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World J Gastroenterol. Nov 14, 2012; 18(42): 6036-6059
Published online Nov 14, 2012. doi: 10.3748/wjg.v18.i42.6036
Celiac disease: Prevalence, diagnosis, pathogenesis and treatment
Naiyana Gujral, Hugh J Freeman, Alan BR Thomson
Naiyana Gujral, Faculty of Pharmacy and Pharmaceutical Sciences, University of Alberta, Edmonton, AB T6G 2E1, Canada
Hugh J Freeman, Department of Medicine, University of British Columbia, Vancouver, BC V6T 2B5, Canada
Alan BR Thomson, Division of Gastroenterology, Department of Medicine, University of Western Ontario, London, ON N6A 5A5, Canada
Author contributions: All authors contributed equally to the literature review; each contributed to the writing; and Thomson ABR assisted in the final editing.
Correspondence to: Alan BR Thomson, Adjunct Professor, Division of Gastroenterology, Department of Medicine, University of Western Ontario, London, ON N6A 5A5, Canada.
Telephone: +1-519-6858300 Fax: +1-519-6633232
Received: May 22, 2012
Revised: July 27, 2012
Accepted: August 3, 2012
Published online: November 14, 2012

Celiac disease (CD) is one of the most common diseases, resulting from both environmental (gluten) and genetic factors [human leukocyte antigen (HLA) and non-HLA genes]. The prevalence of CD has been estimated to approximate 0.5%-1% in different parts of the world. However, the population with diabetes, autoimmune disorder or relatives of CD individuals have even higher risk for the development of CD, at least in part, because of shared HLA typing. Gliadin gains access to the basal surface of the epithelium, and interact directly with the immune system, via both trans- and para-cellular routes. From a diagnostic perspective, symptoms may be viewed as either “typical” or “atypical”. In both positive serological screening results suggestive of CD, should lead to small bowel biopsy followed by a favourable clinical and serological response to the gluten-free diet (GFD) to confirm the diagnosis. Positive anti-tissue transglutaminase antibody or anti-endomysial antibody during the clinical course helps to confirm the diagnosis of CD because of their over 99% specificities when small bowel villous atrophy is present on biopsy. Currently, the only treatment available for CD individuals is a strict life-long GFD. A greater understanding of the pathogenesis of CD allows alternative future CD treatments to hydrolyse toxic gliadin peptide, prevent toxic gliadin peptide absorption, blockage of selective deamidation of specific glutamine residues by tissue, restore immune tolerance towards gluten, modulation of immune response to dietary gliadin, and restoration of intestinal architecture.

Keywords: Celiac disease, Demography, Diagnosis, Pathogenesis, Treatment