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.

Management of celiac disease in daily clinical practice / L. Elli, F. Ferretti, S. Orlando, M. Vecchi, E. Monguzzi, L. Roncoroni, D. Schuppan. - In: EUROPEAN JOURNAL OF INTERNAL MEDICINE. - ISSN 0953-6205. - 61(2019 Mar), pp. 15-24. [10.1016/j.ejim.2018.11.012]

Management of celiac disease in daily clinical practice

L. Elli
;
F. Ferretti;M. Vecchi;E. Monguzzi;L. Roncoroni;
2019-03

Abstract

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.
Autoimmune; Celiac disease; Gluten; T cell; Therapy; Internal Medicine
Settore MED/49 - Scienze Tecniche Dietetiche Applicate
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/2434/637573
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