Pediatric Nutrition in Practice

Food Intolerance and Allergy 199

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food-specific serum IgE antibodies (Immuno-
CAP ® ) [12]. Detection of specific IgE antibodies
(sensitization) on its own, in the absence of clin-
ical symptoms, is not diagnostic ( table 3 ). A neg-
ative SPT or specific IgE test has a high negative
predictive value and makes IgE-mediated food
allergy unlikely [12, 13]. Conversely, high SPT
levels or specific IgE concentrations beyond a
defined cutoff (95% predictive decision point)
are considered diagnostic [12, 13]. In patients
with equivocal results, the diagnosis of IgE-me-
diated food allergy needs to be assessed by for-
mal food challenge in hospital (due to the poten-
tial risk of anaphylaxis) [8]. No useful in vitro

markers for non-IgE-mediated food allergy are

currently available. The diagnosis of non-IgE-

mediated food allergy relies on recognition of

the clinical presentation, demonstration of im-

provement after a 2- to 4-week period of food

allergen elimination, and relapse of symptoms

after a food challenge. The investigation of pos-

sible food intolerances follows the same princi-

ples. In addition, breath hydrogen testing (lac-

tose and fructose) and measurement of disac-

charidase levels in duodenal biopsies may be

useful in patients with suspected carbohydrate

malabsorption syndromes (lactase or sucrase-

isomaltase deficiency).

Ta b l e 2. Lactose malabsorption and its management

Type of
lactose
intolerance

Differential diagnosis Treatment Comments

Primary Congenital (rare) Lactose restriction (long-term) Extremely rare
‘Adult-onset’ hypolactasia Lactose restriction (long-term) Common
Genetic polymorphism
Lactase decline may commence in
childhood

Secondary Acute gastroenteritis/
postenteritic lactose
malabsorption

Short-term lactose restriction

(lactose-free formula)

In breastfed infants, continue

breastfeeding

If not tolerated, incubation of

expressed breast milk with lactase

may be successful

Mainly occurs in infancy

Typically resolves within 1–2 weeks

In very young infants, recovery may be

delayed

Celiac disease (untreated) Ongoing strict gluten-free diet

Lactose restriction until intestinal

mucosa has been restored on

gluten-free diet

Beware of false diagnostic labeling as

‘lactose intolerance’ or ‘irritable bowel

syndrome’

Food protein-induced

enteropathy (non-IgE-mediated

cow’s milk or soy allergy)

Extensively hydrolyzed (first-line

treatment) or amino acid-based

formula (if intolerant to extensively

hydrolyzed formula)

Cow’s milk-based, lactose-free formula

may control the malabsorptive

symptoms but does not allow mucosal

repair (due to ongoing exposure to

cow’s milk protein)

Intestinal dysplasia syndromes

(e.g. microvillus inclusion

disease, tufting enteropathy)

Depends on severity of disease

May require parenteral nutrition

Lactose restriction generally required

Rare

Presents with intestinal failure

Intestinal mucosal transporter

defects (e.g. glucose-galactose

malabsorption)

Strict avoidance of lactose-, glucose-,

galactose- and sucrose-containing

foods

Fructose is tolerated

Rare defect of sodium-glucose

transporter 1

Presents with profuse osmotic

diarrhea and severe dehydration in

first weeks of life

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