References analysis of the Wikipedia article "Doença celíaca" in the Portuguese version

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Fasano A (abril de 2005). «Clinical presentation of celiac disease in the pediatric population». Gastroenterology (Review). 128 (4 Suppl 1): S68-73. PMID 15825129. doi:10.1053/j.gastro.2005.02.015

Lebwohl B, Ludvigsson JF, Green PH (outubro de 2015). «Celiac disease and non-celiac gluten sensitivity». BMJ (Review). 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 celiac 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.

Lundin KE, Wijmenga C (Setembro de 2015). «Coeliac disease and autoimmune disease-genetic overlap and screening». Nat Rev Gastroenterol Hepatol (Review). 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.

Ciccocioppo R, Kruzliak P, Cangemi GC, Pohanka M, Betti E, Lauret E, Rodrigo L (22 de outubro de 2015). «The Spectrum of Differences between Childhood and Adulthood Celiac Disease». Nutrients (Review). 7 (10): 8733–51. PMC 4632446

. PMID 26506381. doi:10.3390/nu7105426. Several additional studies in extensive series of celiac 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)

Lionetti E, Francavilla R, Pavone P, Pavone L, Francavilla T, Pulvirenti A, et al. (2010). «The neurology of coeliac disease in childhood: what is the evidence? A systematic review and meta-analysis». Dev Med Child Neurol. 52 (8): 700–7. PMID 20345955. doi:10.1111/j.1469-8749.2010.03647.x. Cópia arquivada em 25 de abril de 2016

Husby 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 (Janeiro de 2012). «European Society for Pediatric Gastroenterology, Hepatology, and Nutrition guidelines for the diagnosis of coeliac disease» (PDF). J Pediatr Gastroenterol Nutr (Practice Guideline). 54 (1): 136–60. PMID 22197856. doi:10.1097/MPG.0b013e31821a23d0. Cópia arquivada (PDF) em 3 de abril de 2016. 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

Tovoli F, Masi C, Guidetti E, Negrini G, Paterini P, Bolondi L (16 de março de 2015). «Clinical and diagnostic aspects of gluten related disorders». World J Clin Cases (Review). 3 (3): 275–84. PMC 4360499

. PMID 25789300. doi:10.12998/wjcc.v3.i3.275

Vivas S, Vaquero L, Rodríguez-Martín L, Caminero A (6 de novembro de 2015). «Age-related differences in celiac disease: Specific characteristics of adult presentation». World J Gastrointest Pharmacol Ther (Review). 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)

See JA, Kaukinen K, Makharia GK, Gibson PR, Murray JA (Outubro de 2015). «Practical insights into gluten-free diets». Nat Rev Gastroenterol Hepatol (Review). 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.

Fasano, A; Catassi, C (20 de dezembro de 2012). «Clinical practice. Celiac disease». The New England Journal of Medicine (Review). 367 (25): 2419–26. PMID 23252527. doi:10.1056/NEJMcp1113994

Newnham ED (2017). «Coeliac disease in the 21st century: paradigm shifts in the modern age». J Gastroenterol Hepatol (Review). 32 Suppl 1: 82–85. PMID 28244672. doi:10.1111/jgh.13704. Cópia arquivada em 16 de março de 2017. Presentation of CD with malabsorptive symptoms or malnutrition is now the exception rather than the rule

Tonutti E, Bizzaro N (2014). «Diagnosis and classification of celiac disease and gluten sensitivity». Autoimmun Rev (Review). 13 (4–5): 472–6. PMID 24440147. doi:10.1016/j.autrev.2014.01.043

Penagini F, Dilillo D, Meneghin F, Mameli C, Fabiano V, Zuccotti GV (18 de novembro de 2013). «Gluten-free diet in children: an approach to a nutritionally adequate and balanced diet». Nutrients (Review). 5 (11): 4553–65. PMC 3847748

. PMID 24253052. doi:10.3390/nu5114553

Di Sabatino A, Corazza GR (Abril de 2009). «Coeliac disease». Lancet. 373 (9673): 1480–93. PMID 19394538. doi:10.1016/S0140-6736(09)60254-3

Comino I, Moreno Mde L, Sousa C (7 de novembro de 2015). «Role of oats in celiac disease». World J Gastroenterol. 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.

Pinto-Sánchez, María Inés; Causada-Calo, Natalia; Bercik, Premysl; Ford, Alexander C.; Murray, Joseph A.; Armstrong, David; Semrad, Carol; Kupfer, Sonia S.; Alaedini, Armin; Moayyedi, Paul; Leffler, Daniel A.; Verdú, Elena F.; Green, Peter (Abril de 2017). «Safety of Adding Oats to a Gluten-free Diet for Patients with Celiac Disease: Systematic Review and Meta-analysis of Clinical and Observational Studies». Gastroenterology. 153: 395–409.e3. doi:10.1053/j.gastro.2017.04.009

Matthias T, Pfeiffer S, Selmi C, Eric Gershwin M (abril de 2010). «Diagnostic challenges in celiac disease and the role of the tissue transglutaminase-neo-epitope». Clin Rev Allergy Immunol (Review). 38 (2–3): 298–301. PMID 19629760. doi:10.1007/s12016-009-8160-z

Lewis NR, Scott BB (1 de julho de 2006). «Systematic review: the use of serology to exclude or diagnose coeliac disease (a comparison of the endomysial and tissue transglutaminase antibody tests)». Aliment Pharmacol Ther (Review). 24 (1): 47–54. PMID 16803602. doi:10.1111/j.1365-2036.2006.02967.x. Cópia arquivada em 4 de maio de 2016

Rostom A, Murray JA, Kagnoff MF (dezembro de 2006). «American Gastroenterological Association (AGA) Institute technical review on the diagnosis and management of celiac disease». Gastroenterology (Review). 131 (6): 1981–2002. PMID 17087937. doi:10.1053/j.gastro.2006.10.004

Molina-Infante J, Santolaria S, Sanders DS, Fernández-Bañares F (Maio de 2015). «Systematic review: noncoeliac gluten sensitivity». Aliment Pharmacol Ther (Review). 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).

Ludvigsson JF, Card T, Ciclitira PJ, Swift GL, Nasr I, Sanders DS, Ciacci C (abril de 2015). «Support for patients with celiac disease: A literature review». United European Gastroenterol J (Review). 3 (2): 146–59. PMC 4406900

. PMID 25922674. doi:10.1177/2050640614562599

van Heel DA, West J (2006). «Recent advances in coeliac disease». Gut (Review). 55 (7): 1037–46. PMC 1856316

. PMID 16766754. doi:10.1136/gut.2005.075119

US Preventive Services Task, Force.; Bibbins-Domingo, K; Grossman, DC; Curry, SJ; Barry, MJ; Davidson, KW; Doubeni, CA; Ebell, M; Epling JW, Jr; Herzstein, J; Kemper, AR; Krist, AH; Kurth, AE; Landefeld, CS; Mangione, CM; Phipps, MG; Silverstein, M; Simon, MA; Tseng, CW (28 de março de 2017). «Screening for Celiac Disease: US Preventive Services Task Force Recommendation Statement.». JAMA. 317 (12): 1252–1257. PMID 28350936. doi:10.1001/jama.2017.1462

Lionetti E, Gatti S, Pulvirenti A, Catassi C (junho de 2015). «Celiac disease from a global perspective». Best Pract Res Clin Gastroenterol (Review). 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 (Março de 2006). «Review article: safe amounts of gluten for patients with wheat allergy or coeliac disease». Aliment. Pharmacol. Ther. 23 (5): 559–75. PMID 16480395. doi:10.1111/j.1365-2036.2006.02768.x

Losowsky MS (2008). «A history of coeliac disease». Dig Dis. 26 (2): 112–20. PMID 18431060. doi:10.1159/000116768

Di Sabatino A, Corazza GR (Abril de 2009). «Coeliac disease». Lancet. 373 (9673): 1480–93. PMID 19394538. doi:10.1016/S0140-6736(09)60254-3

Ferguson R, Basu MK, Asquith P, Cooke WT (1976). «Jejunal mucosal abnormalities in patients with recurrent aphthous ulceration». Br Med J. 1 (6000): 11–13. PMC 1638254

. PMID 1247715. doi:10.1136/bmj.1.6000.11

Freeman HJ (Dezembro de 2009). «Adult Celiac Disease and Its Malignant Complications». Gut and Liver. 3 (4): 237–46. PMC 2852736

. PMID 20431755. doi:10.5009/gnl.2009.3.4.237

Gujral N, Freeman HJ, Thomson AB (Novembro de 2012). «Celiac disease: prevalence, diagnosis, pathogenesis and treatment.» (PDF). World Journal of Gastroenterology. 18 (42): 6036–59. PMC 3496881

. PMID 23155333. doi:10.3748/wjg.v18.i42.6036. Consultado em 14 de novembro de 2014. Arquivado do original (PDF) em 20 de março de 2014

«American Gastroenterological Association medical position statement: Celiac Sprue». Gastroenterology. 120 (6): 1522–5. 2001. PMID 11313323. doi:10.1053/gast.2001.24055

Tursi A, Brandimarte G, Giorgetti G (2003). «High prevalence of small intestinal bacterial overgrowth in celiac patients with persistence of gastrointestinal symptoms after gluten withdrawal». Am J Gastroenterol. 98 (4): 839–43. PMID 12738465. doi:10.1111/j.1572-0241.2003.07379.x

Cunningham-Rundles C (Setembro de 2001). «Physiology of IgA and IgA deficiency». J. Clin. Immunol. 21 (5): 303–9. PMID 11720003. doi:10.1023/A:1012241117984

Marks J, Shuster S, Watson AJ (1966). «Small-bowel changes in dermatitis herpetiformis». Lancet. 2 (7476): 1280–2. PMID 4163419. doi:10.1016/S0140-6736(66)91692-8

Nicolas ME, Krause PK, Gibson LE, Murray JA (Agosto de 2003). «Dermatitis herpetiformis». Int. J. Dermatol. 42 (8): 588–600. PMID 12890100. doi:10.1046/j.1365-4362.2003.01804.x

Tersigni, C.; Castellani, R.; de Waure, C.; Fattorossi, A.; De Spirito, M.; Gasbarrini, A.; Scambia, G.; Di Simone, N. (2014). «Celiac disease and reproductive disorders: meta-analysis of epidemiologic associations and potential pathogenic mechanisms». Human Reproduction Update. 20 (4): 582–593. ISSN 1355-4786. doi:10.1093/humupd/dmu007

Ferguson A, Hutton MM, Maxwell JD, Murray D (1970). «Adult coeliac disease in hyposplenic patients». Lancet. 1 (7639): 163–4. PMID 4189238. doi:10.1016/S0140-6736(70)90405-8

Schuppan D, Junker Y, Barisani D (Dezembro de 2009). «Celiac disease: from pathogenesis to novel therapies». Gastroenterology. 137 (6): 1912–33. PMID 19766641. doi:10.1053/j.gastro.2009.09.008

Kupper C (2005). «Dietary guidelines and implementation for celiac disease». Gastroenterology. 128 (4 Supl. 1): S121–7. PMID 15825119. doi:10.1053/j.gastro.2005.02.024

Stene LC, Honeyman MC, Hoffenberg EJ, Haas JE, Sokol RJ, Emery L, Taki I, Norris JM, Erlich HA, Eisenbarth GS, Rewers M (2006). «Rotavirus infection frequency and risk of celiac disease autoimmunity in early childhood: a longitudinal study». Am J Gastroenterol. 101 (10): 2333–40. PMID 17032199. doi:10.1111/j.1572-0241.2006.00741.x

Kagnoff MF, Paterson YJ, Kumar PJ, Kasarda DD, Carbone FR, Unsworth DJ, Austin RK (1987). «Evidence for the role of a human intestinal adenovirus in the pathogenesis of coeliac disease». Gut. 28 (8): 995–1001. PMC 1433141

. PMID 2822550. doi:10.1136/gut.28.8.995

Suman S, Williams EJ, Thomas PW, Surgenor SL, Snook JA (2003). «Is the risk of adult coeliac disease causally related to cigarette exposure?». Eur J Gastroenterol Hepatol. 15 (9): 995–1000. PMID 12923372. doi:10.1097/00042737-200309000-00009

Norris JM, Barriga K, Hoffenberg EJ, Taki I, Miao D, Haas JE, Emery LM, Sokol RJ, Erlich HA, Eisenbarth GS, Rewers M (2005). «Risk of celiac disease autoimmunity and timing of gluten introduction in the diet of infants at increased risk of disease». JAMA. 293 (19): 2343–2351. PMID 15900004. doi:10.1001/jama.293.19.2343

Poole JA, Barriga K, Leung DY, Hoffman M, Eisenbarth GS, Rewers M, Norris JM (2006). «Timing of initial exposure to cereal grains and the risk of wheat allergy». Pediatrics. 117 (6): 2175–82. PMID 16740862. doi:10.1542/peds.2005-1803

Akobeng AK, Ramanan AV, Buchan I, Heller RF (2006). «Effect of breast feeding on risk of coeliac disease: a systematic review and meta-analysis of observational studies». Arch Dis Child. 91 (1): 39–43. PMC 2083075

. PMID 16287899. doi:10.1136/adc.2005.082016

Hopper AD, Cross SS, Hurlstone DP, McAlindon ME, Lobo AJ, Hadjivassiliou M, Sloan ME, Dixon S, Sanders DS (2007). «Pre-endoscopy serological testing for coeliac disease: evaluation of a clinical decision tool». BMJ. 334 (7596). 729 páginas. PMC 1847864

. PMID 17383983. doi:10.1136/bmj.39133.668681.BE

van der Windt DA, Jellema P, Mulder CJ, Kneepkens CM, van der Horst HE (2010). «Diagnostic testing for celiac disease among patients with abdominal symptoms: a systematic review». JAMA. 303 (17): 1738–46. PMID 20442390. doi:10.1001/jama.2010.549

Sblattero D, Berti I, Trevisiol C, Marzari R, Tommasini A, Bradbury A, Fasano A, Ventura A, Not T (2000). «Human recombinant tissue transglutaminase ELISA: an innovative diagnostic assay for celiac disease». Am. J. Gastroenterol. 95 (5): 1253–7. PMID 10811336. doi:10.1111/j.1572-0241.2000.02018.x

Hill ID, Dirks MH, Liptak GS, Colletti RB, Fasano A, Guandalini S, Hoffenberg EJ, Horvath K, Murray JA, Pivor M, Seidman EG (2005). «Guideline for the diagnosis and treatment of celiac disease in children: recommendations of the North American Society for Pediatric Gastroenterology, Hepatology and Nutrition». J. Pediatr. Gastroenterol. Nutr. 40 (1): 1–19. PMID 15625418. doi:10.1097/00005176-200501000-00001

Korponay-Szabó IR, Dahlbom I, Laurila K, Koskinen S, Woolley N, Partanen J, Kovács JB, Mäki M, Hansson T (2003). «Elevation of IgG antibodies against tissue transglutaminase as a diagnostic tool for coeliac disease in selective IgA deficiency». Gut. 52 (11): 1567–71. PMC 1773847

. PMID 14570724. doi:10.1136/gut.52.11.1567

Hill ID (Abril de 2005). «What are the sensitivity and specificity of serologic tests for celiac disease? Do sensitivity and specificity vary in different populations?» (PDF). Gastroenterology. 128 (4 Suppl 1): S25–32. PMID 15825123. doi:10.1053/j.gastro.2005.02.012

Nandiwada SL, Tebo AE (Abril de 2013). «Testing for antireticulin antibodies in patients with celiac disease is obsolete: a review of recommendations for serologic screening and the literature». Clinical and vaccine immunology : CVI. 20 (4): 447–51. PMC 3623418

. PMID 23365209. doi:10.1128/CVI.00568-12

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. PMID 15917404. doi:10.1136/jcp.2004.023978

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Qiao SW, Bergseng E, Molberg Ø; et al. (Agosto de 2004). «Antigen presentation to celiac lesion-derived T cells of a 33-mer gliadin peptide naturally formed by gastrointestinal digestion». J. Immunol. 173 (3): 1757–62. PMID 15265905. doi:10.4049/jimmunol.173.3.1757

Shan L, Qiao SW, Arentz-Hansen H, Molberg Ø, Gray GM, Sollid LM, Khosla C (2005). «Identification and analysis of multivalent proteolytically resistant peptides from gluten: implications for celiac sprue». J. Proteome Res. 4 (5): 1732–41. PMC 1343496

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Fleckenstein B, Molberg Ø, Qiao SW, Schmid DG, von der Mülbe F, Elgstøen K, Jung G, Sollid LM (2002). «Gliadin T cell epitope selection by tissue transglutaminase in celiac disease. Role of enzyme specificity and pH influence on the transamidation versus deamidation process». J Biol Chem. 277 (37): 34109–34116. PMID 12093810. doi:10.1074/jbc.M204521200

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