primary prevention of coeliac disease - Associazione Italiana ...

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54 INFANT FEEDING PRACTICES AND COELIAC DISEASE by our study, and that took place before the new national recommendation was launched. A certain delay between changes in exposure and disease occurrence would be expected. Indeed, in the 1980s the change in gluten intake with regard to both amounts consumed during infancy and age at introduction preceded the increase in incidence. In contrast, the decrease in amounts of gluten consumed was first noted in 1995, i.e. the same year as the decline in incidence started. Further, in 1997 the estimated amount of gluten consumed had decreased by one third, while the incidence rate had already returned to the level of the early 1980s. It should also be noted that the proportion of infants breast-fed at six months of age continuously increased during the 1990s without any sharp increase before, or coinciding with, the decrease in incidence. Hence, the changes in exposure caused by each of these factors alone cannot explain the entire epidemic. Considering the combined effects of changes in infant feeding practices over time, it is clear that both the rise and fall in incidence were accompanied by a change in the proportion of infants introduced to gluten in small amounts while still being breast-fed. Thus, Swedish infant feeding practices have shifted over time from a favourable to an unfavourable and then back again to a favourable pattern with respect to coeliac disease risk. Public health impact The public health impact of a change in causal exposures can be estimated by the population attributable fraction (AF), which takes into account the prevalence of different exposures among the cases (Pc), and the adjusted odds ratios (OR) of these exposures [AF = Pc (OR-1)/OR]. We used our case-referent study, performed during the peak of the epidemic, for such estimates. Our analysis revealed that about half of the coeliac disease cases during the epidemic might have been avoided if all infants had been introduced to gluten in small amounts while still being breast-fed (Fig. 6). 120 100 = Preventable cases No of cases 80 60 40 20 0 A B C D Continued Small-medium Continued Large Discontinued Small-medium Discontinued Large Breast-feeding status at introduction of flourand amount of flour given Fig. 6. Preventable coeliac disease cases below two years of age with respect to breastfeeding status at introduction of gluten-containing flour into the diet and the amount of flour given. Risk estimates were based on conditional logistic regression with 392 matched sets of cases and referents, and adjusted for age of the infant when flour was introduced. 37 Odds ratio (95% CI); A) 1.0, B) 2.0 (1.4, 3.0), C) 2.8 (1.9, 4.0), D) 3.3 (2.3, 4.8). From with permission.
INFANT FEEDING PRACTICES AND COELIAC DISEASE 55 Thus, other casual exposures changing over time must also have contributed to the epidemic. However, it is likely that the proportion of coeliac disease cases that might be avoided by appropriate measures varies among different populations, being higher in populations with unusually unfavourable environmental exposures, as was apparently the situation for Swedish infants during the high incidence years of the epidemic. What will follow after the epidemic? In a Swedish study based on symptomatic adult coeliac disease patients, the highest 79 age-specific prevalence was reported for people born between 1927 and 1936 , and interestingly, the majority of cases in our population-based adult screening study were 5 also born during that time period . Thus, these studies indicate a cohort effect, i.e. the life span of certain cohorts coincides with environmental exposures that have resulted in an excess risk for coeliac disease throughout life. Accordingly, it might also be that as a consequence of an unfavourable exposure during their first years of life, the birth cohorts of the epidemic years will carry an excess risk for coeliac disease throughout their lives. If so, the cohorts of the postepidemic period might have a decreased lifetime risk for coeliac disease. Thus far, at comparable ages the cohorts of this later period actually have a lower cumulative 6 1992 6 Cases per 1000 births 5 4 3 2 1 1989-90 1991 1987-88 1985-86 1983-84 1978-82 1973-77 5 4 3 2 1 1993 1994 1995 1996 1997 0 0 2 4 6 8 10 12 14 Age (years) 0 1998 0 2 4 6 Fig. 7. Cumulative incidence of coeliac disease by age for the birth cohorts from 1973 to 1998. To reduce the graph complexity, the cohorts of 1973 to 1982 are aggregated in groups of five, the cohorts of 1983 to 1990 in groups of two, while the cohorts from 1991 to 1998 are reported separately.
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Perspectives on Coeliac Disease Vol
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The AIC Meeting was held in the Aul
Page 8 and 9:
Italian Coeliac Society, Via Picott
Page 11 and 12:
Preface Coeliac disease (CD) is a u
Page 13:
Contents Current understanding of t
Page 16 and 17:
2 THE BASIS OF COELIAC DISEASE hapl
Page 18 and 19: 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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