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Tytuł:
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Management of celiac disease in daily clinical practice.
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Autorzy:
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Elli L; Center for Prevention and Diagnosis of Celiac Disease, Division of Gastroenterology and Endoscopy, Fondazione IRCCS Ca'Granda Ospedale Maggiore Policlinico, Via F. Sforza 35, 20122 Milano, Italy. Electronic address: .
Ferretti F; Center for Prevention and Diagnosis of Celiac Disease, Division of Gastroenterology and Endoscopy, Fondazione IRCCS Ca'Granda Ospedale Maggiore Policlinico, Via F. Sforza 35, 20122 Milano, Italy; Department of Pathophysiology and Transplantation, Università degli Studi di Milano, Via Festa del Perdono, 20122 Milano, Italy.
Orlando S; Center for Prevention and Diagnosis of Celiac Disease, Division of Gastroenterology and Endoscopy, Fondazione IRCCS Ca'Granda Ospedale Maggiore Policlinico, Via F. Sforza 35, 20122 Milano, Italy.
Vecchi M; Center for Prevention and Diagnosis of Celiac Disease, Division of Gastroenterology and Endoscopy, Fondazione IRCCS Ca'Granda Ospedale Maggiore Policlinico, Via F. Sforza 35, 20122 Milano, Italy; Department of Pathophysiology and Transplantation, Università degli Studi di Milano, Via Festa del Perdono, 20122 Milano, Italy.
Monguzzi E; Center for Prevention and Diagnosis of Celiac Disease, Division of Gastroenterology and Endoscopy, Fondazione IRCCS Ca'Granda Ospedale Maggiore Policlinico, Via F. Sforza 35, 20122 Milano, Italy; Department of Pathophysiology and Transplantation, Università degli Studi di Milano, Via Festa del Perdono, 20122 Milano, Italy; Institute for Translational Immunology, Research Center for Immunotherapy (FZI), Johannes Gutenberg University (JGU) Medical Center, 55101 Mainz, Germany.
Roncoroni L; Center for Prevention and Diagnosis of Celiac Disease, Division of Gastroenterology and Endoscopy, Fondazione IRCCS Ca'Granda Ospedale Maggiore Policlinico, Via F. Sforza 35, 20122 Milano, Italy; Department of Pathophysiology and Transplantation, Università degli Studi di Milano, Via Festa del Perdono, 20122 Milano, Italy; Department of Biomedical, Surgical and Dental Sciences, Università degli Studi di Milano, Via Festa del Perdono, 20122 Milano, Italy.
Schuppan D; Institute for Translational Immunology, Research Center for Immunotherapy (FZI), Johannes Gutenberg University (JGU) Medical Center, 55101 Mainz, Germany; Division of Gastroenterology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA.
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Źródło:
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European journal of internal medicine [Eur J Intern Med] 2019 Mar; Vol. 61, pp. 15-24. Date of Electronic Publication: 2018 Dec 05.
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Typ publikacji:
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Journal Article; Review
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Język:
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English
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Imprint Name(s):
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Publication: 1999- : Amsterdam, The Netherlands : Elsevier Science
Original Publication: Basingstoke, Hampshire, UK : Published by the Macmillan Press on behalf of the European Association of Internal Medicine, c1989-
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MeSH Terms:
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Celiac Disease/*diagnosis
Celiac Disease/*therapy
Autoantibodies/immunology ; Diet, Gluten-Free ; GTP-Binding Proteins/immunology ; Genetic Predisposition to Disease ; Glutens/immunology ; HLA-DQ Antigens/genetics ; Humans ; Immune System/physiology ; Immune System/physiopathology ; Immunotherapy ; Intestinal Mucosa/immunology ; Intestinal Mucosa/pathology ; Protein Glutamine gamma Glutamyltransferase 2 ; Risk Assessment ; Risk Factors ; Transglutaminases/immunology
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Contributed Indexing:
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Keywords: Autoimmune; Celiac disease; Gluten; T cell; Therapy
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Substance Nomenclature:
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0 (Autoantibodies)
0 (HLA-DQ Antigens)
8002-80-0 (Glutens)
EC 2.3.2.13 (Protein Glutamine gamma Glutamyltransferase 2)
EC 2.3.2.13 (Transglutaminases)
EC 3.6.1.- (GTP-Binding Proteins)
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Entry Date(s):
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Date Created: 20181212 Date Completed: 20190702 Latest Revision: 20211204
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Update Code:
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20221216
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DOI:
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10.1016/j.ejim.2018.11.012
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PMID:
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30528262
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Celiac disease (CD) is the most common autoimmune enteropathy worldwide. In CD, dietary gluten triggers a T cell driven small intestinal inflammation in a subset of genetically predisposed subjects, expressing the HLA DQ2 and/or DQ8 genes on their antigen presenting cells. HLA DQ2/DQ8 can bind gluten peptides after their prior modification by the CD autoantigen, tissue transglutaminase (TG2). This process leads to the activation of gluten reactive T cells, small bowel villous atrophy, crypt hyperplasia and intraepithelial lymphocytosis, the histological hallmarks of CD. The clinical picture of CD is extremely heterogeneous including intestinal (especially diarrhea, abdominal pain, bloating) and extraintestinal (especially associated autoimmune diseases, anemia, osteoporosis) manifestations. The prevalence of CD in most parts of the world is estimated at 1:100-1:150 and its diagnosis is based on the presence of circulating autoantibodies (anti-TG2) and the histological detection of villous atrophy. Treatment is a lifelong gluten free diet but adjunctive therapies are in development. Although CD is a well-characterized disease, it is grossly underdiagnosed, despite the severe consequences of long-term gluten ingestion in CD, such as enhanced autoimmunity, refractory CD and intestinal T cell lymphoma. The aim of the presented review is to provide a clinical guide and to summarize the most recent clinical progress in CD research.
(Copyright © 2018 European Federation of Internal Medicine. Published by Elsevier B.V. All rights reserved.)
Comment in: Eur J Intern Med. 2019 Apr;62:e17. (PMID: 30598247)