primary prevention of coeliac disease - Associazione Italiana ...

44
INFANT FEEDING PRACTICES AND COELIAC DISEASE
20-23
by means of a cascade of events results in a chronic enteropathy .
The human leukocyte antigen (HLA)-DQ2 molecule is expressed by more than
90% of coeliac disease patients, compared to 20-30% of healthy controls, and the
22
majority of the remaining patients express the DQ8 molecule . It has been estimated
that the HLA-complex confers 40% of the sibling family risk, and that non-HLA genes
24-25
are the most important . However, efforts to identify these contributing non-HLA
26-27
genes have thus far not resulted in conclusive evidence . In assessing the impact of
genetics, the ratio lis crucial. This ratio is constructed by the prevalence in relatives of
28
an affected individual over the prevalence within the general population . Thus, if
causal environmental exposures are aggregated in the family, the impact of genetics
29
will be overestimated .
Most common diseases have a multifactorial aetiology, and they thus develop
through an interaction between an individual's genetic predisposition and various
30
environmental exposures . This has been shown for insulin dependent diabetes
mellitus (IDDM), which is an autoimmune disease with many similarities to coeliac
disease. The immune system has a key function in the pathogenesis of both diseases,
31
and there is an increased risk for coeliac disease in persons with IDDM .
It has recently been suggested that each genetic risk factor, taken separately, may
frequently be present in the general population, and it is the combination of some of
26
these and their interaction with environmental factors that induces coeliac disease .
Thus, in addition to the mere presence of gluten in the diet, environmental exposures
may also be expected to be part of the causal pattern responsible for coeliac disease.
Failure of oral tolerance
Environmental exposures, including infant feeding, influence the immunological
32-34
process resulting in oral tolerance - or intolerance - to a food constituent .
Considering recent knowledge of the aetiology of coeliac disease, this may be viewed at
least hypothetically as a failure in the development of, or the later loss of, oral
35
tolerance .
In most individuals, oral tolerance towards gluten develops and prevails throughout
life. If oral tolerance fails to develop, however, or is later broken down, then gluten may
act like a “dangerous” foreign antigen, resulting in the development of coeliac disease.
The Swedish epidemic
Sweden has experienced an unusual epidemic of symptomatic coeliac disease in
36-37
children . The incidence reached levels higher than ever reported, and the decline
that followed was amazingly abrupt (Fig. 1). Only children below two years of age were
affected, and most of the cases had symptoms as severe as those that had been observed
38-39
earlier . These findings are based on our population-based prospective incidence
register established in 1991, covering 40% of the Swedish child population, and
36
retrospective data collected back to 1973 from 15% of the child population .
Recently it was shown that this was indeed an epidemic of coeliac disease
enteropathy, and not only a shift in the proportion of cases with symptomatic