Celiac Disease (cont.)
In this Article
- Celiac disease facts
- What is celiac disease?
- What causes celiac disease?
- What are the signs and symptoms of celiac disease?
- How do symptoms of celiac disease differ with age of onset?
- What is latent and silent celiac disease?
- What diseases are associated with celiac disease?
- How is celiac disease diagnosed?
- What is the treatment of celiac disease?
- What if individuals don't respond to gluten free diet?
- What is refractory celiac disease?
- What is the treatment of refractory celiac disease?
- What are the complications of celiac disease?
- Can cancer risk be reduced in celiac disease?
- What's new in celiac disease?
- Celiac Disease (Celiac Sprue) FAQs
- Find a local Gastroenterologist in your town
What causes celiac disease?
The destruction of the inner lining of the small intestine in celiac disease is caused by an immunological (allergic) reaction to gluten in the diet that inflames and destroys the inner lining of the small intestine. There is evidence that this reaction is partially genetic and partially inherited. Thus, approximately 10% of the first-degree relatives (parents, siblings or children) of individuals with celiac disease also will have celiac disease. In addition, in approximately 30% of fraternal twins and 70% of identical twins, both twins will have celiac disease. Finally, certain genes have been found to be more common in individuals with celiac disease than in those without celiac disease.
Gluten is a family of proteins present in wheat. Some of the proteins that make up gluten (the ones that are dissolved by alcohol) are called gliadin. It is the gliadin in gluten that causes the immunological reaction in celiac disease. The mechanism whereby gliadin becomes toxic (damaging) is not clear; however, much scientific study is being done, and we are beginning to understand the mechanism.
Proteins, including gliadin, are long chains of amino acids--up to several hundred--attached to each other. Normally during digestion, the digestive enzymes within the small intestine break-up proteins into single amino acids and smaller chains of amino acids. This is necessary because the intestine can only absorb single amino acids or, at most, chains of 3-4 amino acids. Single amino acids and chains of several amino acids do not cause problems for the intestine. It appears, however, that gliadin is not completely broken-up by intestinal enzymes. Several longer chains of amino acids remain intact. Somehow these larger chains enter the cells lining the intestine, perhaps because the cells are abnormally permeable (leaky) to longer chains of amino acids. Some of these longer chains are toxic (damaging) to the intestinal cells. One of the longer chains attaches to an enzyme (tissue transglutaminase) inside the cells. In individuals with celiac disease, the complex of the longer chain of amino acids and tissue transglutaminase sets off an immune reaction that attacks the complex and at the same time damages the intestinal cells.
Barley and rye contain gliadin-like proteins and can cause celiac disease in genetically-predisposed individuals. Oats also contain gliadin-like proteins, but unlike barley and rye, the gliadin-like proteins in oats cause only a mild inflammation and that too in only a few individuals who are predisposed to develop celiac disease. Rice and corn do not cause celiac disease because they do not contain gliadin-like proteins.
What does celiac disease do to the small intestine?
The small intestine has an inner lining of cells that form finger-like projections called villi. The villi are important because they increase the urface area available for the absorption of nutrients from the intestinal lumen into the blood stream. In celiac disease, the inflammation destroys the villi, causing the inner lining of the small intestine to become flattened. This loss of villi reduces the number of cells and the surface area available for absorption of nutrients. The impaired absorption of nutrients is referred to as malabsorption. The malabsorption of nutrients leads to nutrient deficiencies, referred to as malnutrition.
The length (amount) of the small intestine affected by the loss of villi varies from patient to patient, and the length that is involved determines the severity of signs and symptoms. Thus, individuals whose entire small intestine is affected by the loss of villi have more severe signs and symptoms of malabsorption than individuals who have only a part of the small intestine affected. When only a part of the small intestine is affected, usually the upper small intestine (the duodenum and jejunum) is affected more than the lower small intestine (the ileum).
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