You are on page 1of 7

Introduction

Background
Adverse food reactions can be broadly classified into 2 categories.1 The first category consists of immunologically-mediated adverse reactions to foods that are termed food allergies. Food allergies can result in disorders with an acute onset of symptoms following ingestion of the triggering food allergen (eg, anaphylaxis) and in chronic disorders (eg, atopic dermatitis). The second category is composed of adverse reactions that are not immune-mediated. An example is lactose intolerance caused by a deficiency of lactase. Adverse reactions to foods can also occur from toxic (eg, bacterial food poisoning) or pharmacologic (eg, caffeine) effects.

Pathophysiology
Food allergies are primarily the result of immune responses to food proteins.2 Normally, noninflammatory immune responses develop to ingested foods in a process called oral tolerance.3 For reasons that remain unclear, but likely include environmental and genetic factors, tolerance may be abrogated, leading to adverse immune responses. While sensitization (eg, development of an immunoglobulin E [IgE] immune response) to an allergen has been primarily assumed to occur from ingestion, this may not always be the case. For example, oral allergy syndrome (pollen-food related syndrome) describes an allergic response to specific raw fruits or vegetables that share homologous proteins with pollens; the initial route of sensitization is respiratory exposure to pollen proteins rather than oral exposure to food proteins. The skin may be another potential route of sensitization.4 IgE antibody – mediated responses are the most widely recognized form of food allergy and account for acute reactions. Patients with atopy produce IgE antibodies to specific epitopes (areas of the protein) of one or more food allergens. These antibodies bind to high-affinity IgE receptors on circulating basophils and tissue mast cells present throughout the body, including the skin, gastrointestinal tract, and respiratory tract. Subsequent allergen exposure binds and cross links IgE antibodies on the cell surface, resulting in receptor activation and intracellular signaling that initiates the release of inflammatory mediators (eg, histamine) and synthesis of additional factors (eg, chemotactic factors, cytokines) that promote allergic inflammation. The effects of these mediators on surrounding tissues result in vasodilatation, smooth muscle contraction, and mucus secretion, which, in turn, are responsible for the spectrum of clinical symptoms observed during acute allergic reactions to food. Cell-mediated responses to food allergens may also mediate allergic responses, particularly in disorders with delayed or chronic symptoms. For example, food protein – induced enterocolitis syndrome (FPIES), a gastrointestinal food allergy, appears to be mediated by T-cell elaboration of the cytokine tumor necrosis factor (TNF)-alpha.5 Persons with atopic dermatitis that flares with ingestion of milk have been noted to have T cells that, in vitro, express the homing receptor cutaneous lymphocyte antigen, which is thought to home the cell to the skin and mediate the

5%. such as peanut Ara h1. chicken egg white Gal d1.1-4.19 Based upon available studies. can occur following the ingestion of food.11. wheezing. Numerous food allergens are purified and well-characterized.9.6 Celiac disease is the result of an immune response to gluten proteins in grains.23.8% were obtained. and sesame. urticaria. Gal d2.14 In a metaanalysis including allergy to fruits and vegetables (excluding peanut).16 Recent studies from Canada and the United Kingdom indicate allergy rates to peanut of over 1% in children. and estimates of allergy varied widely from 0. wheat.3%. lead to the generation of specific IgE antibodies detectable by skin prick or in vitro testing) but less frequently crossreact clinically. laryngeal edema). 0. delayed allergic reactions to meat proteins have been attributed to reactions to carbohydrate moieties.4% for vegetables to under 1% for wheat. Considering allergy to milk.3% for fruits and tree nuts to 0.1-1. angioedema (eg. 2. 0.22. Closely related foods frequently contain allergens that crossreact immunologically (ie. dysphonia. .21.12 The actual prevalence of food allergies is estimated to be 5-6% in infants and children and 3. including death. Food allergens are typically water-soluble glycoproteins resistant to heating and proteolysis with molecular weights of 10-70 kd. refractory hypotension.15 Studies in the United States and the United Kingdom indicate a rise in peanut allergy among young children in the past decade.response.16. vomiting. and Gal d3. gastrointestinal tract. flushing. Fatalities result from severe laryngeal edema.13 However.17 One study showed an increase of peanut allergy in children from 0. this disorder is reviewed in the eMedicine Pediatrics article Celiac Disease. comprehensive studies that include oral food challenges are few in number. and Ara h3.8%. cough. stridor. or a combination thereof.4% in 1997 to 0. peanuts. Ara h2.13 Allergic reactions to non-protein food additives are uncommon. and soy. estimated rates of 1-10. These characteristics facilitate the absorption of these allergens across mucosal surfaces. 1. and seafood in a meta-analysis of 6 international studies using oral food challenges.20 Mortality/Morbidity  Severe anaphylactic reactions.4%. soybean-Gly m1. eggs. soy. fish-Gad c1. only 6 international studies included oral food challenges. and angioedema. peanut.24 Symptoms observed in a food-induced anaphylactic reaction may involve the skin.4%.7 % in adults. diarrhea. gradual test feeding) are used to confirm patient histories.8% in 2002.18. dyspnea.10 This high rate is not supported by controlled studies in which oral food challenges (a medically supervised. irreversible bronchospasm.8 Frequency General surveys report that as many as 25-30% of households consider at least 1 family member to have a food allergy. nausea. egg. and respiratory tract. 0.7 Recently. and shrimp-Pen a1. Frequently observed symptoms include oropharyngeal pruritus. estimations of the rate of food allergies in children have been summarized as follows for common food allergens: cow milk.

added spices or other ingredients). and (4) a delay or lack of immediate use of epinephrine to treat the allergic reaction. though anaphylactic reactions have been reported to a wide variety of foods.21. the prevalence of food allergy is approximately 5-6%. o Determine the minimum quantity of food exposure required to cause the symptoms. raw. Race  No predilection is known. Sex  Among children.23.7%. o Discuss the manner of preparation of the food (cooked.16 Age   In infants and children younger than 3 years. inhalation) and dose  The timing of the onset of symptoms in relation to food exposure  All observed symptoms and each one’s severity  The duration of the reaction  The treatment provided and the clinical response to treatment  The most recent reaction o Inquire about a personal or family history of other allergic disease. skin contact. especially in patients with poorly controlled disease. . males appear to be more affected. fish. tree nuts. and shellfish are the foods most often implicated in severe foodinduced anaphylactic reactions.22. Fatalities caused by reactions to milk are increasingly noted. (3) a failure to recognize early symptoms of anaphylaxis.13 The estimated prevalence in adults is approximately 3. o Determine the reproducibility of symptoms upon exposure to the food.  Peanuts. females are more frequently affected.13 Clinical History  Necessary elements of a thorough medical history o Develop a complete list of all foods suspected to cause symptoms. (2) previous episodes of anaphylaxis with the incriminated food.24 Teenagers and young adults appear to be overrepresented in registries of food allergy fatalities and present a special risk group. o Obtain a thorough description of each reaction. including the following:  The route of exposure (ingestion. among adults.22 Risk factors or associations for fatal food-induced anaphylaxis include: (1) the presence of asthma.

IgE-mediated gastrointestinal food allergy o These food allergy reactions include immediate hypersensitivity reactions and the pollen-food allergy syndrome (oral allergy syndrome). o Food allergy is rarely the cause of chronic urticaria or angioedema. initial reintroduction of the food after a period of dietary elimination has resulted in more significant symptoms than were observed when the food was regularly ingested. individuals with ragweed allergy may experience oropharyngeal symptoms following the ingestion of bananas or melons. In addition. in some instances. o Elimination of gluten from the diet usually leads to resolution of skin symptoms. o Symptoms range from acute urticaria (most common) to flushing to angioedema to exacerbations of atopic dermatitis. nonsteroidal anti-inflammatory drugs [NSAIDs]. Studies show that of patients with moderate chronic atopic dermatitis.32 o Prophylactic studies show that avoiding particular foods (eg.31 Reintroduction of a suspected food allergen should be performed under medical supervision because. and uvula and a sensation of tightness in the throat may be observed. It is a blistering skin disorder that manifests clinically with a chronic and intensely pruritic rash with a symmetrical distribution. reintroduction of the food exacerbates the atopic dermatitis. Diarrhea is found less frequently.28. and cramping. In fewer than 3% of cases. For example. Atopic dermatitis27 o Controversy surrounds the role of food allergy in the pathogenesis of atopic dermatitis.o Inquire about eliciting factors that can potentiate a food-allergic reaction (eg. such as laryngeal edema or hypotension. Pollen-food allergy syndrome (oral allergy syndrome) o Patients with this syndrome develop itching or tingling of the lips. abdominal pain. 35-40% have IgE-mediated food allergy. exercise25 . Dermatitis herpetiformis o This is a form of non-IgE cell-mediated hypersensitivity related to celiac disease. edema of the lips. symptoms progress to more systemic reactions. and throat following the ingestion of certain foods.30. eggs.33 Celiac disease: Celiac disease is the result of an immune response to gluten proteins in grain. vomiting. cow milk.34 o This syndrome is caused by cross-reactivity between certain pollen and food allergens. tongue. alcohol) Clinical manifestations and disorders26       Cutaneous reactions o These are the most common clinical manifestations of an allergic reaction to a food or food additive. tongue. peanuts) helps delay the onset of atopic dermatitis. o Specific gastrointestinal symptoms include nausea. and . palate. This disorder is reviewed in the eMedicine Pediatrics article Celiac Disease. o Removal of a specific food allergen leads to reduction or resolution of clinical symptoms in affected patients.29 o Both food-specific IgE-mediated and cellular mechanisms appear responsible for chronic eczematous inflammation.

and failure to thrive. o Breastfed infants may have mucus and blood in their stool. An oral food challenge may establish the diagnosis but is not always needed if the history is clear. corticosteroids) may be needed. however. The presentation may mimic sepsis. o Children may experience weight loss or failure to thrive. This allergic proctocolitis does not typically lead to anemia and is not associated with vomiting or poor growth. Eosinophilic esophagitis does not respond to acid blockade therapy. lethargy. and. skin. endoscopy and biopsy must be performed in order to establish the presence of eosinophils in the affected segment of the gut. o CBC count and differential findings may show eosinophilia in approximately 50% of patients. peach or hazelnut. nasal pruritus.38. apple. Mixed IgE/non-IgE gastrointestinal food allergy (eosinophilic esophagitis and gastroenteritis)35 o Symptoms vary according to location of eosinophilia. Maternal exclusion of the allergen resolves the bleeding. Eosinophilic esophagitis may manifest as reflux symptoms and dysphagia. o In addition to diet therapy (or in place of diet therapy). involvement is patchy and variable. primarily cow milk. Non–IgE-mediated gastrointestinal food allergy o Food protein – induced enterocolitis syndrome typically manifests in the first few months of life with severe projectile vomiting. While a dense eosinophil infiltrate may be seen anywhere from the lower esophagus through the large bowel.2 Additional causes of bleeding (eg. food impaction can occur as well. increase in the peripheral blood polymorphonuclear leukocyte count. o Infants who are chronically ingesting the allergen typically appear lethargic. Upper and lower respiratory tract reactions o Upper respiratory reactions typically include nasal congestion. diarrhea. However. diarrhea. Re-exposure prior to resolution results in a delayed (2 h) onset of vomiting. later.   patients with birch pollen allergy may experience these symptoms following the ingestion of raw carrots. wasted. Typically. infection. solid foods may also trigger these reactions. or bronchospasm. celery. symptoms resolve. this is not diagnostic. o IgE-mediated pulmonary symptoms may include laryngeal edema. or rhinorrhea. treatment with antiinflammatory medications (eg. sneezing. Hypotension and methemoglobinemia may occur. o An elemental (no potential allergens) or oligoantigenic diet (a diet that removes common allergenic foods) and trials of food elimination may be required to determine the role of foods in a patient's condition. Typical symptoms include postprandial nausea. No other definitive diagnostic tests are available. especially rice and oats. or gastrointestinal symptoms. potato. They are usually observed in conjunction with ocular. attributed to food allergens ingested by the mother.36 o Cow milk and soy protein formulas are usually responsible for these reactions. and a sensation of early satiety.37 o When the allergen is removed from the diet. Eosinophilic inflammation of the rectum is noted if a biopsy is performed. cough. abdominal pain. fissures) should be considered. and dehydrated. .

Therefore. Food-induced anaphylaxis o Following the ingestion of food. only 5 (2%) of these patients had wheezing as their only objective adverse symptom. periocular swelling  Nasal congestion. and sneezing  Stridor  Dysphonia  Cough  Dyspnea  Wheezing. which included wheezing. 320 children with atopic dermatitis undergoing blinded food challenges at Johns Hopkins Hospital were monitored for respiratory reactions.41 o In a pediatric case-controlled study comparing 19 children who required ventilation for an exacerbation of asthma and 38 control subjects matched by sex. conjunctival edema. rhinorrhea. laryngeal edema)  Urticaria  Ocular injection. o At the National Jewish Center for Immunology and Respiratory Medicine. severe anaphylactic reactions (ie. age. can occur. nasal pruritus. a conservative estimate is that 5-10% of patients with asthma have food-induced allergy symptoms. gastrointestinal blood loss. Food-induced pulmonary hemosiderosis (Heiner syndrome) o This is a rare disorder characterized by recurrent episodes of pneumonia associated with pulmonary infiltrates. and failure to thrive in infants.42 o Wheezing as the only manifestation of an allergic reaction to food is rare. Interestingly. hemosiderosis.40 o In a related report. including death. ocular pruritus. and ethnicity. 34 (17%) of 205 children with positive results from food challenges developed wheezing as part of their reaction. systemic allergic reactions). bronchospasm  Nausea  Emesis  Abdominal pain  Diarrhea  A feeling of impending doom  Cardiovascular collapse 24 o Anaphylaxis can occur without skin symptoms . o Symptoms may include the following:  Oropharyngeal pruritus  Angioedema (eg. coincident food allergy was found to be independently associated with life-threatening asthma. Overall. 67 (24%) of the 279 children with a history of food-induced asthma were documented to have a positive result after a blinded food challenge.   Asthma39 o The role of food allergy in the pathogenesis of asthma is a controversial area of investigation. iron deficiency anemia. o While the precise immunologic mechanism is unknown. it is thought to be secondary to a non-IgE hypersensitivity process.

or asthma. soy.22 . Findings from a comprehensive physical examination can help rule out other conditions that may mimic food allergy. and shellfish. and wheat are the foods most often implicated in allergic reactions that have been confirmed in well-controlled blinded food challenges. and signs of other allergic disease. however.24. only a small group of foods account for most of these reactions. but when exercise follows ingestion of a specific food or foods. Causes    Any food protein can trigger an allergic response. although milk has been increasingly reported. anaphylaxis results. and allergic reactions to a large number of foods have been documented. Eggs. peanuts. milk. exercise-induced anaphylaxis describes a disorder in which exercise is tolerated and a food or foods are tolerated. Sesame appears to be an emerging allergen.43 Physical   The physical examination findings are most useful for assessing overall nutritional status. fish. Investigations of near-fatal or fatal anaphylactic reactions following food ingestion reveal that most are caused by peanuts. tree nuts. such as atopic dermatitis. shellfish.o Food-associated. allergic rhinitis. growth parameters. tree nuts.