Food Intolerance and Allergy 197
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specific serum IgE antibodies [1]. Delayed-onset
reactions occur within several hours to days after
ingestion and may involve the gut, skin or respira-
tory tract. These reactions are cell mediated (lym-
phocytes, eosinophils and mast cells), and individ-
uals lack evidence of systemic IgE sensitization
(skin prick testing, SPT, and food-specific serum
IgE antibodies negative). Finally, some allergic
conditions (e.g. atopic eczema or eosinophilic
esophagitis) display mixed features of IgE-mediat-
ed and non-IgE-mediated immune mechanisms.
An increasing number of major food a llergens
have been characterized at the molecular level,
e.g. β-lactoglobulin in cow’s milk, ovomucin in
hen’s egg or Ara h2 in peanut. On each of these
proteins, specific epitope regions have been
mapped that interact with either specific IgE an-
tibodies or T cell receptors. Conformational epi-
topes (with a three-dimensional structure) may
be inactivated by heating or acidification, while
linear epitopes are more resistant to degradation.
For example, egg-allergic patients may tolerate
baked egg in cakes, while still reacting to un-
cooked egg [7]. By contrast, boiling of cow’s milk
or roa st i ng of nut s gener a l ly doe s not reduc e t hei r
allergenicity.
Clinical Manifestations of Food Allergy
Food allergy may present with a diverse range of
clinical manifestations ( table 1 ) [1]. Immediate
reactions consist of urticaria, angioedema, oral
tingling/itch, vomiting or diarrhea within 30–60
min of allergen ingestion. Atopic dermatitis with
onset in the first months of life is closely associ-
ated with IgE-mediated food allergy [1]. The term
‘anaphylaxis’ is reserved for severe immediate-
type reactions with either respiratory compro-
mise (wheeze, stridor, cough) or systemic hypo-
tension [8]. Anaphylaxis may occur in response
to small allergen doses and can be fatal, particu-
larly in adolescents and young adults with unsta-
ble asthma.
Delayed-onset reactions (non-IgE-mediated
food allergy) typically involve the gastrointesti-
nal tract or skin. While gastrointestinal food al-
lergy is thought to be relatively common in the
first 2–3 years of life, population-based preva-
lence estimates are scarce. In infants and young
children, gastrointestinal food allergies may
cause growth failure due to persistent vomiting/
regurgitation, diarrhea and/or poor feeding [6].
The gastrointestinal allergy syndromes can be
divided into food protein-induced (1) enteropa-
thy, (2) enterocolitis syndrome (FPIES) and (3)
proctocolitis ( table 1 ) [6]. Enteropathy and proc-
tocolitis may occur in exclusively breastfed in-
fants [9] , whereas FPIES seems to require direct
ingestion of the allergen by the infant [10]. Re-
cently, eosinophilic esophagitis has been recog-
nized as a condition associated with food allergy
that often responds to dietary elimination of food
allergens [11].L a c t o s e I n t o l e r a n c eLactose is the main disaccharide in mammalian
milk. It can only be absorbed after digestion into
glucose and galactose by the small intestinal brush
border enzyme lactase. Failure to absorb lactase
results in bacterial fermentation in the colon, pre-
senting as flatulence, diarrhea, acidic stools and
perianal skin excoriation [5]. The abundance of
lactase activity is genetically regulated and slowly
drops after infancy (lactase nonpersistence). This
often leads to symptomatic hypolactasia by adult
age, particularly in non-Caucasian individuals.
Primary lactose intolerance (congenital absence
of lactase) in infants is rare [5]. Secondary forms
of lactose intolerance may be transient and re-
solve after the underlying gastrointestinal condi-
tion (e.g. viral gastroenteritis or celiac disease)
has remitted.
Lactase malabsorption can be confused with
cow’s milk allergy, and both conditions may co-
exist in cow’s milk enteropathy ( table 2 ) [6].Koletzko B, et al. (eds): Pediatric Nutrition in Practice. World Rev Nutr Diet. Basel, Karger, 2015, vol 113, pp 195–202
DOI: 10.1159/000360340