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The lower limb in Coeliac's Disease

Discussion in 'General Issues and Discussion Forum' started by NewsBot, Jan 12, 2013.

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    The occurrence of lower limb enthesopathy in coeliac disease patients without clinical signs of articular involvement
    Mariangela Atteno, et al
    Rheumatology (2013) doi: 10.1093/rheumatology/kes380 First published online: January 7, 2013
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    Coeliac disease

    Coeliac disease, also spelled celiac disease, is a long-term autoimmune disorder primarily affecting the small intestine that occurs in people who are genetically predisposed.[10] Classic symptoms include gastrointestinal problems such as chronic diarrhoea, abdominal distention, malabsorption, loss of appetite and among children failure to grow normally.[1] This often begins between six months and two years of age.[1] Non-classic symptoms are more common, especially in people older than two years.[8][15][16][17] There may be mild or absent gastrointestinal symptoms, a wide number of symptoms involving any part of the body or no obvious symptoms.[1] Coeliac disease was first described in childhood;[8][6] however, it may develop at any age.[1][8] It is associated with other autoimmune diseases, such as diabetes mellitus type 1 and thyroiditis, among others.[6]

    Coeliac disease is caused by a reaction to gluten, which are various proteins found in wheat and in other grains such as barley and rye.[9][18][19] Moderate quantities of oats, free of contamination with other gluten-containing grains, are usually tolerated.[18][20] The occurrence of problems may depend on the variety of oat.[18][21] Upon exposure to gluten, an abnormal immune response may lead to the production of several different autoantibodies that can affect a number of different organs.[4][22] In the small bowel, this causes an inflammatory reaction and may produce shortening of the villi lining the small intestine (villous atrophy).[10][11] This affects the absorption of nutrients, frequently leading to anaemia.[10][19]

    Diagnosis is typically made by a combination of blood antibody tests and intestinal biopsies, helped by specific genetic testing.[10] Making the diagnosis is not always straightforward.[23] Frequently, the autoantibodies in the blood are negative,[24][25] and many people have only minor intestinal changes with normal villi.[16][26] People may have severe symptoms and be investigated for years before a diagnosis is achieved.[27] Increasingly, the diagnosis is being made in people without symptoms, as a result of screening.[28] Evidence regarding the effects of screening, however, is not sufficient to determine its usefulness.[29] While the disease is caused by a permanent intolerance to wheat proteins, it is not a form of wheat allergy.[10]

    The only known effective treatment is a strict lifelong gluten-free diet, which leads to recovery of the intestinal mucosa, improves symptoms and reduces risk of developing complications in most people.[13] If untreated, it may result in cancers such as intestinal lymphoma and a slightly increased risk of early death.[3] Rates vary between different regions of the world, from as few as 1 in 300 to as many as 1 in 40, with an average of between 1 in 100 and 1 in 170 people.[14] In developed countries, it is estimated that 80% of cases remain undiagnosed, usually because of minimal or absent gastrointestinal complaints and poor awareness of the condition.[5][30] Coeliac disease is slightly more common in women than in men.[31] The term "coeliac" is from the Greek κοιλιακός (koiliakós, "abdominal") and was introduced in the 19th century in a translation of what is generally regarded as an Ancient Greek description of the disease by Aretaeus of Cappadocia.[32][33]

    1. ^ a b c d e f Fasano A (Apr 2005). "Clinical presentation of celiac disease in the pediatric population". Gastroenterology (Review). 128 (4 Suppl 1): S68–73. doi:10.1053/j.gastro.2005.02.015. PMID 15825129. 
    2. ^ "Symptoms & Causes of Celiac Disease | NIDDK". National Institute of Diabetes and Digestive and Kidney Diseases. June 2016. Archived from the original on 24 April 2017. Retrieved 24 April 2017. 
    3. ^ a b Lebwohl B, Ludvigsson JF, Green PH (Oct 2015). "Celiac disease and non-celiac gluten sensitivity". BMJ (Review). 351: h4347. doi:10.1136/bmj.h4347. PMC 4596973Freely accessible. PMID 26438584. 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. 
    4. ^ a b Lundin KE, Wijmenga C (Sep 2015). "Coeliac disease and autoimmune disease-genetic overlap and screening". Nat Rev Gastroenterol Hepatol (Review). 12 (9): 507–15. doi:10.1038/nrgastro.2015.136. PMID 26303674. The abnormal immunological response elicited by gluten-derived proteins can lead to the production of several different autoantibodies, which affect different systems. 
    5. ^ a b "Celiac disease". World Gastroenterology Organisation Global Guidelines. July 2016. Archived from the original on 17 March 2017. Retrieved 23 April 2017. 
    6. ^ a b c d Ciccocioppo R, Kruzliak P, Cangemi GC, Pohanka M, Betti E, Lauret E, Rodrigo L (Oct 22, 2015). "The Spectrum of Differences between Childhood and Adulthood Celiac Disease". Nutrients (Review). 7 (10): 8733–51. doi:10.3390/nu7105426. PMC 4632446Freely accessible. PMID 26506381. 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) 
    7. ^ 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. doi:10.1111/j.1469-8749.2010.03647.x. PMID 20345955. Archived from the original on 25 April 2016. open access publication – free to read
    8. ^ a b c d 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 (Jan 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. doi:10.1097/MPG.0b013e31821a23d0. PMID 22197856. Archived (PDF) from the original on 3 April 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 
    9. ^ a b Tovoli F, Masi C, Guidetti E, Negrini G, Paterini P, Bolondi L (Mar 16, 2015). "Clinical and diagnostic aspects of gluten related disorders". World J Clin Cases (Review). 3 (3): 275–84. doi:10.12998/wjcc.v3.i3.275. PMC 4360499Freely accessible. PMID 25789300. 
    10. ^ a b c d e f g "Celiac Disease". NIDDKD. June 2015. Archived from the original on 13 March 2016. Retrieved 17 March 2016. 
    11. ^ a b Vivas S, Vaquero L, Rodríguez-Martín L, Caminero A (Nov 6, 2015). "Age-related differences in celiac disease: Specific characteristics of adult presentation". World J Gastrointest Pharmacol Ther (Review). 6 (4): 207–12. doi:10.4292/wjgpt.v6.i4.207. PMC 4635160Freely accessible. PMID 26558154. 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) 
    12. ^ Ferri, Fred F. (2010). Ferri's differential diagnosis : a practical guide to the differential diagnosis of symptoms, signs, and clinical disorders (2nd ed.). Philadelphia, PA: Elsevier/Mosby. p. Chapter C. ISBN 0323076998. 
    13. ^ a b See JA, Kaukinen K, Makharia GK, Gibson PR, Murray JA (Oct 2015). "Practical insights into gluten-free diets". Nat Rev Gastroenterol Hepatol (Review). 12 (10): 580–91. doi:10.1038/nrgastro.2015.156. PMID 26392070. 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. 
    14. ^ a b Fasano, A; Catassi, C (Dec 20, 2012). "Clinical practice. Celiac disease". The New England Journal of Medicine (Review). 367 (25): 2419–26. doi:10.1056/NEJMcp1113994. PMID 23252527. 
    15. ^ Newnham ED (2017). "Coeliac disease in the 21st century: paradigm shifts in the modern age". J Gastroenterol Hepatol (Review). 32 Suppl 1: 82–85. doi:10.1111/jgh.13704. PMID 28244672. Archived from the original on 16 March 2017. Presentation of CD with malabsorptive symptoms or malnutrition is now the exception rather than the rule Free to read
    16. ^ a b Rostami Nejad M, Hogg-Kollars S, Ishaq S, Rostami K (2011). "Subclinical celiac disease and gluten sensitivity". Gastroenterol Hepatol Bed Bench (Review). 4 (3): 102–8. PMC 4017418Freely accessible. PMID 24834166. 
    17. ^ Tonutti E, Bizzaro N (2014). "Diagnosis and classification of celiac disease and gluten sensitivity". Autoimmun Rev (Review). 13 (4–5): 472–6. doi:10.1016/j.autrev.2014.01.043. PMID 24440147. 
    18. ^ a b c Penagini F, Dilillo D, Meneghin F, Mameli C, Fabiano V, Zuccotti GV (Nov 18, 2013). "Gluten-free diet in children: an approach to a nutritionally adequate and balanced diet". Nutrients (Review). 5 (11): 4553–65. doi:10.3390/nu5114553. PMC 3847748Freely accessible. PMID 24253052. 
    19. ^ a b Di Sabatino A, Corazza GR (April 2009). "Coeliac disease". Lancet. 373 (9673): 1480–93. doi:10.1016/S0140-6736(09)60254-3. PMID 19394538. 
    20. ^ 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 (April 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. 
    21. ^ Comino I, Moreno Mde L, Sousa C (Nov 7, 2015). "Role of oats in celiac disease". World J Gastroenterol. 21 (41): 11825–31. doi:10.3748/wjg.v21.i41.11825. PMC 4631980Freely accessible. PMID 26557006. 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. ^ National Institute for Health and Clinical Excellence. Clinical guideline 86: Recognition and assessment of coeliac disease. London, 2015.
    23. ^ Cite error: The named reference MatthiasPfeiffer2010 was invoked but never defined (see the help page).
    24. ^ Lewis NR, Scott BB (1 July 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. doi:10.1111/j.1365-2036.2006.02967.x. PMID 16803602. Archived from the original on 4 May 2016. 
    25. ^ Cite error: The named reference AGA2006 was invoked but never defined (see the help page).
    26. ^ Molina-Infante J, Santolaria S, Sanders DS, Fernández-Bañares F (May 2015). "Systematic review: noncoeliac gluten sensitivity". Aliment Pharmacol Ther (Review). 41 (9): 807–20. doi:10.1111/apt.13155. PMID 25753138. 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). 
    27. ^ Ludvigsson JF, Card T, Ciclitira PJ, Swift GL, Nasr I, Sanders DS, Ciacci C (Apr 2015). "Support for patients with celiac disease: A literature review". United European Gastroenterol J (Review). 3 (2): 146–59. doi:10.1177/2050640614562599. PMC 4406900Freely accessible. PMID 25922674. 
    28. ^ van Heel DA, West J (2006). "Recent advances in coeliac disease". Gut (Review). 55 (7): 1037–46. doi:10.1136/gut.2005.075119. PMC 1856316Freely accessible. PMID 16766754. 
    29. ^ 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 March 2017). "Screening for Celiac Disease: US Preventive Services Task Force Recommendation Statement". JAMA. 317 (12): 1252–1257. doi:10.1001/jama.2017.1462. PMID 28350936. 
    30. ^ Lionetti E, Gatti S, Pulvirenti A, Catassi C (Jun 2015). "Celiac disease from a global perspective". Best Pract Res Clin Gastroenterol (Review). 29 (3): 365–79. doi:10.1016/j.bpg.2015.05.004. PMID 26060103. 
    31. ^ Hischenhuber C, Crevel R, Jarry B, Mäki M, Moneret-Vautrin DA, Romano A, Troncone R, Ward R (March 2006). "Review article: safe amounts of gluten for patients with wheat allergy or coeliac disease". Aliment. Pharmacol. Ther. 23 (5): 559–75. doi:10.1111/j.1365-2036.2006.02768.x. PMID 16480395. 
    32. ^ Adams F, translator (1856). "On The Cœliac Affection". The extant works of Aretaeus, The Cappadocian. London: Sydenham Society. pp. 350–1. Retrieved 12 December 2009. 
    33. ^ Losowsky MS (2008). "A history of coeliac disease". Dig Dis. 26 (2): 112–20. doi:10.1159/000116768. PMID 18431060. 
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    Risk of Neuropathy Among 28 232 Patients With Biopsy-Verified Celiac Disease
    Sujata P. Thawani, MD, MPH; Thomas H. Brannagan III, MD; Benjamin Lebwohl, MD, MS; Peter H. R. Green, MD; Jonas F. Ludvigsson, MD, PhD
    JAMA Neurol. Published online May 11, 2015

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