Celiac disease is characterized by diffuse damage to the proximal small intestinal mucosa that results in malabsorption of most nutrients.
Typical symptoms may manifest between 6 months and 24 months of age after the introduction of weaning foods, but the majority of cases present with "atypical" symptoms in childhood or adulthood.
Although the precise mechanism of the destruction of villi in the small intestine is unknown, it is clear that removal of gluten from the diet results in resolution of symptoms and intestinal healing in most patients.
Glutens are storage proteins that are present in certain grains such as wheat, rye, and barley but not oats, rice, or corn. It is hypothesized that in genetically predisposed people of all ages, gluten stimulates an inappropriate T cell-mediated autoimmune response in the intestinal submucosa that results in destruction of mucosal enterocytes. One target of this autoimmune response is tissue transglutaminase (tTG), an enzyme that modifies a component of gluten (gliadin) to a form that more strongly stimulates T cells.
83% of people with celiac disease are diagnosed with the wrong condition or not diagnosed at all. Diagnosis is usually first suggested by the presence of transglutaminase (tTG) autoantibodies, but established by biopsy of the small intestine by upper intestinal endoscopy.
Treatment for celiac disease, is a lifelong avoidance of gluten, found in wheat, rye and barley. Gluten-free diet indicates a supposed harmless level of gluten rather than a complete absence.