Copyright ©2012 Baishideng Publishing Group Co.
World J Gastroenterol. Nov 14, 2012; 18(42): 6036-6059
Published online Nov 14, 2012. doi: 10.3748/wjg.v18.i42.6036
Table 9 Key points from recent findings
Environmental (gluten) and genetic factors (HLA and non-HLA genes)
0.5%-1% worldwide in normal at-risk population
Higher risk in the population with diabetes, autoimmune disorder or relatives of CD individuals
Gliadin gains access via trans- and para-cellular routes to the basal surface of the epithelium, and interact directly with the immune system
Types of CD symptoms: “typical” or “atypical”
Positive serological (TGA or EMA) screening results suggestive of CD, should lead to small bowel biopsy followed by a favourable clinical and serological response to the GFD to confirm the diagnosis
Current treatment
Strict life-long GFD
Alternative future CD treatments strategies
Hydrolysis of toxic gliadin peptide
Prevention of toxic gliadin peptide absorption
Blockage of deamidation of specific glutamine residues by tissue
Restoration of immune tolerance towards gluten
Modulation of immune response to dietary gliadin
Restoration of intestinal architecture