Çölyak Hastalığı

ÖzÇölyak hastalığı genetik yatkınlığı olan bireylerde tahıllarda bulunan bir protein olan gliadine karşı immünolojik olarak gelişen inflamatuvar yanıt sonucu intestinal villuslarda hasar ve klinik olarak malabsorpsiyona neden olan kronik otoimmün bir hastalıktır. Ülkemizde çölyak hastalığı seroprevalansı 1:94, biyopsi ile tanı konulanhasta prevalansı ise 1:212’den yüksektir. Çölyak hastalığı klasik olarak kronik ishal,batın distansiyonu ve büyüme geriliği ile seyreden tipik malabsorpsiyon sendromubulguları ile ortaya çıkabilir; ancak son yıllarda bu klasik tablodan çok, gastrointestinal sistem dışı semptomlarla ortaya çıkan atipik form daha sık görülmektedir. Malabsorpsiyonu düşündüren semptom ve bulguları olan hastalarda ilk basamakta hastalığa spesifik serolojik testler istenerek tarama yapılır. Çölyak hastalığında kesin tanı endoskopik olarak alınan duodenal biyopsilerin histopatolojik olarak incelemesiyle konulabilir. Günümüzde çölyak hastalığının tedavisi ömür boyu glutensiz diyettir. Diyet tedavisi kısa sürede klinik bulgularda, uzun dönemde ise histopatolojik bulgularda düCoeliac Diseasezelmeyi sağladığı gibi, çölyak hastalarında daha sık görülen intestinal lenfoma ve ade-nokarsinoma riskini de azaltmaktadır

Coeliac Disease

AbstractCeliac disease, an autoimmune enteropathy that primarily affects the small intestine in genetically predisposed individuals, and caused by ingestion of dietary gluten which is found in grain products. The inflammatory response leads to intestinalvilli damage and malabsorption. Prevalence of celiac disease is increasing worldwide. In our country seroprevalence of celiac disease is 1:94 and biopsy-proved disease prevalence is over 1:212. Celiac disease present itself as a malabsorption syndrome and failure to thrive but in recent years, milder or atypical symptoms such as chronic abdominal pain, short stature, delayed puberty or unexplained elevation of transaminase enzymes might be the presenting symptoms. In children with signs andsymptoms of malabsorption or with symptoms suspicious of celiac, celiac specificserologic tests should be followed by endoscopically obtained duodenal biopsies. Lifelong gluten free diet is the only known effective treatment. Exclusion of gluten fromthe diet leads to histological and clinical remission and prevents the development oflong term complications such as intestinal lymphoma and adenocarcinoma.

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  • Kaynaklar 1.Ludvigsson J, Leffler DA, Bai J, et al. The Oslo definitions forcoeliac disease and related terms. Gut 2013; 62 (1): 43-52. 2.Lionetti E, Catassi . New clues in celiac disease epidemiology,pathogenesis, clinical manifestations and treatment. Int RevImmunol 2011; 30: 219-31. 3.Gujral N, Freeman HJ, Thomson AB. Celiac disease: Preva-lence, diagnosis, pathogenesis and treatment. World J Gas-troenterol 2012; 42: 6036-59. 4.Mustalahti K, Catassi C, Reunanen A, et al. The prevalenceof celiac disease in Europe: results of a centralized, interna-tional mass screening project. Ann Med 2010; 42: 587-95. 5.Dalgıç B, Sarı S, Baştürk B, et al. Prevalence of celiac disea-se in healthy Turkish school children. Am J Gastoenterol 2011;106 (8): 1512-17. 6.Freeman HJ. Risk factors in familial forms of celiac disease.World J Gastroenterol 2010; 16: 1828-31. 7.Book L, Zone JJ, Neuhausen SL. Prevalence of celiac disea-se among relatives of sib pairs with celiac disease in U.S. fa-milies. Am J Gastroenterol 2003; 98: 377-81. 8.Husby S, Koletzko S, Korponay-Szabo IR, et al. ESPGHANWorking Group on Coeliac Disease Diagnosis; ESPGHANGastroenterology Committee; European Society for Pediat-ric Gastroenterology, Hepatology, and Nutrition. EuropeanSociety for Pediatric Gastroenterology, Hepatology, and Nut-rition Guidelines for the Diagnosis of Coeliac Disease. J Pe-diatr Gastroenterol Nutr 2012; 54 (1): 136-60. 9.Arentz-Hansen H, Körner R, Molberg O, et al. The intestinalT cell response to alpha gliadin in adult celiac disease is fo-cused on a single deaminated glutamine targeted by tissuetransglutaminase. J Exp Med 2000; 191: 603-12. 10.Reilly NR, Fasano A, Green PH. Presentation of celiac disea-se. Gastrointest Endosc Clin North Am 2012; 22: 613-21. 11.Rubio-Tapia A, Hill ID, Kelly CP, et al. ACG Clinical Gui-delines: Diagnosis and Management of Celiac Disease. AmJ Gastroenterol 2013; 108 (5): 656-76. 12.Norris JM, Barriga K, Hoffenberg EJ, et al. Risk of celiacdisease autoimmunity and timing of gluten introduction inthe diet of infants at increased risk of disease. JAMA 2005;293: 2343-51. 13.Di Sabatino A, Corazza GR. Coeliac disease. Lancet 2009;373: 14880-493. 14.Nistico L, Fagnani C, Coto I, et al. Concordance, disease prog-ression, and heritability of coeliac disease in Italian twins. Gut2006; 55: 803-808. 15.Sollid LM. Molecular basis of celiac disease. Annu Rev Im-munol 2000; 18: 53-81. 16.Stepniak D, Koning F. Celiac disease –sandwiched between in-nate and adaptive immunity. Hum Immunol 2006; 67: 460-68. 17.Bottaro G, Failla P, Rotolo N, et al. Changes in coeliac disea-se behaviour over the years. Acta Pediatr 1993; 82: 566-68. 18.Garampazzi A, Rapa A, Mura S, et al. Clinical pattern of coe-liac disease is still changing. J Pediatr Gastroenterol Nutr2007; 45: 611-14. 19.Fasano A, Catassi C. Current approaches to diagnosis andtreatment of celiac disease: an evolving spectrum. Gastroen-terology 2001; 120: 636-51. 20.Auricchio R, Tosco A, Piccolo E, et al. Potential celiac child-ren: 9-year follow-up on a gluten-containing diet. Am J Gas-troenterol 2014; 109: 913. 21.Lionetti E, Castellaneta S, Pulvirenti A, et al. Prevalence andnatural history of potential celiac disease in at-family-riskinfants prospectively investigated from birth. J Pediatr2012; 161: 908. 22.Bai JC, Fried M, Corazza GR, et al; World GastroenterologyOrganization. World Gastroenterology Organisation GlobalGuidelines on Celiac Disease. J Clin Gastroenterol 2013; 47(2): 121-26. 23.Lebwohl B, Rubio-Tapia A, Assiri A, Guandalini S. Diagno-sis of Celiac Disease. Gastrointest Endoscopy Clin North Am2012; 22: 661-77. 24.Rostom A, Murray JA, Kagnoff MF. American Gastroentero-logical Association (AGA) Institute technical review on the di-agnosis and management of coeliac disease. Gastroenterology2006; 131: 1981-2002. 25.Kurppa K, Lindfors K, Collin P, et al. Antibodies against dea-midated gliadin peptides in early-stage celiac disease. J ClinGastroenterol 2011; 45: 673–78. 26.Marsh MN. Gluten, major histocompatibility complex, and thesmall intestine. A molecular and immunobiologic approachto the spectrum of gluten sensitivity (celiac sprue). Gastroen-terology 1992; 102: 330-54. 27.Murch S, Jenkins H, Auth M, et al. Joint ESPGHAN and Coe-liac UK guidelines for the diagnosis and management of coe-liac disease in children. Arch Dis Child 2013; 98: 806-11. 28.Ludvigsson JF. Mortality and malignancy in coeliac disease.Gastrointest Endosc Clin North Am 2012; 22: 705-22. 29.Ciacci C, Cirillo M, Auriemma G, et al. Celiac disease andpregnancy outcome. Am J Gastroenterol 1996; 91: 718-22. 30.Malamut G, Murray JA, Christophe C. Refractory celiac disea-se. Gastrointest Endoscopy Clin North Am 2012; 22: 759-72.
Klinik Tıp Pediatri Dergisi-Cover
  • ISSN: 1309-0453
  • Başlangıç: 2009
  • Yayıncı: Selen Medya Yayıncılık Tanıtım ve Organizasyon Hizmetleri
Sayıdaki Diğer Makaleler

Çölyak Hastalığı

Prof. Dr. Deniz ERTEM