The Oslo definitions for coeliac disease and related terms
Jonas F. Ludvigsson1, Daniel A. Leffler2, Julio C. Bai, Federico Biagi3, Alessio Fasano4, Peter H.R. Green5, Marios Hadjivassiliou6, Katri Kaukinen7, Ciaran P. Kelly2, Jonathan N. Leonard8, Knut E.A. Lundin9, Joseph A. Murray10, David S Sanders8, David S Sanders6, Marjorie M. Walker8, Fabiana Zingone11, Carolina Ciacci12 •
Beth Israel Deaconess Medical Center1, Harvard University2, University of Pavia3, University of Maryland, Baltimore4, Columbia University5, Royal Hallamshire Hospital6, University of Tampere7, Imperial College London8, University of Oslo9, Mayo Clinic10, University of Naples Federico II11, University of Salerno12
TL;DR: A multidisciplinary task force of 16 physicians from seven countries used the electronic database PubMed to review the literature for CD-related terms and suggested a definition for each term, followed by feedback through a web survey on definitions and discussions during a meeting in Oslo.
Abstract: Objective The literature suggests a lack of consensus on the use of terms related to coeliac disease (CD) and gluten. Design A multidisciplinary task force of 16 physicians from seven countries used the electronic database PubMed to review the literature for CD-related terms up to January 2011. Teams of physicians then suggested a definition for each term, followed by feedback of these definitions through a web survey on definitions, discussions during a meeting in Oslo and phone conferences. In addition to ‘CD’, the following descriptors of CD were evaluated (in alphabetical order): asymptomatic, atypical, classical, latent, non-classical, overt, paediatric classical, potential, refractory, silent, subclinical, symptomatic, typical, CD serology, CD autoimmunity, genetically at risk of CD, dermatitis herpetiformis, gluten, gluten ataxia, gluten intolerance, gluten sensitivity and gliadin-specific antibodies. Results CD was defined as ‘a chronic small intestinal immune-mediated enteropathy precipitated by exposure to dietary gluten in genetically predisposed individuals’. Classical CD was defined as ‘CD presenting with signs and symptoms of malabsorption. Diarrhoea, steatorrhoea, weight loss or growth failure is required.’ ‘Gluten-related disorders’ is the suggested umbrella term for all diseases triggered by gluten and the term gluten intolerance should not to be used. Other definitions are presented in the paper. Conclusion This paper presents the Oslo definitions for CD-related terms.
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Jonas F. Ludvigsson1, Jonas F. Ludvigsson2, Julio C. Bai3, Federico Biagi, Timothy R. Card4, Carolina Ciacci5, Paul J. Ciclitira6, Peter H.R. Green7, Marios Hadjivassiliou, Anne Holdoway8, David A. van Heel9, Katri Kaukinen, Daniel A. Leffler10, Jonathan N. Leonard11, Knut E.A. Lundin12, Norma McGough, Mike Davidson13, Joseph A. Murray, Gillian L Swift14, Marjorie M. Walker15, Fabiana Zingone5, David S Sanders16 •
Örebro University1, Karolinska Institutet2, Universidad del Salvador3, University of Nottingham4, University of Salerno5, Guy's and St Thomas' NHS Foundation Trust6, Columbia University7, British Dietetic Association8, Queen Mary University of London9, Harvard University10, St Mary's Hospital11, University of Oslo12, Coeliac UK13, Cardiff and Vale University Health Board14, University of Newcastle15, University of Sheffield16
TL;DR: A multidisciplinary panel of 18 physicians and 3 non-physicians from eight countries reviewed the literature on diagnosis and management of adult coeliac disease and the recommendations are presented.
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University of Tübingen1, Queen Mary University of London2, University of Bologna3, Tohoku University4, University of California, Los Angeles5, Heidelberg University6, Cornell University7, University of Belgrade8, Technische Universität München9, University of Gothenburg10, University of Nottingham11
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Cites background from "The Oslo definitions for coeliac di..."
...Likewise, in the intestinal tract, the pathogenesis of celiac disease involves susceptibility genes (HLA-DQ2 and DQ8) and environmental exposure (gluten-containing diet) (81)....
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References
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TL;DR: The nature and basis of nonresponsive celiac sprue require more thoughtful initiatives to elucidate the immunologic mechanism(s) of unresponsiveness and evaluate possible means of reversal.
2,082 citations
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TL;DR: Tissue transglutaminase is identified as the unknown endomysial autoantigen of celiac disease, and gliadin is a preferred substrate for this enzyme, giving rise to novel antigenic epitopes.
Abstract: Celiac disease is characterized by small intestinal damage with loss of absorptive villi and hyperplasia of the crypts, typically leading to malabsorption. In addition to nutrient deficiencies, prolonged celiac disease is associated with an increased risk for malignancy, especially intestinal T-cell lymphoma. Celiac disease is precipitated by ingestion of the protein gliadin, a component of wheat gluten, and usually resolves on its withdrawal. Gliadin initiates mucosal damage which involves an immunological process in individuals with a genetic predisposition. However, the mechanism responsible for the small intestinal damage characteristic of celiac disease is still under debate. Small intestinal biopsy with the demonstration of a flat mucosa which is reversed on a gluten-free diet is considered the main approach for diagnosis of classical celiac disease. In addition, IgA antibodies against gliadin and endomysium, a structure of the smooth muscle connective tissue, are valuable tools for the detection of patients with celiac disease and for therapy control. Incidence rates of childhood celiac disease range from 1:300 in Western Ireland to 1:4700 in other European countries, and subclinical cases detected by serological screening revealed prevalences of 3.3 and 4 per 1000 in Italy and the USA, respectively. IgA antibodies to endomysium are particularly specific indicators of celiac disease, suggesting that this structure contains one or more target autoantigens that play a role in the pathogenesis of the disease. However, the identification of the endomysial autoantigen(s) has remained elusive. We identified tissue transglutaminase as the unknown endomysial autoantigen. Interestingly, gliadin is a preferred substrate for this enzyme, giving rise to novel antigenic epitopes.
1,931 citations
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TL;DR: The most important histological differential diagnoses are given, as well as a definition of the different clinical forms of coeliac disease such as symptomatic, silent, latent, potential, treated and refractory coeliasis.
Abstract: In this paper, we review the histological features of coeliac disease and propose a standardized report scheme based on the Marsh classification. Furthermore, terms used by pathologists are defined. The most important histological differential diagnoses are given, as well as a definition of the different clinical forms of coeliac disease such as symptomatic, silent, latent, potential, treated and refractory coeliac disease.
1,521 citations
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TL;DR: Evidence is provided for a new role of Transglutaminase in the common, HLA-DQ2 (and DQ8) associated celiac disease and it is demonstrated that TGase mediates its effect through an ordered and specific deamidation of gliadins.
Abstract: The action of tissue Transglutaminase (TGase) on specific protein-bound glutamine residues plays a critical role in numerous biological processes. Here we provide evidence for a new role of this enzyme in the common, HLA-DQ2 (and DQ8) associated enteropathy, celiac disease (CD). The intestinal inflammation in CD is precipitated by exposure to wheat gliadin in the diet and is associated with increased mucosal activity of TGase. This enzyme has also been identified as the main target for CD-associated anti-endomysium autoantibodies, and is known to accept gliadin as one of its few substrates. We have examined the possibility that TGase could be involved in modulating the reactivity of gliadin specific T cells. This could establish a link between previous reports of the role of TGase in CD and the prevailing view of CD as a T-cell mediated disorder. We found a specific effect of TGase on T-cell recognition of gliadin. This effect was limited to gliadin-specific T cells isolated from intestinal CD lesions. We demonstrate that TGase mediates its effect through an ordered and specific deamidation of gliadins. This deamidation creates an epitope that binds efficiently to DQ2 and is recognized by gut-derived T cells. Generation of epitopes by enzymatic modification is a new mechanism that may be relevant for breaking of tolerance and initiation of autoimmune disease.
1,121 citations
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What are the key definitions of the terms used in the paper?
The paper provides definitions for terms related to coeliac disease (CD) and gluten, including CD, classical CD, gluten-related disorders, and gluten intolerance.