Allergic Disorders

Allergic illnesses have a significant impact that allergic diseases have on children's health and quality of life. Allergic diseases, including asthma, are among the major causes of chronic illnesses in the United States, affecting approximately 50 million patients or as many as one in five children. The economic impact is enormous; asthma alone is estimated to cost more than 6.2 billion dollars of health care expenditures annually. Of all the chronic illnesses, allergic respiratory problems, including allergic asthma, is the most common cause of school absenteeism. Even though allergic disease usually is not fatal, death can result as a consequence of allergic anaphylaxis related to medication, food, or insect venom allergy or from a complication of asthma. Therefore, the pediatrician must be capable of diagnosing allergic disease so as to institute appropriate management. This review will emphasize those clinical diagnostic features ascertained by history and physical examination as well as the appropriate laboratory studies useful in the diagnosis of respiratory (inhalant) and gastrointestinal (food) allergy.

General Features of Allergic Diseases
Allergic diseases are immunoglobulin E (IgE)-mediated immunologic illnesses that can affect any of the body's major organ systems either individually or collectively. Typically, children are not born having allergies because maternal IgE normally does not cross the placenta. In rare instances, neonates and young infants who apparently were sensitized in utero have been born with specific IgE to foods and had allergic reactions to those foods. Development of an allergy requires a familial predisposition and repeat exposure to an allergen (antigen) that provokes specific IgE antibody.
Epidemiologic surveys indicate that the familial trait for allergy is inherited as autosomal recessive. Whereas the frequency of positive allergy skin tests is similar in boys and girls, asthma is twice as common in males as in females prior to adolescence, but it appears equal in prevalence thereafter. A specific immune response gene has been identified for IgE antibody synthesis in rodents, but it has not yet been demonstrated conclusively in humans. With the recent advances in molecular genetics, it is anticipated that the genetic basis of allergy will be understood better in the near future.
Allergens sensitize by several potential routes and are categorized as inhalants, ingestants, injectants, and contactants (Table 1). It is important for the physician to define the route by which any specific allergen provokes clinical allergy in individual patients.
Of the inhalant IgE-mediated allergies, allergic rhinitis is by far the most common, affecting approximately 15% of all children. Asthma, of which 80% has an allergic inhalant basis, occurs in more than 5% of children. Gastrointestinal (ingestant) allergy typically is associated with food allergy; however, ingestants also may provoke urticaria and atopic dermatitis and less often may trigger respiratory symptoms. Anaphylaxis is a systemic generalized allergic response consisting of hypotension, urticaria, and angioedema as well as upper and lower airway obstruction; it can be caused by severe allergic reactions to foods (ingestant), insect venom stings (injectant), or medications (ingestant, injectant, or contactant).
Although incriminated anecdotally as the cause for hyperactivity, poor school performance, learning disabilities, or abnormal child behavior, there are no definitive, appropriately controlled studies that document an IgE allergic etiology for these predominantly psychosocial or educational problems. The possibility that overgrowth of a yeast such as Candida is important in the pathogenesis of allergy never has been substantiated. The concept of such a candidal syndrome in the context of abnormal child behavior has no validity, and antifungal therapy in the absence of overt clinical candidal infection should be discouraged.

Inhalant Allergy
Microscopic inhaled airborne allergens are responsible for most respiratory allergy (Table 2). In temperate climates, seasonal allergic rhinitis is induced by tree pollens in the early spring, grass pollens in the late spring and early summer, and ragweed in the late summer and early fall. Because of geographic differences in the US, clinicians must become familiar with the pollination patterns in their individual regions. Hay fever is an inappropriate term for allergic rhinitis because these patients neither are allergic to hay nor have fever. Flowering vegetation, such as roses and fruit blossoms, rarely cause allergy because these pollens are too heavy to become airborne; their germination is facilitated by bees and other insects. Fungi (mold) spores may be important outdoor aeroallergens in humid climates throughout the year, but their numbers decrease once there is significant frost in temperate climates. Fungi can be important indoor perennial allergens in damp environments. In perennial allergic rhinitis, house dust, animals, and molds all may be significant indoor inhalant allergens. The principal allergens in house dust are the cuticles and feces of the microscopic house dust mite Dermatophagoides. Animal allergens, such as epidermal danders, salivary proteins, urinary proteins, feces, and feathers, especially from pets such as cats, dogs, and birds are important because about 50% of households in the US have indoor animal pets. Food allergens are of lesser importance in the etiology of allergic rhinitis but cannot be ignored, especially in young children. Patients can be sensitive to one or multiple allergens. Certain individuals react to miniscule amounts of inhaled allergens, while others tolerate a large allergen dose before developing symptoms.
In addition to allergens, viral infections, aerosolized cosmetics, cigarette smoke, industrial fumes, and changes in temperature, humidity, and barometric pressure contribute to exacerbation of both upper and lower respiratory tract symptoms in the allergic child. Psychologic and social stresses also can enhance symptoms. The importance of these additional contributory factors varies greatly from patient to patient but should not be ignored when evaluating any individual.
Symptoms of nasal allergy consist of frequent sneezing, nasal pruritus, watery rhinorrhea, and often, nasal obstruction. Patients also may complain of red, itchy eyes as well as itchy throat and ears. If there is nasal obstruction, the patient will be a mouth breather and snoring can be a bedtime symptom; smell and taste also may be lost. Increased symptoms frequently are noted with increased exposure to the responsible allergen, such as after cutting grass or sleeping on a feather pillow.
When an allergic reaction develops, clear nasal secretions will be evident, and the nasal mucous membranes will become edematous without much erythema. The mucosa appear boggy and blue-gray. With continued exposure to the allergen, the turbinates will appear swollen and can obstruct the nasal airway. Conjunctival edema, itch, tearing, and hyperemia are frequent findings in patients who have associated allergic conjunctivitis. Patients who have allergic rhinitis, particularly children who have significant nasal obstruction and venous congestion, also may demonstrate edema and darkening of the tissues beneath the eyes. These so-called "shiners" are not pathognomonic for allergic rhinitis because they also can be seen in patients who have chronic rhinitis and/or sinusitis. Thick, purulent secretions indicate the presence of infection, including the possibility of sinusitis.

DIAGNOSTIC TESTS
Nonspecific Allergy Tests
Many pediatricians believe in the need for a screening test for allergy. Blood eosinophilia and total serum IgE levels have been proposed as screening tests, but they have relatively low sensitivity and should be used selectively (Table 3). The nasal secretions or sputum of patients who have a respiratory allergy contain increased numbers of eosinophils, which forms the basis of a useful nonspecific test, although not one that will identify any specific allergen etiology. Eosinophilia may not be present in patients who have not been exposed to allergens recently or who have a superimposed upper respiratory tract infection. Both systemic and inhaled steroids can reduce eosinophilia in secretions significantly; antihistamines have no direct effect on eosinophils.
The usefulness of nasal eosinophilia as a diagnostic test depends in large part on the technique used to obtain the specimens to prepare the slides for examination. Patients should expel nasal secretions onto wax paper or parafilm; secretions then are spread on a microscope slide, stained, and eosinophils counted under a microscope. It is difficult to quantify nasal eosinophilia accurately, although a finding of more than 3% eosinophils on stained smear of expelled nasal or bronchial secretions is considered increased. Because cotton or nylon nasal swabs trap secretions, they are not recommended for collecting secretions, except in the young child who will not or cannot expel secretions by blowing the nose. Peripheral blood eosinophilia is observed in allergic asthma but less commonly in allergic rhinitis. Blood eosinophilia is more frequent in atopic dermatitis and other conditions, such as parasite infection.
Total serum IgE is elevated in about 60% of patients who have allergic asthma but only in 30% of those who have allergic rhinitis. Unfortunately, commercial laboratories have promoted tests of total serum IgE excessively, but its usefulness in screening for allergy is limited to positive tests only because more than 60% of patients who have nasal allergy will have normal levels of total serum IgE.
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