Abstract
The only currently accepted and recommended treatment for individuals diagnosed with celiac disease (CD) is a strict life-long gluten-free diet (GFD). While the use of the GFD is well-established, strict adherence to diet is not easy to accomplish. In addition, the administration of a GFD may be compromised by inadvertent exposure to small amounts of gluten. International guidelines define a gluten-free product as one containing less than 20 parts per million (ppm), (20 milligrams of gluten per 1 kg of food) gluten. A number of reports have assessed the safe upper limit for gluten exposure for patients with CD, with general consensus that patients with CD should limit their daily intake to less than 50 mg.
Highlights
Celiac disease (CD) is an immune-mediated small intestinal enteropathy triggered by the ingestion of gluten in genetically susceptible individuals possessing particular HLA genes
Thirty-nine adult patients receiving what the authors called a Codex gluten-free diet (GFD) and 50 patients consuming a non-gluten detectable-GFD (NGD-GFD) were compared
There is no clear consensus on the safe amount of daily gluten intake for individuals with CD on a GFD
Summary
Celiac disease (CD) is an immune-mediated small intestinal enteropathy triggered by the ingestion of gluten in genetically susceptible individuals possessing particular HLA genes. The prolamins are rich in proline and glutamine residues, making them resistant to digestion in the human gastrointestinal tract These residues present in the undigested gluten fragments are excellent substrates for tissue transglutaminase (tTG) within the lamina propria [10]. The deamination of gliadin peptides by tTG generates a complex with high affinity for the DQ2 or DQ8 pockets present on antigen-presenting cells. This enables presentation of the peptides to some subsets of CD4 and CD8 T lymphocytes, prompting direct immune responses. This includes the release of pro-inflammatory cytokines (such as interferon-γ) and metalloproteinases. These events lead to the typical histological changes present in the duodenal mucosa, characterized by villous flattening, crypt hyperplasia, intraepithelial lymphocytosis, and increased cellularity (predominantly lymphocytes and plasmocytes) within the lamina propria [8]
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