Abstract
To date, the only treatment for celiac disease (CD) consists of a strict lifelong gluten-free diet (GFD), which has numerous limitations in patients with CD. For this reason, dietary transgressions are frequent, implying intestinal damage and possible long-term complications. There is an unquestionable need for non-dietary alternatives to avoid damage by involuntary contamination or voluntary dietary transgressions. In recent years, different therapies and treatments for CD have been developed and studied based on the degradation of gluten in the intestinal lumen, regulation of the immune response, modulation of intestinal permeability, and induction of immunological tolerance. In this review, therapeutic lines for CD are evaluated with special emphasis on phase III and II clinical trials, some of which have promising results.
Highlights
Insights into Non-Dietary TreatmentCeliac disease (CD) is a chronic immune-mediated enteropathy triggered by exposure to dietary gluten in genetically predisposed individuals [1,2]
Certain peptides, such as the 19-mer gliadin peptide, trigger an innate immune response mainly characterized by the production of interleukin-15 (IL-15) by epithelial cells and the disruption of the epithelial barrier caused by increased permeability and induction of enterocyte apoptosis [16,17]
Several studies based on nutritional questionnaires, serological tests, and evaluating gluten immunogenic peptides in feces and urine, have reported variable gluten exposure rates in patients with celiac disease (CD), reaching up to 69% in adults, 64% in adolescents, and 45% in children (Figure 1) despite their best efforts to avoid it
Summary
Celiac disease (CD) is a chronic immune-mediated enteropathy triggered by exposure to dietary gluten in genetically predisposed individuals [1,2]. The prevailing hypothesis of immunopathogenesis is the two-signal model, which establishes that gluten has a dual effect on the duodenum of celiac patients mediated by innate and adaptive immune systems [14,15] Certain peptides, such as the 19-mer gliadin peptide, trigger an innate immune response mainly characterized by the production of interleukin-15 (IL-15) by epithelial cells and the disruption of the epithelial barrier caused by increased permeability and induction of enterocyte apoptosis [16,17]. Other peptides such as the 33-mer gliadin can reach the lamina propria to be deamidated by tTG, providing a negative charge to gliadin peptides that activate the immune-adaptive system. Progression of the proinflammatory response, thereby contributing to the symptomatology of the disease [21,22]
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