LETTER TO JMG

Genome screening of coeliac disease

S Popat¹, S Bevan¹, C P Braegger², A Busch³, D O'Donoghue⁴, K Falth-Magnusson⁵, A Godkin⁶, L Hogberg⁷, G Holmes⁸, K B Hosie⁹, P D Howdle¹⁰, H Jenkins¹, D Jewell⁶, S Johnston¹¹, N P Kennedy¹², P Kumar¹³, R F A Logan¹⁴, A H G Love¹¹, M N Marsh¹⁶, C J Mulder¹⁷, K Sjoberg¹⁸, L Stenhammar⁷, J Walker-Smith¹⁹, R S Houlston¹

¹ Section of Cancer Genetics, Institute of Cancer Research, Sutton, Surrey, UK
² University Children's Hospital, Steinwiesstrass 75, Zurich, Switzerland
³ Kinderpoliklinik, Eberhard-Karls-Universitat, Tubingen, Germany
⁴ Gastroenterology and Liver Unit, St Vincent's Hospital, Dublin, Ireland
⁵ Department of Paediatrics, Linkoping University, Sweden
⁶ Gastroenterology Unit, The Radcliffe Infirmary, Oxford, UK
⁷ Department of Paediatrics, Norrkoping Hospital, Sweden
⁸ Department of Medicine, Derbyshire Royal Infirmary, Derby, UK
⁹ University Surgical Unit, Northern General Hospital, Sheffield, UK
¹⁰ Division of Medicine, St James's University Hospital, Leeds, UK
¹¹ Department of Child Health, University Hospital of Wales, Cardiff, UK
¹² Department of Gastroenterology, Belfast City Hospital Trust, Belfast, UK
¹³ Department of Clinical Medicine, Trinity Centre, St James' Hospital, Dublin, Ireland
¹⁴ Department of Gastroenterology, St Bartholomew's Hospital, London, UK
¹⁵ Department of Public Health and Epidemiology, University Hospital, Nottingham, UK
¹⁶ University Department of Medicine, Hope Hospital, Salford, Manchester, UK
¹⁷ Hepatogastroenterology, Rijnstate Hospital, Arnhem, The Netherlands
¹⁸ Department of Medicine, University of Lund, Malmo, Sweden
¹⁹ University Department of Paediatric Gastroenterology, Royal Free Hospital, London, UK

Correspondence to:
Correspondence to:
Dr S Popat, Section of Cancer Genetics, Institute of Cancer Research, Sutton, Surrey, UK;
s.popat@icr.ac.uk

Keywords: coeliac disease; genome screening

Coeliac disease is caused by T cell sensitisation of the intestine to cereal prolamins, which results in a range of mucosal abnormalities that may lead to malabsorption.¹ The population prevalence in western countries is 1 in 200.^2–4 Evidence for an inherited predisposition to coeliac disease comes from studies of first degree relatives of patients and studies of twins.^5,6 A strong association is seen between coeliac disease and the HLA-DQ (1*05, ß1*02) heterodimer (DQ2) which is present in approximately 95% of patients,^7–9 compared with 20-30% of healthy subjects.^10,11 The difference in concordance rates between monozygotic twins and HLA identical sibs (80-100% v 25%) implicates non-HLA genes in the genetic predisposition to coeliac disease.¹¹ The overall relative risk in sibs is at least 20 and is therefore four-fold higher than that attributable to HLA alone under model of inheritance.⁷ Genome linkage searches carried out on Irish,¹² Italian,¹³, and UK¹⁴ coeliac . . . [Full text of this article]

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