نمایش مختصر رکورد

dc.contributor.authorKarjoo, Manoochehren_US
dc.date.accessioned1399-07-09T07:11:34Zfa_IR
dc.date.accessioned2020-09-30T07:11:34Z
dc.date.available1399-07-09T07:11:34Zfa_IR
dc.date.available2020-09-30T07:11:34Z
dc.date.issued2014-08-01en_US
dc.date.issued1393-05-10fa_IR
dc.date.submitted2014-04-12en_US
dc.date.submitted1393-01-23fa_IR
dc.identifier.citationKarjoo, Manoochehr. (2014). Celiac Disease. International Journal of Pediatrics, 2(32), 5-7. doi: 10.22038/ijp.2014.2955en_US
dc.identifier.issn2345-5047
dc.identifier.issn2345-5055
dc.identifier.urihttps://dx.doi.org/10.22038/ijp.2014.2955
dc.identifier.urihttp://ijp.mums.ac.ir/article_2955.html
dc.identifier.urihttps://iranjournals.nlai.ir/handle/123456789/317400
dc.description.abstractCeliac 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. <br/>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.en_US
dc.format.extent316
dc.format.mimetypeapplication/pdf
dc.languageEnglish
dc.language.isoen_US
dc.publisherMashhad University of Medical Sciencesen_US
dc.relation.ispartofInternational Journal of Pediatricsen_US
dc.relation.isversionofhttps://dx.doi.org/10.22038/ijp.2014.2955
dc.subjectCeliac diseaseen_US
dc.subjectDiagnoseen_US
dc.subjectPresentationen_US
dc.titleCeliac Diseaseen_US
dc.typeTexten_US
dc.contributor.departmentPediatrician and Gastroenterologist Upstate Medical University, Syracuse New York USA.en_US
dc.citation.volume2
dc.citation.issue32
dc.citation.spage5
dc.citation.epage7


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