Newnham, Evan D «Coeliac disease in the 21st century: Paradigm shifts in the modern age». Journal of Gastroenterology and Hepatology, 32, 2017, pàg. 82–85. DOI: 10.1111/jgh.13704. PMID: 28244672. «Presentation of CD with malabsorptive symptoms or malnutrition is now the exception rather than the rule.»
«The Spectrum of Differences between Childhood and Adulthood Celiac Disease». Nutrients, 7, 10, 22-10-2015, pàg. 8733–51. DOI: 10.3390/nu7105426. PMC: 4632446. PMID: 26506381. «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)»
«Gluten-free diet in children: an approach to a nutritionally adequate and balanced diet». Nutrients, 5, 11, novembre 2013, pàg. 4553–65. DOI: 10.3390/nu5114553. PMC: 3847748. PMID: 24253052.
«Role of oats in celiac disease». World Journal of Gastroenterology, 21, 41, novembre 2015, pàg. 11825–31. DOI: 10.3748/wjg.v21.i41.11825. PMC: 4631980. 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.»
«Coeliac disease and autoimmune disease-genetic overlap and screening». Nature Reviews. Gastroenterology & Hepatology, 12, 9, setembre 2015, pàg. 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.»
«Age-related differences in celiac disease: Specific characteristics of adult presentation». World Journal of Gastrointestinal Pharmacology and Therapeutics, 6, 4, novembre 2015, pàg. 207–12. DOI: 10.4292/wjgpt.v6.i4.207. PMC: 4635160. 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)»
«Diagnostic challenges in celiac disease and the role of the tissue transglutaminase-neo-epitope». Clin Rev Allergy Immunol, 38, 2–3, abril 2010, pàg. 298–301. DOI: 10.1007/s12016-009-8160-z. PMID: 19629760.
«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, 24, 1, juliol 2006, pàg. 47–54. DOI: 10.1111/j.1365-2036.2006.02967.x. PMID: 16803602.
«Systematic review: noncoeliac gluten sensitivity». Alimentary Pharmacology & Therapeutics, 41, 9, maig 2015, pàg. 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).»
«Support for patients with celiac disease: A literature review». United European Gastroenterology Journal, 3, 2, abril 2015, pàg. 146–59. DOI: 10.1177/2050640614562599. PMC: 4406900. PMID: 25922674.
«Screening for Celiac Disease: US Preventive Services Task Force Recommendation Statement». JAMA, 317, 12, març 2017, pàg. 1252–1257. DOI: 10.1001/jama.2017.1462. PMID: 28350936.
Burkhardt, J. G.; Chapa-Rodriguez, A.; Bahna, S. L. «Gluten sensitivities and the allergist: Threshing the grain from the husks». Allergy, 73, 7, juliol 2018, pàg. 1359–1368. DOI: 10.1111/all.13354. PMID: 29131356.
«Practical insights into gluten-free diets». Nature Reviews. Gastroenterology & Hepatology, 12, 10, octubre 2015, pàg. 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.»
«Celiac disease and non-celiac gluten sensitivity». BMJ, 351, octubre 2015, pàg. h4347. DOI: 10.1136/bmj.h4347. PMC: 4596973. 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 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.»
«Clinical practice. Celiac disease». The New England Journal of Medicine, 367, 25, desembre 2012, pàg. 2419–26. DOI: 10.1056/NEJMcp1113994. PMID: 23252527.
«Celiac disease from a global perspective». Best Practice & Research. Clinical Gastroenterology, 29, 3, juny 2015, pàg. 365–79. DOI: 10.1016/j.bpg.2015.05.004. PMID: 26060103.
«Review article: safe amounts of gluten for patients with wheat allergy or coeliac disease». Alimentary Pharmacology & Therapeutics, 23, 5, març 2006, pàg. 559–75. DOI: 10.1111/j.1365-2036.2006.02768.x. PMID: 16480395.
«Diagnostic testing for celiac disease among patients with abdominal symptoms: a systematic review». JAMA, 303, 17, 2010, pàg. 1738–46. DOI: 10.1001/jama.2010.549. PMID: 20442390. «Most studies used similar histological criteria for diagnosing celiac disease (Marsh grade ≥III), but the level of damage may vary across populations. Only 4 studies presented the proportion of patients in whom only partial villous atrophy was found (Marsh grade of IIIA), which ranged from 4% to 100%. The presence of positive serum antibodies has been shown to correlate with the degree of villous atrophy, and patients with celiac disease who have less severe histological damage may have seronegative findings. This could be important, especially in primary care, in which levels of mucosal damage may be lower, and consequently, more patients with celiac disease may be missed.»
Newnham, Evan D «Coeliac disease in the 21st century: Paradigm shifts in the modern age». Journal of Gastroenterology and Hepatology, 32, 2017, pàg. 82–85. DOI: 10.1111/jgh.13704. PMID: 28244672. «Presentation of CD with malabsorptive symptoms or malnutrition is now the exception rather than the rule.»
«The Spectrum of Differences between Childhood and Adulthood Celiac Disease». Nutrients, 7, 10, 22-10-2015, pàg. 8733–51. DOI: 10.3390/nu7105426. PMC: 4632446. PMID: 26506381. «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)»
«Gluten-free diet in children: an approach to a nutritionally adequate and balanced diet». Nutrients, 5, 11, novembre 2013, pàg. 4553–65. DOI: 10.3390/nu5114553. PMC: 3847748. PMID: 24253052.
«Role of oats in celiac disease». World Journal of Gastroenterology, 21, 41, novembre 2015, pàg. 11825–31. DOI: 10.3748/wjg.v21.i41.11825. PMC: 4631980. 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.»
«Coeliac disease and autoimmune disease-genetic overlap and screening». Nature Reviews. Gastroenterology & Hepatology, 12, 9, setembre 2015, pàg. 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.»
«Age-related differences in celiac disease: Specific characteristics of adult presentation». World Journal of Gastrointestinal Pharmacology and Therapeutics, 6, 4, novembre 2015, pàg. 207–12. DOI: 10.4292/wjgpt.v6.i4.207. PMC: 4635160. 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)»
«Diagnostic challenges in celiac disease and the role of the tissue transglutaminase-neo-epitope». Clin Rev Allergy Immunol, 38, 2–3, abril 2010, pàg. 298–301. DOI: 10.1007/s12016-009-8160-z. PMID: 19629760.
«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, 24, 1, juliol 2006, pàg. 47–54. DOI: 10.1111/j.1365-2036.2006.02967.x. PMID: 16803602.
«Systematic review: noncoeliac gluten sensitivity». Alimentary Pharmacology & Therapeutics, 41, 9, maig 2015, pàg. 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).»
«Support for patients with celiac disease: A literature review». United European Gastroenterology Journal, 3, 2, abril 2015, pàg. 146–59. DOI: 10.1177/2050640614562599. PMC: 4406900. PMID: 25922674.
«Screening for Celiac Disease: US Preventive Services Task Force Recommendation Statement». JAMA, 317, 12, març 2017, pàg. 1252–1257. DOI: 10.1001/jama.2017.1462. PMID: 28350936.
Burkhardt, J. G.; Chapa-Rodriguez, A.; Bahna, S. L. «Gluten sensitivities and the allergist: Threshing the grain from the husks». Allergy, 73, 7, juliol 2018, pàg. 1359–1368. DOI: 10.1111/all.13354. PMID: 29131356.
«Practical insights into gluten-free diets». Nature Reviews. Gastroenterology & Hepatology, 12, 10, octubre 2015, pàg. 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.»
«Celiac disease and non-celiac gluten sensitivity». BMJ, 351, octubre 2015, pàg. h4347. DOI: 10.1136/bmj.h4347. PMC: 4596973. 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 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.»
«Clinical practice. Celiac disease». The New England Journal of Medicine, 367, 25, desembre 2012, pàg. 2419–26. DOI: 10.1056/NEJMcp1113994. PMID: 23252527.
«Celiac disease from a global perspective». Best Practice & Research. Clinical Gastroenterology, 29, 3, juny 2015, pàg. 365–79. DOI: 10.1016/j.bpg.2015.05.004. PMID: 26060103.
«Review article: safe amounts of gluten for patients with wheat allergy or coeliac disease». Alimentary Pharmacology & Therapeutics, 23, 5, març 2006, pàg. 559–75. DOI: 10.1111/j.1365-2036.2006.02768.x. PMID: 16480395.
«Diagnostic testing for celiac disease among patients with abdominal symptoms: a systematic review». JAMA, 303, 17, 2010, pàg. 1738–46. DOI: 10.1001/jama.2010.549. PMID: 20442390. «Most studies used similar histological criteria for diagnosing celiac disease (Marsh grade ≥III), but the level of damage may vary across populations. Only 4 studies presented the proportion of patients in whom only partial villous atrophy was found (Marsh grade of IIIA), which ranged from 4% to 100%. The presence of positive serum antibodies has been shown to correlate with the degree of villous atrophy, and patients with celiac disease who have less severe histological damage may have seronegative findings. This could be important, especially in primary care, in which levels of mucosal damage may be lower, and consequently, more patients with celiac disease may be missed.»
niddk.nih.gov
«Celiac Disease», juny 2015. Arxivat de l'original el 13 març 2016. [Consulta: 17 març 2016].
