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50 INFANT FEEDING PRACTICES AND COELIAC DISEASE 52-54 introduction of dietary gluten is of no importance with respect to coeliac disease risk . In our case-referent study we could move one step further by also adjusting for the differences in amount of gluten-containing foods given at various ages of introduction. Our results also suggested that the age of the infant at introduction of dietary gluten was 57 of no importance for coeliac disease risk , although with the limitation that only the first year of life was evaluated. Thus, present evidence does not support age of the infant at the time of gluten introduction as an independent risk factor for coeliac disease development. However, even when considered together these studies do not encompass all possible ages for introduction of gluten, e.g. after one year of age or even later. Thus, this possibility also needs to be evaluated. Other possible contributing factors Infections 70 71 It has been proposed that adenovirus type 12 , and also other adenoviruses , could initiate coeliac disease as a consequence of sequence similarities between a protein produced in conjunction with the viral infection and A-gliadin. This has been 72-73 questioned , but not convincingly excluded. Gastrointestinal infections cause a 74 disruption of the barrier function of the small intestinal mucosa , which theoretically could result in an increased antigen penetration and unfavourable immune responses. We found a higher risk for coeliac disease in children born during summer as 75 compared to winter, but only in children below two years of age . These findings indicate that environmental exposure(s) with a seasonal pattern may have a causal effect. A temporal relationship suggests that this might be due to a causal effect of infections during foetal life and/or an interaction between infections and introduction of gluten into the diet. However, any exposure with a seasonal pattern might be the explanation, and non-infectious exposures should also be explored. In our case-referent study we found that children who experienced three or more infectious episodes before six months of age had an increased risk for coeliac disease 76 before two years of age (adjusted OR=1.4, 95% CI 1.0-1.9) . This was true even when episodes of gastroenteritis were excluded, and after adjustments were made for differences in infant feeding patterns and family socio-economic group. Infectious episodes later in infancy were not included, as these could be secondary to the disease itself. The risk for coeliac disease increased considerably if in addition to having many infections the child was also introduced to gluten in large amounts, as compared to 76 small and medium amounts . Socio-economic background In our case-referent study children in families belonging to the lower as compared to middle and upper socio-economic strata of Swedish society had an increased risk for 76 coeliac disease (adjusted OR=1.4, 95% CI 1.0-1.8) , but again only in the age group below two years. Our reported estimate was adjusted for differences in infant feeding practices and infectious episodes. This indicates that there are also other as yet unidentified environmental exposures contributing to the causal pattern of coeliac disease.
INFANT FEEDING PRACTICES AND COELIAC DISEASE 51 A multifactorial aetiology A simplified model of the multifactorial aetiology of coeliac disease is outlined below (Fig. 3). It is based on the results of our own studies put into the context of present knowledge of coeliac disease aetiology. The emphasis in the model is on the influence of environmental exposures on coeliac disease risk. Throughout life, including foetal life, an individual's genetic makeup interacts with the continuous and varying exposures of the environment. Theoretically, both genes and the environment, as well as the interaction between them, confer either increased or reduced disease risk. The exposures of causal importance most likely vary throughout life, and the range of potential risk determinants is wide. More specifically, with regard to coeliac disease the immunological response to dietary gluten is shaped. Genetic susceptibility and presence of dietary gluten are considered necessary casual factors, i.e. without these factors coeliac disease will not develop. However, component causal factors also contribute to whether or not coeliac disease develops. Combined, the necessary causes and one or several component causes produce a 77 sufficient cause, i.e. development of the disease is unavoidable . As component causal factors in coeliac disease aetiology we suggest: i) duration of breast-feeding, ii) whether breast-feeding is ongoing or not when gluten is introduced into the diet, iii) amount of gluten given to infants when introduced into the diet, and iv) repeated infectious episodes early in life. Associated factors are not considered to have a causal effect by themselves, but act through other directly causal factors. When identified, however, they may be used as markers for an increased disease risk, and thereby focus the search for causal factors. Such a factor is seasonality in births, with an increased risk for coeliac disease in Season Dietary recommendations Food contents Socioeconomic conditions Structural factors Associated factors Infections Breast feeding ? ? ? Component causal factors Amount DIETARY GLUTEN NECESSARY CAUSAL FACTORS GENETICS sex Immunopathogenesis Fetal life Infancy Childhood Adulthood Fig. 3. Causal model on the multifactorial aetiology of coeliac disease. 37 From , with permission.
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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
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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