Food Allergy

Introduction

 An adverse food reaction is a general term for any untoward response to the ingestion
of a food.
 Adverse food reactions can be divided into food allergies, which are immunologically
mediated, and all other reactions, which are nonimmunologic (food intolerances,
lactose intolerance)
 Worldwide, estimates of food allergy prevalence range from 1–10%;
 food allergies affect an estimated 3.5% of the U.S. population.
 Up to 6% of children experience food allergic reactions in the 1st 3 yr of life, including
approximately 2.5% with cow’s milk allergy, 2% with egg allergy, and 2–3% with
peanut allergy.
Adverse Food Reactions
Pathogenesis

 Food intolerances are the result of a variety of mechanisms, whereas food allergy is
predominantly caused by IgE-mediated and cell-mediated immune mechanisms.
 When food allergens penetrate mucosal barriers and reach cell-bound IgE antibodies,
mediators are released that induce vasodilation, smooth muscle contraction, and mucus
secretion, which result in symptoms of immediate hypersensitivity (allergy)
 acute IgE-mediated reactions can affect the skin (urticaria, angioedema, flushing),
gastrointestinal (GI) tract (oral pruritus, angioedema, nausea, abdominal pain, vomiting,
diarrhea), respiratory tract (nasal congestion, rhinorrhea, nasal pruritus, sneezing, laryngeal
edema, dyspnea, wheezing), and cardiovascular system (dysrhythmias, hypotension, loss
of consciousness)
Pathogenesis

 Children who develop IgE-mediated food allergies may be sensitized by food allergens
penetrating the GI barrier, referred to as class 1 food allergens, or by food allergens that
are partially homologous to plant pollens penetrating the respiratory tract, referred to
as class 2 food allergens.
 Any food may serve as a class 1 food allergen, but egg, milk, peanuts, tree nuts, fish,
soy, and wheat account for 90% of food allergies during childhood.
 Class 2 food allergens are typically vegetable, fruit, or nut proteins that are partially
homologous with pollen proteins
Clinical Manifestation

 Gastrointestinal Manifestations
 Skin Manifestations
 Respiratory Manifestations
 Anaphylaxis
Gastrointestinal Manifestations

 GI food allergies are often the 1st form of allergy to affect infants and young
children and typically manifest as irritability, vomiting or “spitting- up,”
diarrhea, and poor weight gain
 Food protein–induced enterocolitis syndrome (FPIES) typically manifests in
the 1st several mo of life as irritability, intermittent vomiting, and protracted
diarrhea and may result in dehydration
 Vomiting generally occurs 1-4 hr after feeding, and continued exposure may
result in abdominal distention, bloody diarrhea, anemia, and failure to thrive.
 Symptoms are most often provoked by cow’s milk or soy protein–based
formulas
 FPIES usually resolves by age 3-5 yr.
Gastrointestinal Manifestations

 Food protein–induced allergic proctocolitis (FPIAP) presents in the 1st few mo

of life as blood-streaked stools in otherwise healthy infants
 Approximately 60% of cases occur among breastfed infants, with the remainder
largely among infants fed cow’s milk or soy protein–based formula.
 Blood loss is typically modest but can occasionally produce anemia.
 Food protein–induced enteropathy (FPE) often manifests in the 1st several mo
of life as diarrhea, often with steatorrhea and poor weight gain
 Symptoms include protracted diarrhea, vomiting in up to 65% of cases, failure to
thrive, abdominal distention, early satiety, and malabsorption.
 Anemia, edema, and hypoproteinemia occur occasionally.
Gastrointestinal Manifestations

 Cow’s milk sensitivity is the most common cause of FPE in young infants, but it has
also been associated with sensitivity to soy, egg, wheat, rice, chicken, and fish in older
children.
 Oral allergy syndrome (pollen-associated food allergy syndrome) is an IgE-mediated
hypersensitivity that occurs in many older children with birch and ragweed pollen
induced allergic rhinitis.
 Symptoms are usually confined to the oropharynx and consist of the rapid onset of oral
pruritus; tingling and angioedema of the lips, tongue, palate, and throat; and
occasionally a sensation of pruritus in the ears and tightness in the throat.
 Symptoms are generally short lived and are caused by local mast cell activation
following contact with fresh raw fruit and vegetable proteins that cross-react with
birch pollen (apple, carrot, potato, celery, hazel nuts, peanuts, kiwi, cherry, pear), grass
pollen (potato, tomato, watermelon, kiwi), and ragweed pollen (banana, melons such as
watermelon and cantaloupe).
Symptoms of Food-Induced Allergic
Reactions
 Clinical features of food protein-
induced enterocolitis syndrome (FPIES)
Skin Manifestations

 Atopic dermatitis -is a form of eczema that generally begins in early infancy and is
characterized by pruritus, a chronically relapsing course, and association with asthma
and allergic rhinitis. at least 30% of children with moderate to severe atopic dermatitis
have food allergies.
 Acute urticaria and angioedema-The onset of symptoms may be very rapid, within
minutes after ingestion of the responsible allergen. Symptoms result from activation of
IgE- bearing mast cells by food allergens that are absorbed and circulated rapidly
throughout the body (egg, milk, peanuts, and nuts, sesame, fruits (kiwi)
 Perioral dermatitis is often a contact dermatitis caused by substances in toothpaste,
gums, lipstick, or medications.
 Perioral flushing is often noted in infants fed citrus fruits and may be caused by benzoic
acid in the food.
Respiratory Manifestations

 Respiratory food allergies are uncommon as isolated symptoms.

 many parents believe that nasal congestion in infants is often caused by milk allergy,
studies show this not to be the case.
 Food-induced rhinoconjunctivitis - symptoms typically accompany allergic symptoms
in other target organs, such as skin, and consist of typical allergic rhinitis symptoms
(periocular pruritus and tearing, nasal congestion and pruritus, sneezing, rhinorrhea)
 Wheezing occurs in approximately 25% of IgE- mediated food allergic reactions, but
only 10% of asthmatic patients have food-induced respiratory symptom
Diagnosis

 medical history is necessary to determine whether a patient’s symptomatology

represents an adverse food reaction
 The following facts should be established:
 (1) the food suspected of provoking the reaction and the quantity ingested
 (2) the interval between ingestion and the development of symptoms
 (3) the types of symptoms elicited by the ingestion
 (4) whether ingesting the suspected food produced similar symptoms on other
occasions
 (5) whether other inciting factors, such as exercise, are necessary
 (6) the interval from the last reaction to the food.
Diagnosis

 Skin-prick tests and in vitro laboratory tests are useful for demonstrating IgE
sensitization, defined as presence of food-specific IgE antibodies.
 A negative skin test result virtually excludes an IgE-mediated form of food
allergy.
 Conversely, most children with positive skin test responses to a food do not
react when the food is ingested, so more definitive tests, such as quantitative
IgE tests or food elimination and challenge, are often necessary to establish a
diagnosis of food allergy.
Treatment
 Appropriate identification and elimination of foods responsible for food
hypersensitivity reactions are the only validated treatments for food allergies
 Complete elimination of common foods (milk, egg, soy, wheat, rice, chicken, fish,
peanut, nuts) is very difficult because of their widespread use in a variety of processed
foods
 Children with asthma and IgE-mediated food allergy, peanut or nut allergy, or a history
of a previous severe reaction should be given self- injectable epinephrine and a written
emergency plan in case of accidental ingestion
 Because many food allergies are outgrown, children should be reevaluated periodically
by an allergist to determine whether they have lost their clinical reactivity.
 A number of clinical trials are evaluating the efficacy of oral, sublingual, and
epicutaneous (patch) immunotherapy for the treatment of IgE-mediated food allergies
(milk, egg, peanut).
 Combining oral immunotherapy with anti-IgE treatment (omalizumab) may improve
safety compared to oral immunotherapy alone.
ACIP and AAP Recommendations for Administering Vaccines to Patients With Egg Allergy
Milk allergy: Management

 Management of cow's milk allergy (CMA) includes instructions about

avoidance of cow's milk (CM) protein, replacement of CM with alternative
protein and calcium sources
 Eliminating CM from the diet can be difficult and can pose nutritional as well
as quality-of-life concerns since CM is a ubiquitous food in many cultures and
diets and is an important source of fat and protein in early childhood.
 Counseling should include a discussion about CM alternatives
 In addition, evaluation of the allergy followed by an oral food challenge (OFC)
to extensively heated CM is an option since a majority of those with CMA will
tolerate CM in extensively heated (baked) products, such as a muffin
 Autoinjectable epinephrine – Patients with immunoglobulin E (IgE)
mediated CMA are at risk for severe reactions
Nutrients to be replaced on a cow's milk
avoidance diet and alternative dietary sources
Prevetion

 exclusive breastfeeding for the 1st 4-6 mo of life may reduce allergic disorders
 Potentially allergenic foods (eggs, milk, wheat, soy, peanut/tree nut products, fish)
should be introduced after this period of exclusive breastfeeding.
 Use of hydrolyzed formulas may be beneficial if breastfeeding cannot be continued for
4-6 mo or after weaning
 Probiotic supplements may also reduce the incidence and severity of eczema.
 Because some skin preparations contain peanut oil, which may sensitize young infants,
especially those with cutaneous inflammation, such preparations should be avoided.
 Since inflamed/disrupted skin barrier is a risk factor for food allergy, trials are
underway to enhance the skin barrier from birth, using emollients and decreasing
bathing frequency, to reduce the incidence of atopic dermatitis in high-risk neonates.