^ NIDDK. National Institute of Diabetes and Digestive and Kidney Diseases. June 2016 [24 April 2017]. （原始内容存档于2017-04-24）.
^ 3.03.1Lebwohl B, Ludvigsson JF, Green PH. Celiac disease and non-celiac gluten sensitivity. BMJ (Review). October 2015, 351: h4347. PMC 4596973. PMID 26438584. doi:10.1136/bmj.h4347. Celiac disease occurs in about 1% of the population worldwide, although most people with the condition are undiagnosed. It can cause a wide variety of symptoms, both intestinal and extra-intestinal because it is a systemic autoimmune disease that is triggered by dietary gluten. Patients with coeliac disease are at increased risk of cancer, including a twofold to fourfold increased risk of non-Hodgkin’s lymphoma and a more than 30-fold increased risk of small intestinal adenocarcinoma, and they have a 1.4-fold increased risk of death.
^ 4.04.1Lundin KE, Wijmenga C. Coeliac disease and autoimmune disease-genetic overlap and screening. Nature Reviews. Gastroenterology & Hepatology (Review). September 2015, 12 (9): 507–15. PMID 26303674. doi:10.1038/nrgastro.2015.136. The abnormal immunological response elicited by gluten-derived proteins can lead to the production of several different autoantibodies, which affect different systems.
^ 6.06.16.26.3Ciccocioppo R, Kruzliak P, Cangemi GC, Pohanka M, Betti E, Lauret E, Rodrigo L. The Spectrum of Differences between Childhood and Adulthood Celiac Disease. Nutrients (Review). 22 October 2015, 7 (10): 8733–51. PMC 4632446. PMID 26506381. doi:10.3390/nu7105426. Several additional studies in extensive series of coeliac patients have clearly shown that TG2A sensitivity varies depending on the severity of duodenal damage, and reaches almost 100% in the presence of complete villous atrophy (more common in children under three years), 70% for subtotal atrophy, and up to 30% when only an increase in IELs is present. (IELs: intraepithelial lymphocytes)
^ 8.08.18.28.3Husby S, Koletzko S, Korponay-Szabó IR, Mearin ML, Phillips A, Shamir R, Troncone R, Giersiepen K, Branski D, Catassi C, Lelgeman M, Mäki M, Ribes-Koninckx C, Ventura A, Zimmer KP, (( ESPGHAN Working Group on Coeliac Disease Diagnosis; ESPGHAN Gastroenterology Committee; European Society for Pediatric Gastroenterology, Hepatology, and Nutrition)). European Society for Pediatric Gastroenterology, Hepatology, and Nutrition guidelines for the diagnosis of coeliac disease(PDF). J Pediatr Gastroenterol Nutr (Practice Guideline). January 2012, 54 (1): 136–60 [2018-03-29]. PMID 22197856. doi:10.1097/MPG.0b013e31821a23d0. （原始内容(PDF)存档于2016-04-03）. Since 1990, the understanding of the pathological processes of CD has increased enormously, leading to a change in the clinical paradigm of CD from a chronic, gluten-dependent enteropathy of childhood to a systemic disease with chronic immune features affecting different organ systems. (...) atypical symptoms may be considerably more common than classic symptoms温哥华格式错误 (帮助)
^ 11.011.1Vivas S, Vaquero L, Rodríguez-Martín L, Caminero A. Age-related differences in celiac disease: Specific characteristics of adult presentation. World Journal of Gastrointestinal Pharmacology and Therapeutics (Review). November 2015, 6 (4): 207–12. PMC 4635160. PMID 26558154. doi:10.4292/wjgpt.v6.i4.207. In addition, the presence of intraepithelial lymphocytosis and/or villous atrophy and crypt hyperplasia of small-bowel mucosa, and clinical remission after withdrawal of gluten from the diet, are also used for diagnosis antitransglutaminase antibody (tTGA) titers and the degree of histological lesions inversely correlate with age. Thus, as the age of diagnosis increases antibody titers decrease and histological damage is less marked. It is common to find adults without villous atrophy showing only an inflammatory pattern in duodenal mucosa biopsies: Lymphocytic enteritis (Marsh I) or added crypt hyperplasia (Marsh II)
^Ferri, Fred F. Ferri's differential diagnosis : a practical guide to the differential diagnosis of symptoms, signs, and clinical disorders 2nd. Philadelphia, PA: Elsevier/Mosby. 2010: Chapter C. ISBN 978-0323076999.
^ 13.013.1See JA, Kaukinen K, Makharia GK, Gibson PR, Murray JA. Practical insights into gluten-free diets. Nat Rev Gastroenterol Hepatol (Review). 2015年10月, 12 (10): 580–91. PMID 26392070. doi:10.1038/nrgastro.2015.156. A lack of symptoms and/or negative serological markers are not reliable indicators of mucosal response to the diet. Furthermore, up to 30% of patients continue to have gastrointestinal symptoms despite a strict GFD.122,124 If adherence is questioned, a structured interview by a qualified dietitian can help to identify both intentional and inadvertent sources of gluten.
^Newnham, Evan D. Coeliac disease in the 21st century: Paradigm shifts in the modern age. Journal of Gastroenterology and Hepatology. 2017, 32: 82–85. PMID 28244672. doi:10.1111/jgh.13704. Presentation of CD with malabsorptive symptoms or malnutrition is now the exception rather than the rule.
^Comino I, Moreno M, Sousa C. Role of oats in celiac disease. World Journal of Gastroenterology. November 2015, 21 (41): 11825–31. PMC 4631980. PMID 26557006. doi:10.3748/wjg.v21.i41.11825. It is necessary to consider that oats include many varieties, containing various amino acid sequences and showing different immunoreactivities associated with toxic prolamins. As a result, several studies have shown that the immunogenicity of oats varies depending on the cultivar consumed. Thus, it is essential to thoroughly study the variety of oats used in a food ingredient before including it in a gluten-free diet.
^ 22.022.1Matthias T, Pfeiffer S, Selmi C, Eric Gershwin M. Diagnostic challenges in celiac disease and the role of the tissue transglutaminase-neo-epitope. Clin Rev Allergy Immunol (Review). 2010年4月, 38 (2–3): 298–301. PMID 19629760. doi:10.1007/s12016-009-8160-z.
^Lewis NR, Scott BB. Systematic review: the use of serology to exclude or diagnose coeliac disease (a comparison of the endomysial and tissue transglutaminase antibody tests). Alimentary Pharmacology & Therapeutics. July 2006, 24 (1): 47–54. PMID 16803602. doi:10.1111/j.1365-2036.2006.02967.x.
^Molina-Infante J, Santolaria S, Sanders DS, Fernández-Bañares F. Systematic review: noncoeliac gluten sensitivity. Alimentary Pharmacology & Therapeutics (Review). May 2015, 41 (9): 807–20. PMID 25753138. doi:10.1111/apt.13155. Furthermore, seronegativity is more common in coeliac disease patients without villous atrophy (Marsh 1-2 lesions), but these ‘minor’ forms of coeliac disease may have similar clinical manifestations to those with villous atrophy and may show similar clinical–histological remission with reversal of haematological or biochemical disturbances on a gluten-free diet (GFD).
^Bibbins-Domingo K, Grossman DC, Curry SJ, Barry MJ, Davidson KW, Doubeni CA, Ebell M, Epling JW, Herzstein J, Kemper AR, Krist AH, Kurth AE, Landefeld CS, Mangione CM, Phipps MG, Silverstein M, Simon MA, Tseng CW. Screening for Celiac Disease: US Preventive Services Task Force Recommendation Statement. JAMA. March 2017, 317 (12): 1252–1257. PMID 28350936. doi:10.1001/jama.2017.1462.
^Burkhardt, J. G.; Chapa-Rodriguez, A.; Bahna, S. L. Gluten sensitivities and the allergist: Threshing the grain from the husks. Allergy. July 2018, 73 (7): 1359–1368. PMID 29131356. doi:10.1111/all.13354.
^Lionetti E, Gatti S, Pulvirenti A, Catassi C. Celiac disease from a global perspective. Best Practice & Research. Clinical Gastroenterology (Review). June 2015, 29 (3): 365–79. PMID 26060103. doi:10.1016/j.bpg.2015.05.004.
^Hischenhuber C, Crevel R, Jarry B, Mäki M, Moneret-Vautrin DA, Romano A, Troncone R, Ward R. Review article: safe amounts of gluten for patients with wheat allergy or coeliac disease. Alimentary Pharmacology & Therapeutics. March 2006, 23 (5): 559–75. PMID 16480395. doi:10.1111/j.1365-2036.2006.02768.x.