A history of coeliac disease
ABSTRACT Coeliac disease may have an ancient history dating back to the 1st and 2nd centuries AD. The first clear description was given by Samuel Gee in 1888. He suggested that dietary treatment might be of benefit. In the early 20th century various diets were tried, with some success, but without clear recognition of the toxic components. The doctoral thesis of Wim Dicke of 1950 established that exclusion of wheat, rye and oats from the diet led to dramatic improvement. The toxicity was shown to be a protein component, referred to as gluten. Dicke's colleagues, Weijers and Van de Kamer, showed that measurement of stool fat reflected the clinical condition. Early studies were in children but stool fat measurements documented that the condition could be recognised in adults. Histological abnormalities of the lining of the small intestine were demonstrated beyond doubt by Paulley in 1954 and techniques of per-oral biopsy described by Royer in 1955 and Shiner in 1956 afforded reliable diagnosis. Concurrence in monozygotic twins suggested a genetic component, confirmed by studies of HLA antigens. Additional, non-genetic factors seem likely. Circulating antibodies suggest an immunological mechanism of damage and provide non-invasive screening tests. Lymphoma, adenocarcinoma and ulceration of the small intestine and a range of immunological disorders are associated. A relationship with dermatitis herpetiformis was suggested by Samman in 1955 and established by Shuster and Marks in 1965 and 1968. The Coeliac Society (now Coeliac UK) was founded in 1968 and similar societies now exist across the world. They provide an extremely valuable service. Present problems include definition of the tolerated levels of gluten, whether oats are toxic for some or all coeliacs and the likelihood that the condition is relatively common and frequently without classical symptoms. Hope for the future is that more convenient methods of treatment will follow better understanding.
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ABSTRACT: Celiac disease (CD) is an autoimmune disorder that can be divided into typical and atypical forms. Atypical forms can show extraintestinal manifestations among which oral signs are very frequent. Considering that the pathogenesis of CD is related to a positivity to specific HLA-DQB1 haplotypes, we tested whether the presence of the HLA-DQB1*02 allele could be a hypothetical cause of the development of oral manifestations. For this study was been examined the oral condition of 98 Sardinian patients, all affected by CD and all on a gluten-free diet for at least 1 year. Then was been determined each patient's HLA-DQB1 haplotype and compared these results with clinical information. The statistical analysis evidenced that the absence of the HLA-DQB1*02 allele predisposes to oral manifestations such as dental enamel defects (DED) and recurrent aphthous stomatitis (RAS) (Pvalue=5.98x10(-05), OR = 0.23, CI: (0.10 - 0.45) per each copy of the HLA allele). These results showed that the presence of the HLA-DQB1*02 allele influences the development of oral signs in a dose-dependent manner and also how the HLA haplotype connected to oral signs could have a fundamental role for the diagnosis of atypical forms of CD.The Open Dentistry Journal 11/2011; 5:174-8. DOI:10.2174/1874210601105010174
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ABSTRACT: : Celiac disease is an autoimmune disorder with genetic predisposition that affects as many as 1 in 100 individuals. Treatment is a lifelong, strict adherence to a gluten-free diet. Management by a primary care provider may lead to increased adherence and can minimize effects of nonadherence to the diet.The Nurse Practitioner 01/2015; DOI:10.1097/01.NPR.0000459728.54533.ac
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ABSTRACT: The basis for celiac disease (CD) treatment is a strict lifelong gluten-free diet. On the diet, the small intestinal mucosal injury heals and gluten-induced symptoms and signs disappear. The mucosal healing is a prerequisite for sustaining health and is also obtained with a diet containing oats and trace amounts of gluten, industrially purified wheat starch-based gluten-free products. The small intestinal mucosa does not heal in noncompliant people, nor when a patient is inadvertently ingesting gluten. Development of adjunctive or alternative therapies is on its way. There are several novel treatment pipelines within academy and industry. Examples are the ideas of using glutenases as a drug to degrade the ingested gluten, polymers to bind and sequester the gluten to the feces, and also vaccine development for an immunotherapy to induce tolerance towards gluten. Clinical drug trials are to be foreseen in CD, soon also in children.Journal of Pediatric Gastroenterology and Nutrition 07/2014; 59 Suppl 1:S15-S17. DOI:10.1097/01.mpg.0000450397.76521.f9 · 2.87 Impact Factor