Recent developments in the pathogenesis, diagnosis and treatment of celiac disease

Celiac disease (CD) is a syndrome characterised by damage of the small intestinal mucosa, caused by the gliadin fraction of wheat gluten and similar alcohol-soluble proteins (prolamines) of barley and rye in genetically susceptible subjects. The clinical manifestations of CD are protean in nature and vary markedly with the age of the patient, the duration and extent of disease and the presence of extra-intestinal pathology. This article reviews three patents from the last four years which claim methods and tools for the diagnosis and treatment of CD. They are related to the antigenic role of tissue transglutaminase, the immunodominant gliadin peptide recognised by the cells in the peripheral blood of individuals with CD and the pro-inflammatory role of IL-15; however, only the first invention found application worldwide. In spite of this, the current gold standard for the diagnosis of CD is still the histological confirmation of the intestinal damage and the keystone treatment of CD patients is a life-long elimination diet, in which food products containing gluten are avoided.

[1]  E. Iannitto,et al.  Sideropenic Anemia and Celiac Disease (One Study, Two Points of View) , 1998, Digestive Diseases and Sciences.

[2]  E. Thorsby,et al.  EVIDENCE FOR A PRIMARY ASSOCIATION OF CELIAC DISEASE TO A PARTICULAR HLA-DQ a/ß HETERODIMER , 2003 .

[3]  A. Pound Length of gestation period linked to chronic lung disease , 2001, The Lancet.

[4]  G. Aimo,et al.  Diagnostic accuracies for celiac disease of four tissue transglutaminase autoantibody tests using human antigen. , 2001, Clinical chemistry.

[5]  G. Corrao,et al.  For Personal Use. Only Reproduce with Permission from the Lancet Publishing Group , 2022 .

[6]  A. Fasano,et al.  Current approaches to diagnosis and treatment of celiac disease: an evolving spectrum. , 2001, Gastroenterology.

[7]  A. Fasano,et al.  Human zonulin, a potential modulator of intestinal tight junctions. , 2000, Journal of cell science.

[8]  E. Iannitto,et al.  Tissue Transglutaminase Autoantibodies in Patients with Non-Hodgkin’s Lymphoma , 2000, Digestion.

[9]  L. Maiuri,et al.  Interleukin 15 mediates epithelial changes in celiac disease. , 2000, Gastroenterology.

[10]  D. Schuppan,et al.  Current concepts of celiac disease pathogenesis. , 2000, Gastroenterology.

[11]  R. Marzari,et al.  Human recombinant tissue transglutaminase ELISA: an innovative diagnostic assay for celiac disease , 2000, American Journal of Gastroenterology.

[12]  A. Fasano,et al.  Zonulin, a newly discovered modulator of intestinal permeability, and its expression in coeliac disease , 2000, The Lancet.

[13]  J. Murray,et al.  Prevalence of celiac disease among risk groups and the general population in USA , 2000 .

[14]  L. Sollid,et al.  Role of tissue transglutaminase in celiac disease. , 2000, Journal of pediatric gastroenterology and nutrition.

[15]  R. Pratesi,et al.  Prevalence of celiac disease among blood donors in Brazil , 2000, American Journal of Gastroenterology.

[16]  D. Jewell,et al.  In vivo antigen challenge in celiac disease identifies a single transglutaminase-modified peptide as the dominant A-gliadin T-cell epitope , 2000, Nature Medicine.

[17]  R. Pratesi,et al.  Why is coeliac disease endemic in the people of the Sahara? , 1999, The Lancet.

[18]  L. Greco,et al.  Duration of exposure to gluten and risk for autoimmune disorders in patients with celiac disease. SIGEP Study Group for Autoimmune Disorders in Celiac Disease. , 1999, Gastroenterology.

[19]  G. Davies-Jones,et al.  Idiopathic cerebellar ataxia associated with celiac disease: lack of distinctive neurological features , 1999, Journal of neurology, neurosurgery, and psychiatry.

[20]  R. Marzari,et al.  HUMAN TISSUE TRANSGLUTAMINASE ELISA: A POWERFUL MASS SCREENING DIAGNOSTIC ASSAY FOR COELIAC DISEASE , 1999, Journal of Pediatric Gastroenterology and Nutrition.

[21]  G. Corazza,et al.  The clinical pattern of subclinical/silent celiac disease: an analysis on 1026 consecutive cases Figure 1 , 1999, American Journal of Gastroenterology.

[22]  J. Schulzke,et al.  Epithelial Tight Junction Structure in the Jejunum of Children with Acute and Treated Celiac Sprue , 1998, Pediatric Research.

[23]  J. Partanen,et al.  Celiac disease risk in the USA: high prevalence of antiendomysium antibodies in healthy blood donors. , 1998, Scandinavian journal of gastroenterology.

[24]  M. Färkkilä,et al.  Undiagnosed coeliac disease is common in Finnish adults. , 1998, Scandinavian journal of gastroenterology.

[25]  K. Lundin,et al.  Autoantibodies in coeliac disease: tissue transglutaminase—guilt by association? , 1997, Gut.

[26]  D. Schuppan,et al.  Identification of tissue transglutaminase as the autoantigen of celiac disease , 1997, Nature Medicine.

[27]  T. Macdonald,et al.  A major role for matrix metalloproteinases in T cell injury in the gut. , 1997, Journal of immunology.

[28]  G. Coppa,et al.  The coeliac iceberg in Italy. A multicentre antigliadin antibodies screening for coeliac disease in school‐age subjects , 1996, Acta paediatrica (Oslo, Norway : 1992). Supplement.

[29]  E. Thorsby,et al.  Identification of a putative motif for binding of peptides to HLA-DQ2. , 1996, International immunology.

[30]  R. Luchetti,et al.  In vitro assessment of acetic-acid-soluble proteins (glutenin) toxicity in celiac disease. , 1996, Journal of biochemical toxicology.

[31]  A. Fasano,et al.  Epidemiology of celiac disease. , 1995, The American journal of gastroenterology.

[32]  H. Wieser The precipitating factor in coeliac disease. , 1995, Bailliere's clinical gastroenterology.

[33]  C. Catassi,et al.  Coeliac disease in the year 2000: exploring the iceberg , 1994, The Lancet.

[34]  E. Thorsby,et al.  HLA susceptibility genes in celiac disease: genetic mapping and role in pathogenesis. , 1993, Gastroenterology.

[35]  A. Ferguson,et al.  Clinical and pathological spectrum of coeliac disease--active, silent, latent, potential. , 1993, Gut.

[36]  H. Cornell,et al.  Characterization of the gliadin-derived peptides which are biologically active in coeliac disease. , 1992, Clinica chimica acta; international journal of clinical chemistry.

[37]  L. Franzén,et al.  High prevalence of celiac disease in healthy adults revealed by antigliadin antibodies. , 1992, Annals of allergy.

[38]  I. Krantz,et al.  Increasing incidence of coeliac disease in Sweden. , 1991, Archives of disease in childhood.

[39]  E. Thorsby,et al.  Evidence for a primary association of celiac disease to a particular HLA-DQ alpha/beta heterodimer , 1989, The Journal of experimental medicine.

[40]  M. A. Saper,et al.  The foreign antigen binding site and T cell recognition regions of class I histocompatibility antigens , 1987, Nature.

[41]  M. De Vos,et al.  Histopathology of intestinal inflammation related to reactive arthritis. , 1987, Gut.

[42]  J. Tanner,et al.  SHORT STATURE AS THE PRIMARY MANIFESTATION OF COELIAC DISEASE , 1981, The Lancet.

[43]  J. Tanner,et al.  SHORT STATURE AS THE PRIMARY MANIFESTATION OF COELIAC DISEASE , 1980, The Lancet.

[44]  J. Madara,et al.  Structural abnormalities of jejunal epithelial cell membranes in celiac sprue. , 1980, Laboratory investigation; a journal of technical methods and pathology.