Pediatric Nutrition in Practice

Celiac Disease 193

3

bility with anti-zonulin antibodies, preventing
gliadin presentation to T cells by blocking HLA
binding sites and the use of tissue TG inhibitors.
The efficacy of these approaches needs to be as-
sessed in more in vivo studies.

Prevention

Evidence suggests that the first months of life are
crucial for CD development; breastfeeding has a
protective role, and indeed there is a negative cor-
relation between its duration and the develop-
ment of CD. Moreover, the age at introduction of
gluten to the diet is important: exposure to gluten
in the first 3 months significantly increases the
risk of CD in genetically susceptible individuals.

One study has suggested the existence of a win-

dow of opportunity as the late introduction of

gluten to the diet (after the 7th month of life) has

been found to be associated with a higher risk. On

the basis of the present evidence, breastfeeding

should be strongly encouraged and gluten should

not be introduced before the 4th month of life,

preferably while the baby is still breastfed [13].

Finally, increasing attention is being devoted to

the possible role of viruses, which could trigger

CD autoimmunity in genetically susceptible chil-

dren by increasing intestinal permeability and ac-

tivating innate immune pathways linked to CD

pathophysiology.

Other Conditions Requiring GFD

The spectrum of gluten-related disorders also in-

cludes wheat allergy (WA) and nonceliac gluten

sensitivity (NCGS). WA is defined as an adverse

immunologic reaction to wheat proteins. De-

pending on the allergen exposure and the immu-

nologic mechanisms, WA is classified into (1)

classic food allergy affecting the skin, gastrointes-

tinal tract or respiratory tract, (2) wheat-depen-

dent, exercise-induced anaphylaxis, (3) occupa-

tional asthma (baker’s asthma) and rhinitis as

well as (4) contact urticaria. IgE antibodies play a

central role in the pathogenesis of these diseases.

WA is treated by GFD, and the same limits as dis-

cussed for CD seem to apply to WA [14].

NCGS refers to individuals who show distress

when eating gluten and improvement when fol-

lowing a GFD. CD autoantibodies are absent, the

small intestine is usually normal, and allergy tests

are negative. Thus, NCGS is a diagnosis by exclu-

sion criteria. However, many suggest caution, as

there is a noticeable lack of controlled studies un-

equivocally demonstrating the role of gluten. Oth-

er food components (fermentable oligo-, di- and

monosaccharides and polyols or FODMAPs) have

been suspected to be responsible for symptoms at-

tributed to NCGS. Further caution is required due

Ta b l e 2. Alternative therapies for CD

1. Intraluminal therapies
   Wheat varieties
   (Ancient) wheat variants with low
   immunogenicity
   Genetically modified wheat variants or deletion
   lines of common wheat with lower
   immunogenicity
   Flour/dough treatment
   Pretreatment with lactobacilli
   Transamidation of gliadin
   Ingested gliadin peptide modifications
   Prolyl endopeptidases from Aspergillus niger or
   Sphingomonas capsulata
   Intraluminal gliadin binding by polymers


2. Transepitelial uptake
   Epithelial tight junctions
   ZOT receptor antagonist AT1001


3. Adaptive immune response
   TG2
   TG inhibitors
   HLA-DQ2
   Blocking DQ2 analogs


4. Immune modulators
   Gluten vaccination


5. Biologicals (T cell or cytokine blockers)

Koletzko B, et al. (eds): Pediatric Nutrition in Practice. World Rev Nutr Diet. Basel, Karger, 2015, vol 113, pp 190–194
DOI: 10.1159/000367874