Up-date on the etiopathogenesis of celiac disease

Wheat, oat, rye and barley flours are toxic for celiac patients. Prevalence and incidence of Celiac Disease (CD), quite variable from country to country, are very high in Austria (1 out of 476 born alive) and low in France (1 out of 41.667 born alive). This difference is probably due to its multifac...

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Bibliographic Details
Published inLa Pediatria medica e chirurgica Vol. 10; no. 1; p. 7
Main Authors Ansaldi, N, Tavassoli, K, Forni, M, Lerro, P, Poli, E
Format Journal Article
LanguageItalian
Published Italy 01.01.1988
Subjects
Celiac Disease - enzymology
Celiac Disease - etiology
Celiac Disease - immunology
Humans
Hypersensitivity - immunology
Immunity
Jejunum - enzymology
Lectins - adverse effects
Lectins - metabolism
T-Lymphocytes - classification
T-Lymphocytes - immunology
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Summary:Wheat, oat, rye and barley flours are toxic for celiac patients. Prevalence and incidence of Celiac Disease (CD), quite variable from country to country, are very high in Austria (1 out of 476 born alive) and low in France (1 out of 41.667 born alive). This difference is probably due to its multifactorial genesis. In a multicentric Italian study, histocompatibility antigens of HLA complex II were typed in 460 CD children. DR3 was present in 63% of the cases (Relative Risk = RR: 6.8), DR7 in 67% (RR: 3.8) and DR3/DR7 in 22.5% (RR: 10.5), while in 7.7 of patients both antigens were absent. Therefore in a certain percentage of CD patients these risk antigens are absent, while in the normal population they can be present. The probability of CD increases when HLA DR3 and DR7 are present (but their absence cannot exclude the disease. The main etiological factor is gluten and its fractions (B, B1, B2, fraction 9 etc.). It seems that breast feeding can prevent or delay the onset of CD, while the age at gluten introduction does not modify the risk. Pathogenetic mechanisms are still under discussion: 3 theories are under investigation. 1) Enzymatic theory: a proteolytic enzyme for gluten digestion could be lacking. This theory is not yet proven, while Bruce et al. found in the jejunal mucosa of CD patients an elevation of a transglutaminase, which binds the gluten to enterocytes. Its level does not seem to vary with the diet. 2) Lectinic theory: the gluten bind the enterocyte membrane by a lectinic mechanism and damage it.
ISSN:0391-5387