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Found 5 results

  1. Celiac.com 10/17/2016 - Refractory celiac disease is a severe condition with few good treatment options, and which often eventually results in death. A group of researchers recently set out to create a prognostic model to estimate survival of patients with refractory celiac disease. The research team included A. Rubio-Tapia, G. Malamut, W. H. M. Verbeek, R. L. J. van Wanrooij, D. A. Leffler, S. I. Niveloni, C. Arguelles-Grande, B. D. Lahr, A. R. Zinsmeister, J. A. Murray, C. P. Kelly, J. C. Bai, P. H. Green, S. Daum, C. J. J. Mulder, and C. Cellier. They are variously affiliated with the Mayo Clinic, Rochester, MN, USA, the Hopital Europeen Georges-Pompidou, Paris, France, the Hospital Dr. Carlos Nonorino Udaondo, Buenos Aires, Argentina, the Columbia University Medical Center, New York, NY, USA, Beth Israel Deaconess Medical Center, Boston, MA, USA, the Charite-University Medicine Berlin, Berlin, Germany, and the VU University Medical Centre, Amsterdam, The Netherlands. Before setting up their prognostic model, the team first assessed predictors of 5-year mortality using Cox proportional hazards regression on subjects from a multinational registry. The team used bootstrap resampling to internally validate the individual factors and overall model performance. To calculate a risk score for 5-year mortality, the team averaged all estimated regression coefficients gathered from 400 bootstrap models that they formulated from their multinational cohort of 232 patients diagnosed with refractory celiac disease across seven centers. Average patient age was 53 years and the group included 150 women out of the 232 patient total. A total of 51 subjects died during a 5-year follow-up, which put the cumulative 5-year all-cause mortality at 30%. The results from a multiple variable Cox proportional hazards model showed that the following variables were significantly associated with 5-year mortality: age at refractory celiac disease diagnosis (per 20 year increase, hazard ratio = 2.21; 95% confidence interval, CI: 1.38–3.55), abnormal intraepithelial lymphocytes (hazard ratio = 2.85; 95% CI: 1.22–6.62), and albumin (per 0.5 unit increase, hazard ratio = 0.72; 95% CI: 0.61–0.85). A simple weighted three-factor risk score was created to estimate 5-year survival. The team's prognostic model for predicting 5-year mortality among patients with refractory celiac disease may help clinicians to guide treatment and follow-up. Source: Alimentary Pharmacology & Therapeutics. DOI: 10.1111/apt.13755View/save citation
  2. Celiac.com 01/18/2016 - How come only 2% to 5% of genetically susceptible individuals develop celiac disease? Researchers attempting to answer that question have turned their focus to environmental factors, including gut microorganisms, that may contribute to the development of celiac disease. In a recent study, published in The American Journal of Pathology, researchers using a humanized mouse model of gluten sensitivity found that the gut microbiome can play an important role in the body's response to gluten. Their data show that the rise in overall celiac disease rates over the last 50 years may be driven, at least partly, by variations in gut microbiota. If this proves to be true, then doctors may be able to craft "specific microbiota-based therapies" that "aid in the prevention or treatment of celiac disease in subjects with moderate genetic risk," says lead investigator Elena F. Verdu, MD, PhD, Associate Professor, Division of Gastroenterology, Department of Medicine, Farncombe Family Digestive Health Research Institute, McMaster University, Hamilton, ON (Canada). For their study, the team used mice that express the human DQ8 gene, which makes them genetically susceptible to inflammatory responses to gluten, researchers compared immune responses and pathology in the guts of mice that differed in their gut microorganisms. The three groups included germ-free mice, clean–specific-pathogen-free (SPF) mice with microbiota free of opportunistic pathogens and Proteobacteria, and conventional SPF mice that were colonized with a mixture of microorganisms including opportunistic pathogens and Proteobacteria. For example, the microbial profile of conventional SPF mice included Staphylococcus, Streptococcus, and Helicobacter, while the clean SPF had none. Researchers already know that growth and activation of intraepithelial lymphocytes (IELs) is an early sign of celiac disease. This research team saw that gluten treatment led to increased IEL counts in germ-free mice, but not in clean SPF mice. The gluten-induced IEL response in germ-free mice was accompanied by increased cell death in the cells lining the gastrointestinal tract (enterocytes), as well as anatomical changes in the villi lining the small intestine. The germ-free mice also developed antibodies to a component of gluten, known as gliadin, and displayed pro-inflammatory gliadin-specific T-cell responses. A non-gluten protein, zein, did not affect IEL counts, indicating that the response was gluten specific. Meanwhile, the mice colonized with limited opportunistic bacteria (clean SPF), did not develop gluten-induced pathology, compared to germ-free mice or conventional SPF mice with a more diverse microbiota. Interestingly, this protection was suppressed when clean SPF mice were supplemented with an enteroadherent E. coli isolated from a patient with celiac disease. These results are preliminary, and other researchers stress that the specific role of Proteobacteria in celiac disease should not be over interpreted. In an accompanying Commentary, Robin G. Lorenz, MD, PhD, of the Department of Pathology at the University of Alabama at Birmingham, writes that these findings "implicate opportunistic pathogens belonging to the Proteobacteria phylum in celiac disease; however, this does not indicate that Proteobacteria cause celiac disease." Instead, Dr. Lorenz suggests, there may be numerous possible avenues by which Proteobacteria enhance the exposure and immune response to gluten or gliadin. So, the takeaway here is that, while these early results are highly interesting and certainly merit follow-up, it's way too early to say that certain types of gut bacteria may be driving celiac disease, and any types of bacterial treatments that might prevent celiac disease from developing are just the stuff of imagination. Still, this is an important discovery that might pave the way for exactly such types of therapy in the future, so stay tuned. Source: The American Journal of Pathology
  3. Celiac.com 08/15/2011 - People with potential celiac disease have similar HLA, and positive anti-transglutaminase antibodies, but do not suffer damage to small intestinal mucosa. Very few of these patients develop mucosal lesions. So far, scientists know of more than forty genes associated with celiac disease, but exactly how these pathways act to trigger celiac disease in genetically predisposed individuals remains a mystery. A team of researchers recently set out to shed some light on that mystery. The research team included Maria Pia Sperandeo, Antonella Tosco, Valentina Izzo, Francesca Tucci, Riccardo Troncone, Renata Auricchio, Jihane Romanos, Gosia Trynka, Salvatore Auricchio, Bana Jabri, and Luigi Greco. They are variously affiliated with the European Laboratory for Food Induced Disease, and the Department of Pediatrics at the University of Naples Federico II in Naples, Italy, the Department of Genetics at the University Medical Centre at the University of Groningen, Groningen in The Netherlands, and with the Department of Medicine, the Department of Pathology and the Department of Pediatrics at University of Chicago. To more fully explore the genetic features of potential celiac disease individuals, the team enrolled 127 patients with potential celiac disease, positive anti-tissue transglutaminase and no mucosal lesions. Ultimately, about 30% of those followed for four years developed celiac disease. The team then genotyped each of the subjects for 13 polymorphisms of the 'candidate genes’ and compared the results to control subjects, and to patients with known celiac disease. They used 60 biopsy specimens to more fully evaluate gene expression. They found that people with potential celiac disease have less HLA-related risk compared to those with celiac disease (χ2 = 48.42; p value = 1×10−8). Those with potential celiac disease also share most of the polymorphisms of the celiacs, but the frequency of c-REL* G allele was suggestive for a difference compared to celiac (χ2 = 5.42; p value = 0.02). There was one marker of the KIAA1109/IL-2/IL-21 region that differentiated those with potential celiac disease from those with clinical celiac disease (rs4374642: χ2 = 7.17, p value = 0.01). In people with potential celiac disease, the expression of IL-21 was completely suppressed, whereas, in those with celiac disease (p value = 0.02) and in control subjects (p value = 0.02), IL-2, KIAA1109 and c-REL expression were over-expressed. The study reveals that people with potential celiac disease show different genetic features expression markers than those with celiac disease. The study also shows potential celiac disease to be a useful biological model of the pathways leading to the small intestinal mucosal damage in genetically predisposed individuals. Source: PLoS ONE 6(7): e21281. doi:10.1371/journal.pone.0021281
  4. 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
  5. Oberhuber G, Schwarzenhofer M, Vogelsang H Dig Dis 1999 Nov- Dec;16(6):341-4 Department of Clinical Pathology, University of Vienna, Vienna, Austria. The in vitro challenge of duodenal mucosa with gliadin is a useful model to reproduce the immunological features of celiac disease (celiac disease) and allows the study of early pathogenetic events in this disease. With this model it was shown that antigens such as ICAM-1 and HLA-DR are upregulated as early as 1-2 h after gliadin challenge in patients with celiac disease. After 24 h the lamina propria contained CD4+ T cells expressing the IL-2 receptor alpha-chain, which is a sign of activation. Intraepithelial lymphocytes increased in number and showed proliferative activity. After in vitro stimulation with gliadin, endomysial antibodies were found in the supernatant of the cultured mucosa from patients with celiac disease following a gluten-free diet. This supported the notion that endomysial antibodies are at least in part produced locally. The model was also successfully used to identify toxic constituents of gliadin. Presently, organ culture is not commonly used for diagnostic purposes.
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