Cows' milk is an important weaning food in many countries. In recent years it has become practically ubiquitous, being found in an increasing range of commercially produced foods (Sampson 1998). There is extensive cross-reactivity between milks of different species (Businco et al. 1995, Carroccio et al. 1999). Cows' milk is one of the first foods to enter an infant's diet and therefore is often the first to cause problems. Adverse reactions to cows' milk can be divided into two main groups, immunological (IgE or non-IgE mediated) or non-immunolo-gical (Host et al. 1997, Host and Halken 1998). This latter group is mainly due to lactase deficiency and may be difficult to differentiate clinically from non-IgE mediated cows' milk allergy (Host et al. 1997, Bruinjzeel-Koomen et al. 1995). Cows' milk allergy gives rise to a spectrum of disease from immediate symptoms ranging from urticaria to anaphylaxis (Goldman et al. 1963, Sampson et al. 1992) and late symptoms which may not develop for 24 to 48 hours. Most early reactors have specific IgE to cows' milk (Hill et al. 1988, Host and Halken 1990).
Adverse reactions to milk presents early, median age 4-8 weeks with a range of 152 weeks (Jakobson and Lindberg 1979, Host 1990, Schrander et al. 1993). In general, infants do not develop symptoms on their first exposure to cows' milk (Host 1990). Half react within a week of first exposure and three-quarters within four weeks (Host 1990, Jakobson and Lindberg 1979). Of note, a quarter of the children have their first symptoms while being exclusively breast fed (Host 1990).
Symptoms suggestive of cows' milk allergy or intolerance are relatively common and are seen in 2-15% of infants (Table 10.1). This variability is probably due to different diagnostic criteria, study design, geographical differences and different ages. Where subjects have been prospectively recruited and diagnosis is based on food challenge, the cumulative incidence has been found to be remarkably similar at 1.9-2.3% in the first three years of life (Table 10.1). Unfortunately few of these studies differentiate between the different types of adverse reactions or whether specific IgE is present. Where they do, 2550% of infants develop symptoms within 1-3 hours (Schrander et al. 1993, Jakobson and Lindberg 1979, Host 1990).
The peak prevalence of cows' milk allergy is seen at 1-2 years of age. After this age, children start to lose their reactivity (Table 10.1). The remission rate in one study was 56% at 1 year, 77% at 2 years, 87% at 3 years and 92% at 5 and 10 years (Host 1990, Host 1997). The majority of children with persistent cows' milk allergy beyond 5 years of age have IgE to cows' milk (Host 1990, Host et al. 1997).
Within the adult population, adverse reactions to cows' milk are reported by 0.7% of the population but only 10% of these have specific IgE to cows' milk. The prevalence of IgE-mediated cows' milk allergy in adults is therefore extremely low at 0.07% and is probably due largely to persistent allergy from childhood (Bjornsson et al. 1996, Niestijl et al. 1994) (Table 10.1). Lactase deficiency is probably responsible for most adverse reactions to cows' milk in adults (Bruinjzeel-Koomen et al. 1995).
Soy is a fairly recent addition to the Western diet although soybeans have been eaten for centuries in the Far East. The most commonly reported adverse reactions to soy are gastrointestinal symptoms, often as an enterocolitis syndrome or colitis (Powell 1978). Specific IgE to soy is not thought to be involved (Zeiger et al. 1999). Skin lesions are occasionally seen but IgE-mediated symptoms or anaphylaxis are extremely rare (Cantani and Lucenti 1997).
It had been thought that most cows' milk allergic children also reacted to soy (Cantani and Lucenti 1997). However, the early studies relied on the history, RAST tests or skinprick tests to make the diagnosis. When open or blinded challenges are used to diagnose both the cows' milk and soy allergy, 11-32% of children are found to react to both (Table 10.2). This variation in results between studies probably stems from the fact that they each enrolled different populations with different proportions of children with IgE and non-IgE mediated cows' milk allergy.
In general, adverse reactions to soy are first seen in the later part of infancy although when infants are exposed to soy at a young age, reactions can occur (Bruno et al. 1997). The prevalence of self-reporting of soy allergy is very low unless a selected, atopic population is studied (Table 10.3). In atopic children presenting to allergy clinics the prevalence is 1.2-3% when diagnosed by open challenge. In unselected childhood population, the prevalence is only 0-0.3%. Most of these children have positive specific IgE to soy and react within four hours. Where soy allergic children have been followed up, all have been found to outgrow their allergy within seven years (Bock 1982). This correlates with adult studies where the prevalence of soy allergy has been estimated as zero (Table 10.3). Soy may behave as an aeroallergen in both adults and children; in Barcelona, aerosolised soy from the port has been linked to epidemics of asthma (Navarro et al. 1993).
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