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.
Metabolomics 11/2014; DOI:10.1007/s11306-014-0752-9 · 3.97 Impact Factor
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ABSTRACT: The diagnostic criteria for celiac disease (CD) have undergone significant change during the past several decades following a better understanding of the pathogenesis of the disease and the identification of sensitive and specific serum markers. In 2012, the European Society for Pediatric Gastroenterology, Hepatology, and Nutrition published new diagnostic algorithms, which for the first time questioned the need for histological evaluation in all patients, and identified specific requirements for omitting intestinal biopsies from diagnosis requirements. Here, we briefly review the evolution of the diagnostic algorithms, emerging data which may be integrated into the diagnosis algorithm in the future and suggest key points which should be considered while we continue to develop and refine the diagnostic criteria for CD in an age of personalized medicine.Journal of Pediatric Gastroenterology and Nutrition 07/2014; 59 Suppl 1:S13-S15. DOI:10.1097/01.mpg.0000450396.76521.b0 · 2.87 Impact Factor
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ABSTRACT: Celiac disease (CD) is a multifactorial chronic inflammatory condition that results in injury of the mucosal lining of the small intestine upon ingestion of wheat gluten and related proteins from barley and rye. Although the exact mechanisms leading to CD are not fully understood, the genetic basis of CD has been relatively well characterized. In this review we briefly review the history of discovery, clinical presentation, pathophysiology, and current understanding of the genetics underlying CD risk. Then, we discuss what is known about the current distribution and evolutionary history of genes underlying CD risk in light of other evolutionary models of disease. Specifically, we conclude that the set of loci underlying CD risk did not cohesively evolve as a response to a single past selection event such as the development of agriculture. Rather, deterministic and stochastic evolutionary processes have both contributed to the present distribution of variation in CD risk loci. Selection has shaped some components of this network, but this selection appears to have occurred at diffferent points in the past. Other parts of the CD risk network have likely arisen due to stochastic processes such as genetic drift.Human Biology 02/2014; 86(1):19-36. DOI:10.3378/027.086.0102 · 1.52 Impact Factor