Celiac Disease (CD) is a lifelong autoimmune intestinal disorder resulting from an abnormal response of the small bowel mucosa to gluten peptides derived from food. Gluten protein is found in all forms of wheat and related grains like rye, barley, and triticale. In individuals genetically susceptible to CD, the ingested gluten triggers an autoimmune response that damages the intestinal villi, leading to malabsorption and malnutrition. Symptoms of the disease are related to defects in absorption of nutrients, and include diarrhea, failure to thrive, fatigue, weight loss, anemia (due to iron malabsorption), osteopenia and osteoporosis (due to calcium and vitamin D malabsorption) and abnormal bleeding (malabsorption of vitamin K).
Diagnosis of the disease is complicated by the fact that the symptoms overlap with many other common diseases. However, patients of CD have increased levels of IgA anti-tissue transglutaminase (tTGA), and IgA anti-endomysium antibodies, and this feature is used for confirming the diagnosis. The only way to manage this disease is to switch to a gluten free diet. Symptoms ease within days of switching to this diet. However, in patients with severely damaged intestines, nutrients may have to be directly given through the blood until the villi heal.
CD is a genetic disease that runs in families. The disease has been shown to have a strong association with the HLA-DQ locus. Both HLA-DQA1 and HLA-DQB1 have been implicated in CD. It has been postulated that certain alleles at these loci may be involved in the production of receptors that bind very tightly to gliadin peptides, thereby activating T lymphocytes, and initiating the autoimmune response.