Medication and Supplement Use in Celiac Disease
Medication and Supplement Use in Celiac Disease
CD affects an estimated 0.2% to 1% of the U.S. population, with a higher incidence in females, and its prevalence has increased. The disorder is characterized by an autoimmune reaction to gluten that causes inflammation of the mucosa of the small intestine, damaging the villi of the epithelial lining and leading to obstructed nutrient absorption. Gluten is a protein found in wheat, barley, and rye (containing gliadin, hordein, and secalin glycoproteins, respectively). Gliadin, which is not fully broken down by the intestine, may pass through the intestinal mucosa in patients with gluten intolerance, producing an immune response by activating class II human leukocyte antigen (HLA)-DQ2 and HLA-DQ8 T-cell genetic molecules.
The gluten intolerance specifically characterized by CD is genetically based and typically develops in individuals with a familial (first- or second-degree relative) history of immune intolerance to the protein in gluten. Genetic predisposition of the HLA-DQ2 and HLA-DQ8 alleles is correlated with the development of gluten sensitivity. Individuals with neurodevelopmental syndromes, such as Down, Williams, and Turner syndromes, have a higher prevalence of CD. Additionally, patients with diagnosed autoimmune disease, such as type 1 diabetes mellitus, thyroid disorders, and immunoglobulin (Ig) A deficiency, are at greater risk for developing CD. See Table 1.
The exact cause of autoimmune gluten intolerance is unknown, but various contributing factors to CD development have been suggested. Possible triggers include viral infections such as Giardia lamblia, rotavirus, enterovirus, Campylobacter jejuni, hepatitis C, and adenovirus type 12; gluten consumption during the first year of life; decreased protection against infection from early termination of breastfeeding; and tissue damage. The introduction of gluten in infant diets should occur between 3 and 7 months of age to decrease the risk of developing intolerance. Cesarean delivery and rotavirus infection have been suggested as potential risk factors for CD development owing to the disruption of normal flora in neonates and children. All potential risk factors for CD that occur during pediatric development have unknown mechanisms and require further investigation.
To prevent consumption of gluten, patients with CD must avoid all wheat, barley, and rye products. Exposure to as little as 30 to 50 mg of the protein (roughly 1/48th the size of a slice of bread) per day can damage the mucosa of the small intestine.
Etiology and Risk Factors
CD affects an estimated 0.2% to 1% of the U.S. population, with a higher incidence in females, and its prevalence has increased. The disorder is characterized by an autoimmune reaction to gluten that causes inflammation of the mucosa of the small intestine, damaging the villi of the epithelial lining and leading to obstructed nutrient absorption. Gluten is a protein found in wheat, barley, and rye (containing gliadin, hordein, and secalin glycoproteins, respectively). Gliadin, which is not fully broken down by the intestine, may pass through the intestinal mucosa in patients with gluten intolerance, producing an immune response by activating class II human leukocyte antigen (HLA)-DQ2 and HLA-DQ8 T-cell genetic molecules.
The gluten intolerance specifically characterized by CD is genetically based and typically develops in individuals with a familial (first- or second-degree relative) history of immune intolerance to the protein in gluten. Genetic predisposition of the HLA-DQ2 and HLA-DQ8 alleles is correlated with the development of gluten sensitivity. Individuals with neurodevelopmental syndromes, such as Down, Williams, and Turner syndromes, have a higher prevalence of CD. Additionally, patients with diagnosed autoimmune disease, such as type 1 diabetes mellitus, thyroid disorders, and immunoglobulin (Ig) A deficiency, are at greater risk for developing CD. See Table 1.
The exact cause of autoimmune gluten intolerance is unknown, but various contributing factors to CD development have been suggested. Possible triggers include viral infections such as Giardia lamblia, rotavirus, enterovirus, Campylobacter jejuni, hepatitis C, and adenovirus type 12; gluten consumption during the first year of life; decreased protection against infection from early termination of breastfeeding; and tissue damage. The introduction of gluten in infant diets should occur between 3 and 7 months of age to decrease the risk of developing intolerance. Cesarean delivery and rotavirus infection have been suggested as potential risk factors for CD development owing to the disruption of normal flora in neonates and children. All potential risk factors for CD that occur during pediatric development have unknown mechanisms and require further investigation.
To prevent consumption of gluten, patients with CD must avoid all wheat, barley, and rye products. Exposure to as little as 30 to 50 mg of the protein (roughly 1/48th the size of a slice of bread) per day can damage the mucosa of the small intestine.
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