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Found 16 results

  1. Celiac.com 10/29/2018 - Researchers Emma L. Smith with UCB Pharma Ltd., Slough, United Kingdom, and Mark Peakman from the Department of Immunobiology, King’s College London, London, United Kingdom recently set out to catalog clinical advances in peptide immunotherapy for Type 1 diabetes. Autoimmune and allergic diseases occur when a person’s body has an incorrect immune response to an antigen from the person’s own body, or to an innocuous antigen from outside the body. This triggers a pathogenic T-cell response which causes damage to certain tissues and organs. In Type 1 diabetes, this process results in the destruction of the insulin-secreting β cells, which leads to permanent need for recombinant insulin to make up for the loss. The best way to restore immune homeostasis and prevent further tissue damage is to reduce or cease the pathogenic T-cell response by using antigen-specific peptide immunotherapy. Smith and Peakman found that recent clinical advances with peptide therapy approaches in both Type 1 diabetes and other diseases are beginning to show encouraging results. New treatments that target peptides specific to certain cell types are also moving from the development stages into clinical use. Drug developers still face numerous hurdles in reaching full clinical use, including determining optimal dose and dosing frequency, but peptide immunotherapy for Type 1 diabetes is clearly becoming a very active field of drug development. Read their full report: Front Immunol. 2018; 9: 392.Published online 2018 Feb 28. doi:  10.3389/fimmu.2018.00392PMCID: PMC5836708PMID: 29541078
  2. Hi, I have some questions that I hope to get some answers to. First of all, I am not diagnosed and have not been tested for celiac. Only bloodtest I have taken that's relevant is Ferritin and Iron. I'm not anemic, but both my levels are on the lower range of normal (Ferritin 20-25 and Iron 9 and Iron binding capacity a bit over the normal range). My first question is if this is normal in celiacs, or would the Ferritin and Iron be lower if I was celiac? I eat meat and vegetables and my periods are normal. Second Question is related to abdominal pain. I have these IBS related pains (cramping before going to the bathroom) sometimes and also some bloating and stuff. But sometimes I get this lower abdominal pain that is different, it's much much worse when I press my stomach in or touch it. It almost feel normal when I sit still in one position, but when i lean forward, touch it or press it in, it's really bad. Does anyone else with celiac relate to this kind of abdominal pain? The reason I'm asking these questions is because I'm wondering if I should get tested for celiac. I've had symptoms for a while now, and I want to suggest different blood tests to my doctor. I have a feeling I should get tested for something autoimmune. There are already three different Autoimmune diseases in my mother's family (grandmother with psoriasis, cousin with diabetes, mother with ulcerus colitis), and I've been having diffuse symptoms for a while now, like abdominal pain, diarrhea, muscle/bone pain, some joint pain, muscles falling asleep, some tingling, anxiety, neck pain, fever feeling without fever, chills, fatigue (especially after lunch), bad hangovers etc etc. The list is long. So I'm just trying to get some answers so I can be more clear with my doc. Thanks!
  3. Celiac.com 03/26/2018 - Researchers are making serious headway in understanding critical aspects of celiac disease and other autoimmune conditions. However, despite numerous studies showing links between gut microbiota and immune diseases, researchers still don’t know very much about role of gut microbiota in autoimmunity. One team of researchers recently found that translocation of a gut pathobiont, Enterococcus gallinarum, to the liver and other systemic tissues triggers autoimmune responses in a genetic background predisposing to autoimmunity. What does that mean, exactly, and what else did they find? First of all, it’s important to understand that a pathobiont is any potentially disease-causing organism which, normally, lives in symbiosis with its host. So, these are organisms that normally cause no problems at all, but which, under certain circumstances, can cause disease. The research team included S. Manfredo Vieira, M. Hiltensperger, V. Kumar, D. Zegarra-Ruiz, C. Dehner, N. Khan, F. R. C. Costa, E. Tiniakou, T. Greiling, W. Ruff, A. Barbieri, C. Kriegel, S. S. Mehta, J. R. Knight, D. Jain, A. L. Goodman, and M. A. Kriegel. They are variously affiliated with the Department of Immunobiology, the Department of Medicine, and the Department of Pathology, the Yale Center for Genome Analysis, the Department of Microbial Pathogenesis and Microbial Sciences Institute at the Yale School of Medicine in New Haven, CT, USA, the Department of Biochemistry and Immunology, Ribeirao Preto Medical School, Ribeirao Preto, SP, Brazil, the Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA, and the Department of Dermatology, Oregon Health and Science University, Portland, OR, USA. The team’s study data for this model showed that antibiotic treatment prevented mortality, suppressed growth of E. gallinarum in tissues, and eliminated pathogenic autoantibodies and T cells, while Hepatocyte–E. gallinarum cocultures induced autoimmune-promoting factors. Pathobiont translocation in monocolonized and autoimmune-prone mice induced autoantibodies and caused mortality, which could be prevented by an intramuscular vaccine targeting the pathobiont. Liver biopsies of autoimmune patients yielded E. gallinarum–specific DNA, while cocultures with human hepatocytes replicated the murine findings, which means that similar processes likely occur in susceptible humans. This study shows that a gut pathobiont can change locations and can promote autoimmunity in people with a genetic predisposition. This is an important revelation that will help researchers to better understand the mechanisms that trigger celiac disease, and may lead to better diagnosis and treatment options in the future. Source: Science  09 Mar 2018: Vol. 359, Issue 6380, pp. 1156-1161. DOI: 10.1126/science.aar7201
  4. Celiac.com 01/15/2018 - Cerebellar ataxia with sensory ganglionopathy is a disabling combination of neurological dysfunction that usually occurs as part of certain hereditary ataxias. However, some patients present this combination with no apparent genetic cause. A team of researchers recently set out to if autoimmunity might have a role to play in SG. The research team included Panagiotis Zis, Ptolemaios Georgios Sarrigiannis, Dasappaiah Ganesh Rao, Nigel Hoggard, David Surendran Sanders, and Marios Hadjivassiliou. They are variously affiliated with the Academic Department of Neurosciences, Sheffield Teaching Hospitals NHS Foundation Trust, Sheffield, UK; the University of Sheffield, Sheffield, UK; the Department of Neuroradiology, Sheffield Teaching Hospitals NHS Foundaiton Trust, Sheffield, UK; the University of Sheffield, Sheffield, UK; and the Academic Unit of Gastroenterology, Sheffield Teaching Hospitals NHS Foundation Trust, Sheffield, UK. The team reviewed records of all patients that have been referred to the Sheffield Ataxia Centre who had neurophysiological and imaging data suggestive of SG and cerebellar ataxia respectively. We excluded patients with Friedreich's ataxia, a common cause of this combination. All patients were screened for genetic causes and underwent extensive investigations. They found 40 patients with combined cerebellar ataxia and sensory ganglionopathy. The majority of patients were initially diagnosed with cerebellar dysfunction, and about one-third were initially diagnosed with sensory ganglionopathy. For that one-third, the two diagnoses were made together. The average time between the two diagnoses was 6.5 ± 8.9 years, ranging from 0 up to 44 years. The most common initial symptom was unsteadiness, in 77.5% of patients, followed by patchy sensory loss in 17.5%, and peripheral neuropathic pain in 5%. Nineteen patients had gluten sensitivity, of whom 3 patients had biopsy proven celiac disease. Other abnormal immunological tests were present in another 15 patients. Six patients had malignancy, which was diagnosed within 5 years of the neurological symptoms. Only 3 patients were classified as having a truly idiopathic combination of cerebellar ataxia with sensory ganglionopathy. This study shows that immune pathogenesis plays a significant role in patients with the unusual combination of cerebellar ataxia and sensory ganglionopathy. Source: Cerebellum & Ataxias 20174:20
  5. Celiac.com 11/07/2017 - Researchers still don't have much good data on the consequences of antibiotic use in early life and how that relates to the risk of certain autoimmune diseases. A team of researchers recently set out to test the association between early-life antibiotic use and islet or celiac disease autoimmunity in genetically at-risk children prospectively followed up for type 1 diabetes (T1D) or celiac disease. Their study is part of a larger study called The Environmental Determinants of Diabetes in the Young, or TEDDY, for short. The reasearch team enrolled HLA-genotyped newborns from Finland, Germany, Sweden, and the United States between November 20, 2004, and July 8, 2010, and analyzed data from November 20, 2004, to August 31, 2014. They also enrolled individuals from the general population, and those having a first-degree relative with T1D, with any 1 of 9 HLA genotypes associated with a risk for T1D. The team charted parental reports of the most common antibiotics, such as cephalosporins, penicillins, and macrolides, used between age 3 months and age 4 years. Islet autoimmunity and celiac disease autoimmunity were defined as being positive for islet or tissue transglutaminase autoantibodies at 2 consecutive clinic visits at least 3 months apart. The team used Cox proportional hazards regression models to assess the relationship between antibiotic use in early life before seroconversion and the development of autoimmunity, and to calculate hazard ratios and 95% CIs. The team conducted tests for islet and tissue transglutaminase autoantibodies on 8,495 children (49.0% female), and 6,558 children (48.7% female) who were enrolled in the TEDDY study, and they found that antibiotic exposure and frequency of use in early life or before seroconversion did not influence the risk of developing islet autoimmunity or celiac disease autoimmunity. Additionally, cumulative use of any antibiotic during the first 4 years of life was not tied to the appearance of any autoantibody (hazard ratio , 0.98; 95% CI, 0.95-1.01), multiple islet autoantibodies (HR, 0.99; 95% CI, 0.95-1.03), or the transglutaminase autoantibody (HR, 1.00; 95% CI, 0.98-1.02). Using any of the most common antibiotics during the first 4 years of life, in any geographic region, did not influence the later development of autoimmunity for T1D or celiac disease. Based on these results, the team concluded that doctors recommending antibiotics for young children at risk for T1D or celiac disease need not be concerned that the use will lead to islet or tissue transglutaminase autoimmunity. Source: JAMA Pediatr. Published online October 9, 2017. doi:10.1001/jamapediatrics.2017.2905 The research team included Kaisa M. Kemppainen, PhD; Kendra Vehik, PhD; Kristian F. Lynch, PhD; Helena Elding Larsson, MD, PhD; Ronald J. Canepa, BSc; Ville Simell, MSc; Sibylle Koletzko, MD, PhD; Edwin Liu, MD; Olli G. Simell, MD, PhD; Jorma Toppari, MD, PhD; Anette G. Ziegler, MD, PhD; Marian J. Rewers, MD, PhD; Åke Lernmark, PhD; William A. Hagopian, MD, PhD; Jin-Xiong She, PhD; Beena Akolkar, PhD; Desmond A. Schatz, MD; Mark A. Atkinson, PhD; Martin J. Blaser, MD; Jeffrey P. Krischer, PhD; Heikki Hyöty, MD, PhD; Daniel Agardh, MD, PhD; and Eric W. Triplett, PhD; for The Environmental Determinants of Diabetes in the Young (TEDDY) Study Group. They are variously affiliated with the Department of Microbiology and Cell Science, Institute of Food and Agricultural Sciences, University of Florida, Gainesville; the Health Informatics Institute, Morsani College of Medicine, University of South Florida, Tampa; the Department of Clinical Sciences, Lund University Clinical Research Center, Skåne University Hospital, Malmö, Sweden; the MediCity Laboratory, University of Turku, Turku, Finland; the Division of Paediatric Gastroenterology and Hepatology, Dr von Hauner Children's Hospital, Ludwig Maximilian University, München, Germany; the Digestive Health Institute, Children's Hospital Colorado, Anschutz Medical Campus, University of Colorado Denver, Aurora; the Research Centre of Applied and Preventive Cardiovascular Medicine, University of Turku, Turku, Finland; the Department of Pediatrics, University of Turku, Turku University Hospital, Turku, Finland; the Department of Physiology, Institute of Biomedicine, University of Turku, Turku, Finland Institute of Diabetes Research, Helmholtz Zentrum München, München, Germany; the Klinikum Rechts der Isar, Technische Universität München, München, Germany; the Forschergruppe Diabetes e.V., Neuherberg, Germany; the Barbara Davis Center for Childhood Diabetes, University of Colorado Denver, Aurora; the Pacific Northwest Diabetes Research Institute, Seattle, Washington; the Center for Biotechnology and Genomic Medicine, Medical College of Georgia, Augusta University, Augusta National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland; the Department of Pediatrics, College of Medicine, University of Florida, Gainesville; the Department of Pathology, Immunology, and Laboratory Medicine, College of Medicine, University of Florida, Gainesville; the Department of Medicine and Microbiology, New York School of Medicine, New York; the Department of Virology, Faculty of Medicine and Life Sciences, University of Tampere, Tampere, Finland; and with Fimlab Laboratories, Pirkanmaa Hospital District, Tampere, Finland.
  6. Celiac.com 03/13/2017 - A team of researchers recently set out to determine whether there might exist ethnic differences in celiac disease autoimmunity in children at 6 years of age, and if present, to assess how these differences may be explained by known sociodemographic and environmental factors. The research team included Michelle A E Jansen, Sytske A Beth, Diana van den Heuvel, Jessica C Kiefte-de Jong, Hein Raat, Vincent W V Jaddoe, Menno C van Zelm, and Henriette A Moll. They are variously affilated with the Generation R Study Group, Erasmus MC, University Medical Center, Rotterdam, The Netherlands; the Department of Paediatrics, the Department of Immunology, and the Department of Epidemiology, Erasmus MC, University Medical Center, Rotterdam, The Netherlands, and with the Department of Public Health, University Medical Center, Rotterdam, the Department of Global Public Health at Leiden University College, The Hague, The Netherlands, and with the Department of Immunology and Pathology, Central Clinical School, Monash University, Melbourne, Australia. The team embedded their study within a multi-ethnic population-based prospective cohort study of 4442 six-year-old children born between 2002 and 2006. They used questionnaires to assess information on ethnicity, environmental and lifestyle characteristics. They divided ethnicity into Western, which included Dutch, European, Indonesian, American, Oceanian, and non-Western, which included Turkish, Moroccan, Cape Verdean, Antillean, Surinamese. The team then used fluorescence enzyme immunoassay to measure serum transglutaminase type 2 antibody (TG2A) levels . They used ELISA to measure serum IgG levels against cytomegalovirus (CMV). They defined TG2A positivity as TG2A ≥7 U/mL, strong TG2A positivity as TG2A ≥10 upper limit normal (70 U/mL). Of the 4,442 children they assessed, just 60, or 1.4%, tested TG2A positive. Of these 60, 31 registered strong positive. In all, 66% of these children were Western, 33% non-Western. Western ethnicity, high socioeconomic position and daycare attendance were positively associated with strong TG2A positivity (odds ratio (OR) 6.85 (1.62 to 28.8) p Together, these factors explained up to 47% (−67 to −17; p=0.02) of the ethnic differences in TG2A positivity between Western and non-Western children. Ethnic differences in children with celiac disease autoimmunity are present in childhood. Socioeconomic position, daycare attendance and CMV seropositivity partly explained these differences, and may serve as targets for prevention strategies for CDA. Source: BMJ Publishing Group Limited
  7. Celiac.com 10/13/2016 - Researchers don't currently know much about rates of celiac disease autoimmunity or tissue transglutaminase autoantibodies (TGA) in patients with type 1 diabetes (T1D) and autoimmune thyroid disease (AITD) in the Chinese population. A team of researchers recently set out to assess rate of celiac disease autoimmunity amongst patients with T1D and AITD in the Chinese population. The research team included Zhiyuan Zhao, Jing Zou, Lingling Zhao, Yan Cheng, Hanqing Cai, Mo Li, Edwin Liu, Liping Yu, and Yu Liu. The study included 178 patients with type 1 diabetes, along with 119 with AITD where 36 had both T1D and AITD, classified as autoimmune polyglandular syndrome type 3 variant (APS3v). The study also included 145 patients with type 2 diabetes (T2D), 97 patients with non-autoimmune thyroid disease (NAITD), and 102 healthy control subjects. The team used radioimmunoassay to measure serum islet autoantibodies, thyroid autoantibodies and TGA. They found TGA positivity in 22% of patients with either type 1 diabetes or AITD, much higher than the 3.4% seen in T2D patients (p< 0.0001) the 3.1% seen in NAITD patients (P < 0.0001) or the 1% seen in healthy controls (1%; p<0.0001). Thirty-six percent of patients with APS3v who had both T1D and AITD positive for TGA, significantly higher than patients with T1D alone (p = 0.040) or with AITD alone (p = 0.017). At diagnosis, T1D and AITD showed overlap frequencies of 20% and 30%, respectively. Chinese population with existing T1D and/or AITD shows high rates of TGA positivity, which are even higher in people with both diseases. The study team recommends routine TGA screening in patients with T1D or AITD will help to identify celiac disease autoimmunity early on, and will yield better clinical patient care. Source: Plos.org
  8. Celiac.com 06/13/2016 - Researchers Umberto Volta, Giacomo Caio, and Roberto De Giorgio, of the Department of Medical and Surgical Sciences at the University of Bologna in Bologna, Italy, recently submitted a letter to the medical journal Gastroenterology. In their letter, the researchers respond to a recent paper, published by Carroccio et al, reporting on the prevalence of autoimmunity (as identified by positivity of antinuclear antibodies [ANA] and associated autoimmune disorders) in non-celiac wheat sensitivity (NCWS) compared with celiac disease and irritable bowel syndrome (IBS). They note that the study results, based on retrospective and prospective data, showed that the prevalence of ANA in NCWS was significantly higher than in celiac disease and IBS (46% in NCWS vs 24% in celiac disease and 2% in IBS, retrospectively; and 28% in NCWS vs 7.5% in celiac disease and 6% in IBS, prospectively). They note also that both retrospective and prospective analysis show autoimmune disorders (mainly autoimmune thyroiditis) in a slightly higher proportion in NCWS (29% vs 24%) than celiac disease (21% vs 20%). Meanwhile, both NCWS and celiac patients showed substantially higher rates of autoimmune disorders than IBS. In both both retrospective and prospective data, ANA showed a strong relation to HLA-DQ2 and -DQ8 in NCWS, whereas these autoantibodies were associated with autoimmune disorders only in the prospective arm. The team found these results from the Carroccio study to be scientific interesting because NCWS, more than better known autoimmune disorders, such as celiac disease, shows a surprisingly high autoimmune profile. They note that celiac disease is a well-established autoimmune condition often marked by different types of autoantibodies and associated autoimmune disorders. Such autoimmune features have not been seen so far in NCWS and the odds of these patients developing autoimmune dysfunction remains unknown. The team's data showed that only 14% of 486 patients with NCWS had an associated autoimmune disorder including thyroiditis, psoriasis, Graves disease, type 1 diabetes mellitus, and atrophic gastritis. In contrast, about 30% of 770 celiac patients showed the same autoimmune manifestations. These findings are in line with previously published data. They point out that another interesting aspect that came out of Carroccio study is the very high rate of ANA in their cohort of NCWS versus celiac disease and IBS patients. The team notes that their own experience shows ANA to be higher in celiac disease than NCWS and IBS (49% vs 37% vs 6%), which indicates a substantial autoimmune profile in celiac disease, compared with the two other conditions. They also note that evidence showing patients with NCWS to have higher rates of ANA compared with IBS is in line with the results presented by Carroccio et al. They conclude their letter by stating that consistent evidence supports a major role of adaptive immunity in celiac disease more than NCWS, and this peculiarity is reflected by a predominant occurrence of autoimmune disorders and autoantibodies (eg, ANA). However, the challenging data shown by Carroccio et al provide the basis to understand whether NCWS, like celiac disease, show a wide array of autoimmune expressions mediated by adaptive mechanisms. They call for further studies to better understand what they term the "intriguing relationship between autoimmunity and NCWS." Source: Gastroenterology. 2016 Jan;150(1):282. doi: 10.1053/j.gastro.2015.08.058. Epub 2015 Nov 23.
  9. Celiac.com 02/10/2015 - A number of studies have shown a connection between celiac autoimmunity and type 1 diabetes mellitus (T1DM). Doctors recommend celiac screening for T1DM patients, but screening is not always conducted. Meanwhile, reports about the impact of celiac autoimmunity in T1DM have been varied. A team of researchers recently set out to determine rates of celiac autoimmunity in patients with T1DM, and to study the impact of celiac autoimmunity on nutritional parameters, glycaemic control, endocrine axes and bone health. The research team included A.S. Joshi, P.K. Varthakavi, N.M. Bhagwat, M.D. Chadha, AND S.S. Mittal. They are variously associated with the Department of Endocrinology of Topiwala National Medical College and BYL Nair Charitable Hospital, Mumbai Central in Maharashtra, India. For their study, the team conducted celiac autoimmunity screens on eighty-six consecutive patients with T1DM using immunoglobulin A (IgA) tissue transglutaminase as a marker (TTG; IgG anti-gliadin in IgA-deficient case). They compared CA positive (CA+) T1DM cases with age-matched and sex-matched CA negative (CA-) T1DM cases for anthropometry, glycaemic control (as assessed by glycated haemoglobin (HbA1c) and hypoglycaemic/hyperglycaemic episodes), endocrine (thyroid function, cortisol, growth hormone (GH) axis, gonadal axes), haematological (haemoglobin, iron profile and vitamin B12 status) and calcium metabolism parameters and bone densitometry (by dual-energy X-ray absorptiometry (DXA)). Consenting patients with celiac autoimmunity also underwent upper gastrointestinal (GI) endoscopy with duodenal biopsy. Results showed that 11 of the 86 patients, about 12.75%, screened positive for celiac autoimmunity. Of those, seven patients underwent duodenal biopsies which suggested two cases of Marsh grade III, three cases of Marsh grade II and two cases of Marsh grade I celiac disease. In terms of anthropometry, CA+ T1DM patients were comparable with CA- T1DM patients. Overall, CA+ patients had higher HbA1c (10.7±1.8 vs. 8.4±1.0 (93±19 vs. 68±11 mmol/mol); p The incidence of fractures in the past 3 years was four CA+ patients, and one CA- patient (p<0.05). There is an important autoimmune connection between celiac disease and T1DM. For people with T1DM, celiac disease adversely affects stature, bone health, glycaemic control and iron and B12 levels. The study team recommends that IgA sufficiency be established before using an IgA-based screening test for celiac autoimmunity. Source: Arab J Gastroenterol. 2014 Jun;15(2):53-7. doi: 10.1016/j.ajg.2014.04.004. Epub 2014 Jun 7.
  10. The following was written by one of the CEDAR staff, Stephanie Tudor - TudorS@jove.uchsc.edu. Anyone with further questions should contact her directly. If you live in Denver and are biopsy-confirmed, they would love to hear from you. The Celiac Disease Autoimmunity Research (CEDAR) project is affiliated with the Department of Preventive Medicine and Biometrics in the School of Medicine of the University of Colorado, Health Sciences Center. It is a project supported by a grant from the National Institutes of Health (NIH), and will collect data for a total of five years. The principal investigator is Marian J. Rewers, MD, MPH, Ph.D. Other co-investigators include: Jill Norris, Ph.D.; George Eisenbarth, MD, Ph.D.; Ronald J. Sokol, MD; and Edward Hoffenberg, MD. The goals of this study are primarily to investigate the genetic and environmental causes of celiac disease, through the determination of the prevalence of anti-endomysial antibodies (EMA) in children considered to be at risk based on their family history (first degree relative) of either diabetes mellitus (Type I) or celiac disease or based on their HLA genotype (DR3) that is suspected to put them at an increased risk. The study is anticipating an enrollment of approximately 3,000 eligible children under the age of ten years. Most of the children reside in the Denver metro area, and a large proportion (approximately 40%) of the children involved with this research are concurrently enrolled in the Diabetes Autoimmunity Study in the Young (DAISY), which is run by the same principal investigator. The DAISY project is evaluating the presence of autoimmunity in relation to a pre-diabetic (insulin dependent diabetes mellitus) condition. The enrolled subjects are screened initially between the ages of two and five years of age with a serum sample tested using an IgA-based anti-endomysial antibody assay. The serum samples are also screened for IgA levels in order to rule out the potential for false negative results in IgA deficient children. For the subjects who are tested at a positive titration, follow-up includes a clinic evaluation and small bowel biopsy at the Pediatric Gastroenterology Department at the Childrens Hospital of Denver, Colorado. If a diagnosis of celiac is made, the subject is referred for nutritional counseling and follow-up serum testing is done six months after the diagnosis to confirm effective treatment. Dietary factors are also collected upon enrollment of the subjects, reflecting dietary changes that are made between the ages of one and two years of age, as the introduction of gluten into the diet usually occurs in this time frame. Information on family history of other autoimmune conditions is also collected. Subjects who test negative for the presence of anti-endomysial antibodies will be re-screened two years after their initial testing, to verify their immune status with respect to the anti-endomysial antibodies. By the end of the study period, we hope to have data that more accurately defines the prevalence of celiac disease in a United States population. The children recruited based on their HLA type are from a general population screening, and their data should be able to provide more accurate statistics on prevalence, and perhaps incidence, as some of these children have been followed since birth. We also hope to have identify associations with potential environmental exposures which may increase susceptibility to celiac disease.
  11. Celiac.com 12/05/2012 - Regulatory T cells (Tregs) are play a pivotal role in helping our bodies tolerate self-antigens and dietary proteins. Interleukin (IL)-15 is a cytokine that is overly present in the intestines of patients with celiac disease. Studies have shown that Interleukin (IL)-15 does not interfere with the generation of functional Tregs, but causes human T cells to resist Treg suppression. To better understand how control of effector T cells by regulatory T cells is inhibited, a team of researchers compared Treg numbers and responses of intestinal and peripheral T lymphocytes to suppression by Tregs in celiac disease patients and in a control group. The research team included N.B. Hmida, M. Ben Ahmed, A. Moussa, M.B. Rejeb, Y. Said, N. Kourda, B. Meresse, M. Abdeladhim, H. Louzir, and N. Cerf-Bensussan. They are affiliated with the Department of Clinical Immunology and the Institut Pasteur de Tunis in Tunis, Tunisia. For their study, the team isolated intraepithelial lymphocytes (IELs) and lamina propria lymphocytes (LPLs) from duodenal biopsy specimens of patients with celiac disease and in a control group. The team then purified CD4+CD25+ T lymphocytes (Tregs) from blood. By analyzing anti-CD3-induced proliferation and interferon (IFN)-γ production in the presence or absence of peripheral Tregs, they were able to test responses of IELs, of LPLs, and peripheral lymphocytes (PBLs) to suppression by Tregs. The team used flow cytometry to measure lamina propria and peripheral CD4+CD25+FOXP3+ T cells. They found that, although patients with active celiac disease showed significantly increased percentages of CD4+CD25+FOXP3+ LPLs, they also showed less inhibited proliferation and IFN-γ production of intestinal T lymphocytes by autologous or heterologous Tregs (P < 0.01). IEL for subjects with celiac disease showed no response to Tregs. Also, the team noted resistance of LPLs and PBLs to Treg suppression in patients with villous atrophy who had substantially higher blood levels of IL-15 compared with patients without villous atrophy and controls. From their results, the research team concludes that effector T lymphocytes in people with active celiac disease become resistant to suppression by Tregs. This resistance may result in loss of tolerance to gluten, and to self-antigens. Source: Am J Gastroenterol. 2012 Apr;107(4):604-11. doi: 10.1038/ajg.2011.397. Epub 2011 Nov 22.
  12. Celiac.com 06/08/2011 - A team of researchers recently set out to determine whether delaying gluten introduction in infants with genetic risk for islet autoimmunity is feasible, safe, and able to reduce the risk of type 1 diabetes–associated islet autoimmunity. The research team included Sandra Hummel, PHD, Maren Pflüger, PHD, Michael Hummel, MD, Ezio Bonifacio, PHD, and Anette-G. Ziegler, MD. They are variously affiliated with the Institute for Diabetes Research, Helmholtz Zentrum München, Forschergruppe Diabetes der Technischen Universität München, the Institut für Diabetesforschung der Forschergruppe Diabetes e.V. am Helmholtz Zentrum München, Munich, Germany, and the Deutsche Forschungsgemeinschaft Center for Regenerative Therapies Dresden, Technische Universität Dresden, Germany. For the study, the team recruited a total of 150 infants with a first-degree family history of type 1 diabetes and a risk HLA genotype. They then randomly assigned each infant to a first gluten exposure at age 6 months (control group) or 12 months (late-exposure group). The team followed-up on each infant at three month-intervals until the age of 3 years, and then yearly thereafter. The team tested for growth and autoantibodies to transglutaminase C [TGCAs]), islet autoantibodies to insulin, GAD, insulinoma-associated protein 2, and type 1 diabetes. A total of 70% of families reported following the dietary-intervention protocol. For the first three years, children in the control and late-exposure groups showed similar weight and height, along with similar probability of developing TGCAs (14 vs. 4%; P = 0.1). A total of eleven children in the control group and 13 children in the late-exposure group developed islet autoantibodies (3-year risk: 12 vs. 13%; P = 0.6). Seven children developed diabetes, including four in the late-exposure group. The team saw no significant differences when analyzing children as per protocol on the basis of the first reported reported gluten exposures for the children. From the data, the team concluded that delaying gluten exposure until the age of 12 months is safe, but does not significantly reduce the likelihood of islet autoimmunity in genetically at-risk children. Source: DiabetesCare.com
  13. Celiac.com 08/05/2010 - A myriad of autoimmune disordersincluding, Addison's disease, type 1 diabetes and celiac disease areclosely associated with the HLA-DR3 haplotype. However it is has beenhypothesized that alleles of other genes in linkage disequilibriumwith HLA-DRB1 also contribute to the diseases. Researchers at the Barbara Davis Centerfor Childhood Diabetes, University of Colorado Denver, Aurora,Colorado, conducted a study to characterize major histocompatabilitycomplex (MHC) haplotypes which put patients at high risk forAddison's disease. Between 1992 and 2009, eighty-sixCaucasian subjects with 21-hydroxylase autoantibody-positive ,nonautoimmune polyendocrine syndrome type 1, were genotyped forJLA-DRB1, HLA-DQB1, MICA, HLA-B, HLA-A and high density MHCsingle-nucleotide polymorphism analysis for 34. Measuring AD and genotype, 97% of themultiplex subjects, 60% of the simplex AD subjects and 13% of thegeneral population control group had both HLA-DR3 and HLA-B8. The study also found that 85% of the ADmultiplex subjects, 24% of the simplex patients and 1.5% of thecontrol group subjects presented with DR3/DR4 and B8. Also discovered through this study wasthat the DR3-B8 haplotype of AD subjects only 47% had HLA-A1,compared to the control subjects at 81% and the type 1 diabeticsubjects at 73%. Researchers of this study concludedthat severe risk for Addison's disease, specifically in multiplexfamilies, is connected to haplotypic DR3 variants in specific a part(3.8) though not all of the conserved 3.8.1 haplotype. Source: PubMed.govJClin Endocrinol Metab. 2010 Jul 14.
  14. Celiac.com 03/03/2010 - A team of researchers set out to assess long-term outcomes of thyroid function and autoimmunity in a large population of children with celiac disease. The research team included Alessandra Cassio, MD, Giampaolo Ricci, MD, Federico Baronio, MD, Angela Miniaci, MD, Milva Bal, MD, Barbara Bigucci, MD, Veronica Conti, MD, and Alessandro Cicognani, MD. To accomplish this, they conducted a longitudinal, retrospective study at the Pediatric Department, University of Bologna, Italy (duration of follow-up, 8.9 +- 4.0 years). In all, the team examined one hundred thirty-five consecutive patients diagnosed between June 1990 and December 2004 and followed on a gluten-free diet. To be included, researchers required study subjects to maintain good dietary compliance and duration of follow-up for at least 3 years. A total of 101 patients showed no positive antithyroid titers during the follow-up, while 86 remained euthyroid; 15 showed high thyroid-stimulating hormone values at diagnosis that normalized in 11 cases after 12 to 18 months of gluten withdrawal. A total of 31 patients showed persistently positive antibody titers, with 23 of those (74%) remained consistently euthyroid during the follow-up and 8 (26%) had a subclinical hypothyroidism. Children with growth retardation or gastroenterological symptoms at diagnosis and different lengths of gluten exposure showed similar rates of positive antibodies. In children with celiac disease, antithyroid antibodies have a low clinical value for predicting the development of thyroid hypo-function during the indicated surveillance period. They encourage a more comprehensive follow-up. Source: J Pediatr. Volume 156, Issue 2, Page A2; February 2010
  15. Celiac.com 03/09/2009 - Due to seemingly low rates of beta-cell autoimmunity among children with celiac disease, there is no need to screen these children for beta-cell autoimmunity markers, according to a report by Italian doctors in the February issue of Diabetes Care. Dr. Giuseppe D'Annunzio, of the University of Genoa, and colleagues recently set out to determine which pediatric celiac patients might warrant beta-cell autoimmunity screening. His research team assessed 188 children who received celiac disease diagnosis at an average age of 5.8 years, and who had had the disease for 4.2 years on average. The doctors confirmed gluten-free diet compliance by testing for anti-endomysial antibodies and endomysial tissue transglutaminase antibodies. Nine of the children (4.8%) tested positive for diabetes-related auto-antibodies. However, all of these children showed normal fasting blood glucose and A1C levels and, after 36 months of follow-up, none developed type 1-diabetes. The researchers note that there is, between celiac disease and juvenile diabetes, a shared prodromic stage, with “auto-antibodies to islet or gut antigens.” Still, they note that their findings support those of other investigators, and that routine screening for diabetes-related antibodies in children with celiac disease is not warranted. Diabetes Care 2009; 32:254-256.
  16. JAMA. 2005;293:2343-2351, 2410-2412 Celiac.com 05/31/2005 – Researchers in the United States have found that introducing gluten too early or too late in an infants diet may play a key role in whether or not they eventually develop celiac disease autoimmunity. From 1994 to 2004 the researchers followed 1,560 high-risk children (those with either HLA-DR3 or DR4 alleles, or with a first-degree relative with type 1 diabetes) who were periodically screened for celiac disease autoimmunity. Positive results were defined by two positive tissue transglutaminase (tTG) blood serum tests, or one positive tTG and a positive small bowel biopsy. The researchers conducted a prospective observational study in which the parents of the children in the study responded to a questionnaire regarding the timing of gluten introduction into their childrens diets. To avoid a bias on the answers the researchers purposely did not include children who already had celiac disease. During the mean duration period of the study (4.8 years), 51 children developed celiac disease autoimmunity. Their findings indicate that children who were first introduced to gluten when they were less than 3 months of age had a five-fold increased risk of developing celiac disease autoimmunity when compared to children who were first introduced to gluten at 4-6 months old. Additionally, those who were first introduced at 7 months or older had a marginally increased risk of getting celiac disease autoimmunity when compared with the same group. Based on these findings the researchers recommend that parents should introduce cereals into their childrens diets at 4-6 months of age—even though this conflicts with recent recommendations by the American Academy of Pediatrics, who recommend breast-feeding only until 6 months of age. The researchers stress that much larger international prospective studies need be done in this area to answer the many questions that this study raises.
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