@article { author = {Karjoo, Manoochehr}, title = {Celiac Disease}, journal = {International Journal of Pediatrics}, volume = {2}, number = {3.2}, pages = {5-7}, year = {2014}, publisher = {Mashhad University of Medical Sciences}, issn = {2345-5047}, eissn = {2345-5055}, doi = {10.22038/ijp.2014.2955}, abstract = {Celiac disease also known as gluten-sensitive enteropathy is characterized by intestinal mucosal damage and malabsorption from dietary intake of wheat, rye or barley. Symptoms may appear with introduction of cereal in the first 3 years of life. A second peak in symptoms occurs in adults during the third or forth decade and even as late as eight decade of life. The prevalence of this disease is approximately 1 in 250 adults. The disease is more prevalent in Ireland as high as 1 in 120 adults. The disorder occurs in Arab, Hispanics, Israeli Jews, Iranian and European but is rare in Chinese and African American. To have celiac disease the patient should have the celiac disease genetic markers as HLA DQ 2 and HLA DQ 8. Patient with celiac disease may have 95 per cent for DQ 2 and the rest is by DQ 8. Someone may have the genetic marker and never develops the disease. In general 50 percent with markers may develop celiac disease. To develop the disease the gene needs to become activated. This may happen with a viral or bacterial infection, a surgery, delivery, accident, or psychological stress. After activation of gene cause the tight junction to opens with the release of Zonulin This results in passage of gluten through the tight junction and formation of multiple antibodies and autoimmune disease. This also allows entrance of other proteins and development of multiple food allergies. As a result is shortening, flattening of intestinal villi resulting in food, vitamins and minerals malabsorption.}, keywords = {Celiac disease,Diagnose,Presentation}, url = {https://ijp.mums.ac.ir/article_2955.html}, eprint = {https://ijp.mums.ac.ir/article_2955_8b4cc6c89fc3406983e45d866093e91e.pdf} }