingone, David S Sanders, and Joseph A Murray.
    The research team is variously affiliated with the Department of Paediatrics, Örebro University Hospital, Örebro, Sweden, the Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden, the Department of Epidemiology and Public Health, University of Nottingham, Nottingham, UK, the School of Medicine, University of Tampere, Tampere, Finland, the Department of Internal Medicine, Hospital, Tampere University Hospital, Tampere, Finland, the Department of Internal Medicine, Seinäjoki Central Hospital, Seinäjoki, Finland, the Department of Medicine, C Bonorino Udaondo Gastroenterology Hospital, Universidad del Salvador, Buenos Aires, Argentina, the Department of Medicine and Surgery, University of Salerno, Salerno, Italy, the Regional GI and Liver Unit, Royal Hallamshire Hospital, Sheffield, UK, the Department of Medicine, Department of Immunology, Mayo Clinic College of Medicine, Rochester, USA.
    The team conducted a PubMed search for all indexed papers on celiac disease screening published from 1900 until mid-2014. For all relevant abstracts the team read the corresponding paper in full.
    Their search revealed that current evidence is not sufficient to support mass screening for celiac disease.
    However, they do note that this strategy will help most patients with celiac disease, so active case-finding may be appropriate.

    They also note that, even though proof of benefit is lacking, screening for celiac disease may be appropriate in high-risk groups.

    Source:
    United European Gastroenterology Journal April 2015 vol. 3 no. 2 106-120

    Jefferson Adams
    Celiac.com 11/18/2015 - Researchers have known for some time that first-degree relatives (FDRs) of celiac patients are at high risk for developing the disease, and that prevalence among them varies from 1.6 to 38%. However, not much is known about specific risk levels when the FDR is sister, brother, mother, father, son, or daughter of a celiac patient.
    A team of researchers recently conducted a meta-analysis and calculated pooled prevalence of celiac disease among FDRs, second-degree relatives (SDRs), and specific relations with given celiac patients. The research team included P. Singh, S. Arora, S. Lal, T.A. Strand, G.K. Makharia. They are variously affiliated with the Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts, USA; Department of Medicine, Brigham and Women's Hospital, Boston, Massachusetts, USA; Max Healthcare, Gurgaon, India; Medical Services Division, Innlandet Hospital Trust, Lillehammer, Norway; and the Department of Gastroenterology and Human Nutrition at the All India Institute of Medical Sciences, New Delhi, India.
    The team searched 2,259 related medical articles, and found 54 articles relevant for their meta-analysis. They defined celiac disease diagnosis using standard biopsy and Marsh criteria. Analysis of their data group showed an overall celiac disease prevalence of 7.5% (95% confidence interval (CI) 6.3%, 8.8%) in 10,252 FDRs and 2.3% (95% CI 1.3%, 3.8%) in 642 SDRs.
    Pooled celiac disease rates were highest in siblings, at 8.9%, followed by offspring, at 7.9%, and parents, at 3.0%.
    A total of 8.4% of female FDRs showed rates of celiac disease compared to 5.2% male FDRs (P=0.047).
    Sisters and daughters of a primary patient had the highest risk of having celiac disease, at 1 in 7 and 1 in 8, respectively), compared to a risk of 1 in 13 in sons, 1 in 16 in brothers, 1 in 32 in mothers, and 1 in 33 in fathers.
    The data also revealed differences in the pooled prevalence of celiac disease in FDRs according to their geographic location.
    Average pooled rates of celiac disease among FDRs is 7.5%, but the actual rate for a given individual varies widely based on their relationship with the primary celiac patient, and is also influenced by gender and geographical location.
    Source:
    Am J Gastroenterol. 2015 Sep 29. doi: 10.1038/ajg.2015.296.

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