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  • Jefferson Adams
    Jefferson Adams

    Anti-transglutaminase 6 Antibody Development in Children with Celiac Disease Correlates With Length of Gluten Exposure

    Reviewed and edited by a celiac disease expert.

    Anti-transglutaminase 6 Antibody Development in Children With Celiac Disease Correlates With Length of Gluten Exposure

    Anti-transglutaminase 6 Antibody Development in Children with Celiac Disease Correlates With Length of Gluten Exposure - Photo: CC--Shakreez
    Caption: Photo: CC--Shakreez

    Celiac.com 03/06/2018 - A number of clinicians and researchers have suspected that antibodies against transglutaminase 6 (anti-TG6) play a role in neurological issues in adult patients with genetic gluten intolerance, but it is not known if autoimmunity to TG6 develops after long-term consumption of gluten.

    A team of researchers recently set out to establish a correlation between these autoantibodies and the duration of gluten exposure by measuring the anti-TG6 in children with celiac disease at diagnosis. The team then investigated a correlation between anti-TG6 and the presence of neurological disorders.



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    The research team included L De Leo, D Aeschlimann, M Hadjivassiliou, P Aeschlimann, N Salce, S Vatta, F Ziberna, G Cozzi, S Martelossi, A Ventura, and T Not. They are variously affiliated with the Institute for Maternal and Child Health-IRCCS "Burlo Garofolo" Trieste, Trieste, Italy; Matrix Biology and Tissue Repair Research Unit, School of Dentistry, and Arthritis Research UK Biomechanics and Bioengineering Centre of Excellence, College of Biomedical and Life Sciences, Cardiff University, Cardiff; the Department of Neurology at the Royal Hallmshire Hospital, Sheffield, UK; and with the University of Trieste in Trieste, Italy.

    The team used ELISA to measure anti-TG6 (IgA/IgG) in children with biopsy-proven celiac disease and of children experiencing gastrointestinal disorders. Celiac disease patients who tested positive for anti-TG6 were retested after 2 years of gluten-free diet. In all, the team analyzed test results for 274 children with celiac disease, along with 121 control subjects.

    They found anti-TG6 in 68 out of 274 celiac disease patients and in 19/121 control subjects, though the differences between the two groups was significant. None of the celiac patients or the controls who tested positive for anti-TG6 suffered from neurological disorders. Eleven of 18 celiac disease patients with other autoimmune diseases tested positive for anti-TG6. 

    Among the celiac disease patients, the team found a significant correlation between the gluten exposure before the celiac disease diagnosis and anti-TG6 concentration. The gluten-free diet substantially reduced the anti-TG6 concentrations. The team found no significant correlation between anti-TG6 and anti-TG2 serum concentrations.

    Anti-TG6 is much more common in children with untreated celiac disease , but with no apparent neurological disorders. The synthesis of the anti-TG6 is associated with longer exposure to gluten prior to celiac diagnosis, while the autoimmunity against TG6 is gluten dependent and disappears with a gluten-free diet.

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  • About Me

    Jefferson Adams

    Jefferson Adams is Celiac.com's senior writer and Digital Content Director. He earned his B.A. and M.F.A. at Arizona State University, and has authored more than 2,500 articles on celiac disease. His coursework includes studies in science, scientific methodology, biology, anatomy, medicine, logic, and advanced research. He previously served as SF 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.


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    Jefferson Adams
    Celiac.com 11/04/2016 - Patients in the earliest stages of celiac disease have TG2-autoantibodies present in serum and small-intestinal mucosa. Many suffer abdominal symptoms long before the development of villus atrophy.
    The classic small-bowel mucosal damage that marks celiac disease develops over time and in stages; from normal villi to inflammation and finally to villus atrophy with crypt hyperplasia. Previously, researchers have shown that intraperitoneal injections of sera from celiac patients or of purified immunoglobulin fraction into mice trigger a condition mimics early-stage celiac disease.
    Those same researchers recently set out to show whether re-combinantly produced, patient-derived TG2-targeted autoantibodies are alone sufficient to trigger such condition in immune-compromised mice. The research team included Suvi Kalliokoski, Victoria Ortín Piqueras, Rafael Frías, Ana-Marija Sulic, Juha A. E. Määttä, Niklas Kähkönen, Keijo Viiri, Heini Huhtala, Arja Pasternack, Kaija Laurila, Daniele Sblattero, Ilma R. Korponay-Szabó, Markku Mäki, Sergio Caja, Katri Kaukinen, Katri Lindfors.
    They are various affiliated with the Tampere Center for Child Health Research, the Tampere School of Health Sciences, the Department of Internal Medicine, with BioMediTech at Tampere University Hospital and School of Medicine at the University of Tampere in Tampere, Finland, with the Department of Equine and Small Animal Medicine, Faculty of Veterinary Medicine, and Department of Bacteriology and Immunology at the University of Helsinki in Helsinki, Finland, with the Central Animal Laboratory at the University of Turku in Turku, Finland, with the Comparative Medicine Karolinska Institutet in Stockholm, Sweden, with the Department of Life Sciences at the University of Trieste in Trieste, Italy, and with the Celiac Disease Center, Medical and Health Science Center, Heim Pál Children’s Hospital and Department of Pediatrics at the University of Debrecen in Debrecen, Hungary.
    Interestingly, mice injected with celiac patient TG2-antibodies showed changes to small-intestinal mucosa, increased lamina propria cellular infiltration and disease-specific autoantibodies in the small bowel, but did not show any clinical signs of celiac disease.
    Thus, celiac patient-derived TG2-specific autoantibodies seem to be enough to trigger small-bowel mucosal changes in mice, but probably not enough to trigger clinical features on their own. Triggering clinical celiac features likely requires other factors, such as other antibody populations implicated in celiac disease.
    Source:
    Amino Acids, pp 1–12. DOI: 10.1007/s00726-016-2306-0


    Jefferson Adams
    Celiac.com 01/23/2017 - It makes some kind of sense that kids with celiac disease who follow a gluten-free diet will recover, their guts will normalize, and their levels of IgA tissue transglutaminase antibodies would drop to reflect this change; whereas high antibodies likely mean no recovery, right? But is that true? Is there really a correlation on any level?
    To test this idea, a team of researchers recently set out to document the rate of mucosal recovery in kids with celiac disease on a gluten-free diet. They also wanted to figure out whether IgA tissue transglutaminase (tTG) correlates with mucosal damage at the time of a repeat endoscopy with duodenal biopsy.
    The research team included Maureen M. Leonard, Dascha C. Weir, Maya DeGroote, Paul D. Mitchell, Prashant Singh, Jocelyn A. Silvester, Alan M. Leichtner, and Alessio Fasano.
    Their team conducted a retrospective chart review of one-hundred and three pediatric patients, under 21 years of age, with a diagnosis of celiac disease defined as Marsh 3 histology, and who underwent a repeat endoscopy with duodenal biopsy at least twelve months after initiating a gluten free diet.
    Their result showed that 19% of these pediatric patients treated with a gluten-free diet still had persistent enteropathy.
    At the time of the repeat biopsy, tTG was elevated in 43% of cases with persistent enteropathy, and in 32% of cases in which there was mucosal recovery. So, high tTG levels could be seen in both recovered patients, and non-recovered patients.
    The overall positive predictive value of the autoantibody tissue transglutaminase was 25%, and the negative predictive value was 83%, in patients on a gluten free diet for a average of 2.4 years.
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    These findings could help improve current monitoring and management criteria of celiac disease in children.
    Source:
    Journal of Pediatric Gastroenterology & Nutrition. doi: 10.1097/MPG.0000000000001460


    Jefferson Adams
    Celiac.com 10/13/2017 - Tissue transglutaminase (tTG) immunoglobulin A (IgA) testing is a sensitive adjunct to the diagnosis of coeliac disease. The threshold for positivity was developed for diagnosis, with negative results reported as below the reference value (<4 U/mL).
    A team of researchers recently set out to investigate if an undetectable tissue transglutaminase IgA antibodies (tTG IgA<1.2 U/mL) is more predictive of healing compared to patients with negative but detectable serology (1.2-3.9 U/mL).
    The research team included H. Fang, K. S. King, J. J. Larson, M. R. Snyder, T. T. Wu, M. J. Gandhi, and J. A. Murray. They are variously affiliated with the Department of Medicine, the Division of Gastroenterology and Hepatology, the Division of Anatomic Pathology, the Division of Clinical Biochemistry and Immunology, the Division of Biomedical Statistics and Informatics, and the Division of Transfusion Medicine at the Mayo Clinic, Rochester, MN, USA.
    The research team conducted a retrospective study of 402 treated coeliac disease patients seen at the Mayo Clinic with negative tTG IgA values drawn within 1 month of duodenal biopsy between January 2009 and December 2015.
    The team used Corazza-Villanacci scores to assess mucosal healing, and logistic regression to assess the relationship of clinical variables with a normal biopsy. They also noted the presence of gastrointestinal symptoms.
    Their results showed that patients with undetectable test levels more frequently had normal duodenal histology, as compared with patients with detectable tTG IgA levels. Asymptomatic patients more often showed normal duodenal histology as compared to symptomatic patients.
    Patients with undetectable blood levels, and who followed a gluten-free diet for ≥2 years were more likely to have no villous atrophy, as compared to patients with detectable blood levels.
    Follow-up biopsies revealed that people recovering from celiac disease with negative tTG IgA serology showed that undetectable test levels are associated with normal histology.
    Source:
    AP&T


    Jefferson Adams
    Celiac.com 03/01/2018 - Mortality rates for children under five have been falling steadily for decades. Additionally, there's plenty of data to indicate that rates of celiac disease have been rising in general population.
    Before doctors understood the role that gluten played in celiac disease, the prognosis for young children with the condition was grim. Since doctors didn't understand the underlying disease, many of these deaths were simply logged as deaths due to wasting or failure to thrive. Could fewer children dying from celiac disease help explain the apparent rise in celiac rates? In an attempt to answer that question, a team of researchers recently set out to to investigate a possible relationship between mortality rates in children under five years old and rates of celiac disease.
    The research team included F Biagi, A Raiteri, A Schiepatti, C Klersy, and GR Corazza. They are variously affiliated with the First Department of Internal Medicine, Coeliac Centre, and the Biometry and Clinical Epidemiology, Fondazione IRCCS Policlinico San Matteo, University of Pavia, Pavia, Italy.
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    Over the last twenty years or so, mortality rates for kids under 5 have been decreasing all over the world. This reduction has mirrored an increase of the rates of celiac disease. The Spearman correlation coefficient was -63%, 95% confidence interval -82% to -33% (P < 0.001). The data show that higher mortality rates mirrored lower rates of celiac disease. This finding is confirmed by the meta-analysis of the four Italian studies.
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    Source:
    J Pediatr Gastroenterol Nutr. 2018 Feb;66(2):289-294. doi: 10.1097/MPG.0000000000001696.


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