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56 INFANT FEEDING PRACTICES AND COELIAC DISEASE incidence than the cohorts of the epidemic period (Fig. 7). A longer follow-up will reveal to what extent this lower risk continues, and to what extent new cases develop later in life. Large screening studies of cohorts from both the epidemic and post-epidemic periods, with repeated screening for a considerable number of years, would increase our understanding of the natural history of coeliac disease development in relation to exposures early in life. These exposures would be complicated, of course, by the addition of exposures later in life. An option for primary prevention Primary prevention of coeliac disease is a clearly desirable option, as it would contribute substantially to the health of the general population. By definition, it aims at intervening before the disease has developed. Genetic modification of the gluten-containing cereals so that they lose their ability to trigger celiac disease might someday become an alternative, although this is something for the distant future. Another option, at least theoretically, would be induction of immune tolerance to gluten peptides by giving a vaccine. Even today, coeliac disease could be effectively prevented if the use of gluten-containing cereals was abandoned, but in most countries such a suggestion would be considered unacceptable. However, if coeliac disease has a multifactorial aetiology, which is likely, then primary prevention would be possible, at least in some individuals, without completely abandoning the use of dietary gluten. This might be attained through a change in component causal exposures, thereby increasing the chance for infants to develop oral tolerance to gluten, and possibly also promoting the maintenance of tolerance throughout life (Fig. 3). When knowledge is consolidated from the clinical, epidemiological and basic sciences, it seems likely that infant feeding practices, in addition to the mere presence of gluten in the diet, have an important role in coeliac disease development. Thus, a significant contribution to primary prevention seems possible through a gradual introduction of gluten-containing foods into the infant diet before breast-feeding is discontinued. The duration of breast-feeding in itself seems to reduce the risk even further, and a long duration should thus be promoted. The risk for coeliac disease is then clearly reduced, at least up to two years of age. This infant feeding pattern most likely also contributes to a decreased lifetime risk of coeliac disease, although this remains to be established. Only a few of all the potential causal environmental exposures have thus far been explored, and the search for such factors, which exhibit their effect during different periods in the life span, should be intensified. This approach most likely will lead to the identification of other entry-points for primary prevention. Acknowledgements We thank Don Kasarda, US Department of Agriculture, Albany, California, for valuable comments on the manuscript.
INFANT FEEDING PRACTICES AND COELIAC DISEASE 57 References 1. Grodzinsky E, Franzen L, Hed J, Ström M. High prevalence of celiac disease in healthy adults revealed by antigliadin antibodies. Ann Allergy 1992; 69: 66-70. 2. Catassi C, Rätsch I-M, Fabiani E, Rossini M, Bordicchia F, Candela F, et al. Coeliac disease in the year 2000: exploring the iceberg. Lancet 1994; 343: 200-3. 3. Not T, Horvath K, Hill ID, Partanen J, Hammed A, Magazzu G, et al. Celiac disease risk in the USA: High prevalence of antiendomysium antibodies in healthy blood donors. Scand J Gastroenterol 1998; 33: 494-8. 4. Johnston SD, Watson RGP, McMillan SA, Sloan J, Love AHG. Coeliac disease detected by screening is not silent--simply unrecognized. QJM 1998; 91: 853-60. 5. Ivarsson A, Persson LÅ, Juto P, Peltonen M, Suhr O, Hernell O. High prevalence of undiagnosed coeliac disease in adults: a Swedish population-based study. J Intern Med 1999; 245: 63-8. 6. Catassi C, Rätsch IM, Gandolfi L, Pratesi R, Fabiani E, El Asmar R, et al. Why is coeliac disease endemic in the people of the Sahara? [letter]. Lancet 1999; 354: 647-8. 7. Csizmadia CGDS, Mearin ML, von Blomberg BME, Brand R, Verloove-Vanhorick SP. An iceberg of childhood coeliac disease in the Netherlands [letter]. Lancet 1999; 353: 813-4. 8. Gandolfi L, Pratesi R, Cordoba JC, Tauil PL, Gasparin M, Catassi C. Prevalence of celiac disease among blood donors in Brazil. Am J Gastroenterol 2000; 95: 689-92. 9. Rabassa EB, Sagaró E, Fragoso T, Castañeda C, Gra B. Coeliac disease in Cuban children. Arch Dis Child 1981; 56: 128-31. 10. Sher KS, Fraser RC, Wicks AC, Mayberry JF. High risk of coeliac disease in Punjabis. Epidemiological study in the south Asian and European populations of Leicestershire. Digestion 1993; 54: 178-82. 11. Rawashdeh MO, Khalil B, Raweily E. Celiac disease in Arabs. J Pediatr Gastroenterol Nutr 1996; 23: 415-8. 12. Demir H, Yuce A, Kocak N, Ozen H, Gurakan F. Celiac disease in Turkish children: presentation of 104 cases. Pediatr Int 2000; 42: 483-7. 13. Marsh MN. Screening for latent gluten sensitivity: questions many, but answers few [editorial; comment]. Eur J Gastroenterolog Hepatol 1996; 8: 3-6. 14. Catassi C, Fabiani E, Ratsch IM, Coppa GV, Giorgi PL. Celiac disease in the general population: should we treat asymptomatic cases? J Pediatr Gastroenterol Nutr 1997; 24: S10-2. 15. Lohiniemi S. Tricky to find, hard to treat, impossible to cure. Lancet 2001; 358: 14. 16. Ellis A. Coeliac disease: Previous family studies. In: McConnell RB, ed. The genetics of coeliac disease: International symposium on the genetics of coeliac disease, 1979, Liverpool, England. MTP, Lancaster: 1981; 197-9. 17. Polanco I, Biemond I, van Leeuwen A, et al. Gluten sensitive enteropathy in Spain: Genetic and environmental factors. In: McConnell RB, ed. The genetics of coeliac disease: International symposium on the genetics of coeliac disease, 1979, Liverpool, England. MTP, Lancaster: 1981; 211-31. 18. Bardella MT, Fredella C, Prampolini L, Marino R, Conte D, Giunta AM. Gluten sensitivity in monozygous twins: a long-term follow-up of five pairs. Am J Gastroenterol 2000; 95: 1503-5. 19. Hervonen K, Karell K, Holopainen P, Collin P, Partanen J, Reunala T. Concordance of Dermatitis Herpetiformis and Celiac Disease in Monozygous Twins. J Invest Dermatol 2000; 115: 990-3. 20. Ferguson A. Coeliac disease research and clinical practice: maintaining momentum into the twenty-first century. Baillieres Clin Gastroenterol 1995; 9: 395-412. 21. Walker-Smith J, Murch S. Coeliac disease. Diseases of the small intestine in childhood. 4 ed. Isis Medical Media; Oxford: 1999; 235-77.
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Perspectives on Coeliac Disease Vol
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The AIC Meeting was held in the Aul
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Italian Coeliac Society, Via Picott
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Preface Coeliac disease (CD) is a u
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Contents Current understanding of t
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2 THE BASIS OF COELIAC DISEASE hapl
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4 THE BASIS OF COELIAC DISEASE 1 pr
Page 20 and 21: 6 THE BASIS OF COELIAC DISEASE spre
Page 22 and 23: 8 THE BASIS OF COELIAC DISEASE Ackn
Page 24 and 25: 10 THE BASIS OF COELIAC DISEASE glu
Page 27 and 28: Catassi C, Fasano A, Corazza GR (ed
Page 29: T CELL RESPONSES TO GLUTEN PEPTIDES
Page 32 and 33: 18 A DOMINANT EPITOPE IN GLUTEN PEP
Page 42 and 43: 28 ROLE OF A-GLIADIN 31-49 PEPTIDE
Page 47 and 48: COELIAC DISEASE IN THE SAHARAWI 33
Page 55: COELIAC DISEASE IN THE SAHARAWI 41
Page 58 and 59: 44 INFANT FEEDING PRACTICES AND COE
Page 66 and 67: Age (years) 52 INFANT FEEDING PRACT
Page 76 and 77: 62 MECHANISMS OF ORAL TOLERANCE the
Page 78 and 79: 64 MECHANISMS OF ORAL TOLERANCE pot
Page 80 and 81: 66 MECHANISMS OF ORAL TOLERANCE Epi
Page 82 and 83: 68 MECHANISMS OF ORAL TOLERANCE typ
Page 84 and 85: 70 MECHANISMS OF ORAL TOLERANCE 51
Page 86 and 87: 72 MECHANISMS OF ORAL TOLERANCE 23.
Page 91 and 92: GENETICALLY DETOXIFIED GRAINS 77 to
Page 93 and 94: • • GENETICALLY DETOXIFIED GRAI
Page 95 and 96: GENETICALLY DETOXIFIED GRAINS 81 3.
Page 99 and 100: IMMUNOTHERAPY OF COELIAC DISEASE 85
Page 101 and 102: IMMUNOTHERAPY OF COELIAC DISEASE 87
Page 105 and 106: RECENT ADVANCES ON GLUTEN TOXICITY
Page 107 and 108: Index A Antiendomysium antibodies (
Page 109: INDEX 95 W Wheat, 7, 23, 27, 31, 53
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