CHAPTER 95
Allergic Disease
Nasser Redjal, MD, and Niloufar Tehrani, MD
CASE STUDY
A 3-year-old girl is rushed to an urgent care center by her mother after the girl developed a pruritic rash, facial swelling, and hoarseness shortly after eating a peanut butter sandwich. She had eaten peanut butter once before, and her parents noticed a few small hives on her cheek that self-resolved. Previously, the girl has been well except for recurrent nasal congestion every spring that has responded to antihistamines. She has also had an intermittent skin rash that has been managed with topical steroid creams. She has never before had an acute reaction and has no history of asthma. Her father had asthma as a child.
Physical examination reveals a well-developed, 3-year-old girl with marked facial swelling and a generalized rash who is in mild respiratory distress. Vital signs, including blood pressure, are normal. The girl has a diffuse, blotchy, erythematous rash with central wheals; a hoarse voice; and a mild expiratory wheeze on auscultation of her chest. The remainder of the examination is normal.
Questions
1. What are the various symptoms of allergic disease?
2. What is the appropriate evaluation of a child with manifestations of allergic disease?
3. What allergens are common triggers for allergic symptoms?
4. What treatment is helpful for the child with manifestations of allergic disease?
5. Can allergic disease be prevented?
Allergic disease occurs frequently in the general population and manifests in many ways. Types of allergic disease include asthma, atopic dermatitis, allergic rhinitis, allergic conjunctivitis, urticaria, angioedema, anaphylaxis, and food, insect, and drug allergies. Allergic symptoms result from the production of specific immunoglobulin (Ig) E antibody after exposure to a foreign antigen. The process has 2 steps. The first step is the sensitization or antibody induction stage. The individual develops IgE antibody against an inhaled, ingested, or injected substance. The process usually takes from several days to weeks for medications and foods to months to years for inhalant allergens, such as pollens. Newly formed antigen- specific IgE antibody adheres to IgE receptors on circulating blood basophils or to tissue mast cells. On reexposure, the allergen binds to several specific IgE antibodies on the surface of these cells and triggers degranulation of preformed and rapidly formed mediators, such as histamine and leukotrienes, resulting in the early phase of the reaction. Clinically, this is manifested by sneezing, rhinorrhea, and pruritus in allergic rhinitis; wheal and/or flare in urticaria or angioedema; and shock in anaphylaxis. Mast cell degranulation also releases peptides that attract inflammatory peptides, such as interleukin-4 and interleukin-5, which release mediators that result in chronic inflammation. This late phase of inflammation is responsible for congestion and hyperreactive mucosa in allergic rhinitis and delayed reactions in anaphylaxis. The remaining manifestations of allergies, including allergic rhinitis, conjunctivitis, food allergies, and anaphylaxis are the focus of this chapter.
Epidemiology
Allergic disease or some form of allergic symptoms occur in 12% to 20% of the general population in the United States. The prevalence of symptoms varies depending on the population being investigated. Factors such as age, genetic background, and place of residence are significant. Allergic rhinitis occurs in 10% of children, as does asthma. Up to 6% of children younger than 3 years develop food allergies. Urticaria occurs at some time in approximately 10% to 20% of the population.
It is generally accepted that if neither parent is atopic (ie, has the allergic tendency to manufacture IgE on antigen exposure), the chance that a child of theirs will develop allergic symptoms is less than 1 in 5. If 1 parent is atopic, however, the risk doubles. If both parents are atopic, the chance of their child developing allergic symptoms is better than 3 in 5.
Clinical Presentation
Children with allergic disease frequently present with persistent, clear rhinorrhea; sneezing; postnasal drip; or injected pruritic conjunctivitis. Skin manifestations include dry, scaling, erythematous rashes; wheals; and subcutaneous swelling (Box 95.1). A recurrent cough or wheezing on chest examination is further evidence of allergic disease.
Pathophysiology
Allergic rhinitis, like all allergic manifestations, is caused primarily by an antigen-antibody reaction involving IgE. Antigen-specific IgE is produced by the B lymphocytes of allergic patients on exposure to a particular antigen, which attaches to immune cell receptors located on basophils in the circulation and mast cells in the tissue. On reexposure, the antigen reacts with this specific IgE on the mast cells, releasing vasoactive mediators, including histamine, leukotrienes, kinins, and prostaglandins. These mediators produce vasodilation and edema, and they also stimulate neural reflexes to produce mucous hypersecretion and sneezing. Eosinophils, basophils, and other inflammatory cells induced by chemotactic factors enter the affected organ, releasing mediators and thereby worsening the inflammation and damaging tissues. Secretions and released tissue proteins exacerbate existing edema. Other immunologic mechanisms can also be involved.
Box 95.1. Diagnosis of Allergic Disease in the Pediatric Patient
•Chronic, clear rhinorrhea
•Nasal congestion
•Conjunctival tearing and pruritus
•Conjunctival injection
•Wheezing
•Chronic cough
•Postnasal drip
•Mouth breathing
•Snoring
•Skin findings of atopic dermatitis or urticaria
•Seasonal variability of symptoms
•Occurrence of symptoms after exposure to an antigen
•Family history of allergic disease
•Acute onset of symptoms following exposure to possible allergen
Children with allergic rhinitis often present with rhinorrhea, sneezing, nasal pruritus, and congestion. Allergic eye symptoms (ie, allergic rhinitis, conjunctivitis) may accompany nasal rhinitis with ocular pruritus, injection of the conjunctiva, and clear tearing. Younger children may present with repeated sniffing, snorting, coughing, or scratching an itchy palate with their tongue (ie, palatal clicking) because they usually cannot blow their nose.
Urticaria, the clinical rash produced by capillary leak vasodilation and edema of the skin, occurs when histamine and other vasoactive peptides, such as prostaglandins and leukotrienes, are released from the epidermal mast cells. Basophils have been identified in biopsies of these lesions. Mast cell degranulation occurs commonly in sensitized patients on reexposure to antigens found in food, medications, supplements, and insect venom when antigen-specific IgE found on mast cells is triggered by these allergens. The mast cell, however, can also be activated and release mediators by a wide number of stimuli independent of IgE mechanisms, including viral, bacterial, parasitic, and fungal infections; collagen vascular disease; malignancy; and endocrine disease. Some patients also experience urticaria to physical factors, such as heat, cold, pressure, sun, and vibration.
An urticarial rash appears as erythematous lesions of various sizes with pale, papular centers that typically are not painful unless traumatized by scratching. Lesions may coalesce, the rash blanches on pressure, and the skin is intact. Usually, individual lesions last less than 24 hours at a single location, although they often recur in the same area.
Angioedema is the extension of the urticarial process deeper into the dermis of the skin, producing swelling. The mucous membranes may be affected. Pathophysiology is similar to that of urticaria. A hereditary type of angioedema, which is not allergy related, is caused by an inherited deficiency of the C1 esterase inhibitor, resulting in unopposed production of the potent vasoactive amine bradykinin. Unlike urticaria, no distinct rash exists and the skin is not pruritic. Capillary leak and edema of the dermis results in tissue swelling, a sense of tightness, and sometimes pain. Involvement of the abdominal viscera may result in colicky abdominal pain.
Chronic urticaria and angioedema is that which persists beyond 6 weeks. More than 90% of chronic urticaria and angioedema in an otherwise healthy patient is idiopathic and is termed chronic idiopathic urticaria. Up to one-half of patients with chronic idiopathic urticaria have the circulating mast cell anti-IgE receptor antibody IgG, which repeatedly causes degranulation of cutaneous mast cells in these patients.
Anaphylaxis is an acute, systemic allergic reaction resulting from antigen-specific IgE on mast cells and basophils. Pathophysiology is similar to that of allergic rhinitis, but the reaction occurs in mast cells in many locations simultaneously, and prior sensitization to an allergen is essential. Anaphylactic reactions may be life-threatening. Massive vasoactive mediator release results in large reductions in peripheral resistance caused by capillary leak and vasodilation. This eventually overwhelms compensatory increases in cardiac output (blood pressure = cardiac output × total peripheral resistance), resulting in hypotension and shock. Pooling of blood in the periphery also reduces venous return, resulting in diminished preload and cardiac output. Reactions can occur in seconds or as late as 1 hour after exposure. Up to 20% of adults and 15% of children may experience a late or biphasic phase (ie, a recurrence of symptoms after resolution of anaphylaxis without trigger reexposure) hours after the first reaction because of late recruitment and activation of basophils and other inflammatory cells. Children with anaphylaxis have a reduced risk for late phase reaction, likely of approximately 3% to 5%. Common causes of anaphylaxis include food, medications and biologic agents, and stinging insect venom. The drug most frequently implicated in anaphylaxis is penicillin. Patients initially experience tightness and intense itching of the skin. Nausea, vomiting, and abdominal pain may ensue, followed by the full spectrum of anaphylaxis. Certain agents, such as radiocontrast media and blood products, may cause massive mast cell degranulation via an IgE-independent mechanism, resulting in clinical symptoms that are indistinguishable from anaphylaxis; these reactions, termed anaphylactoid reactions, are generally less severe than anaphylaxis.
Confusion exists among less experienced clinicians as to what combination of symptoms constitutes anaphylaxis, which may result in either overdiagnosis or underdiagnosis. Generally, anaphylaxis is highly likely in the setting of cutaneous findings plus respiratory or hemodynamic compromise; involvement of 2 or more of the following systems: skin, respiratory, and gastrointestinal (GI) organ; and hemodynamic compromise (Box 95.2).
A food allergy may produce IgE-mediated reactions and diseases, including acute urticaria or angioedema, anaphylaxis, acute rhinitis, and atopic dermatitis. The localization of IgE-sensitized mast cells to that specific antigen determines the symptoms produced by an allergy. The antigen enters through the GI mucosal barrier. Intact food proteins may enter the circulation, stimulating the production of antigen-specific IgE. Additionally, food allergens may result in some non–IgE-mediated diseases, including eosinophilic esophagitis, food protein-induced enterocolitis syndrome (FPIES), allergic proctocolitis, and Heiner syndrome, a rare reaction to cow’s milk protein. Finally, many patients have a nonimmune-mediated reaction to foods termed food intolerance (eg, lactose intolerance).
In young children, the most common food allergens are milk, egg, soy, wheat, peanuts, and tree nuts, whereas adults and older children are allergic to peanuts, shellfish, and fish. Adults and older children with atopic predisposition and allergic rhinitis or asthma often become sensitized to tree and weed pollens via the respiratory tract. They exhibit cross-reactivity between common elements of these inhalant tree or weed pollen peptides and similar peptides found in fruits and vegetables, resulting in local (ie, oral) IgE symptoms of tingling and mild swelling when ingesting these foods. These mild reactions are called pollen-food allergy syndrome.
Patients with IgE-mediated food allergy may experience urticaria or angioedema, eczematoid dermatitis, vomiting, wheezing, and, in severe cases, anaphylaxis. Eosinophilic esophagitis presents with nonspecific symptoms, including vomiting, reflux, dyspepsia, poor appetite, and failure to thrive. Infants with FPIES present with severe vomiting and bloody stool, generalized edema, and, in some cases, shock on initial ingestion of cow’s milk, although soy and other foods have, in rare cases, been implicated. Allergic proctocolitis presents in infants on first exposure to cow’s milk protein, including via human milk, but symptoms are mild and involve only blood-streaked stool. Heiner syndrome is a rare IgG-mediated reaction to cow’s milk protein that results in anemia, wheezing, hemoptysis, melena, and pulmonary infiltrates. Older patients with pollen-food allergy syndrome to fruits and vegetables experience lip, oral mucosa, and tongue tingling as well as minimal swelling. These reactions are local and mild and rarely progress to anaphylaxis.
Box 95.2. Practical Definition of Anaphylaxis
One of the following criteria is fulfilled:
1. Acute onset of mucosa or cutaneous findings, such as hives, pruritus, lip swelling, AND 1 of the following:
•Respiratory compromise
•Cardiovascular compromise (eg, hypotension) or end-organ dysfunction (eg, syncope)
2. TWO of the following after likely exposure to allergen:
•Respiratory compromise
•Mucocutaneous symptoms
•Hypotension
•Persistent gastrointestinal symptoms
3. Reduced blood pressure appropriate for age
Adapted from Sampson HA, Muñoz-Furlong A, Campbell RL, et al. Second symposium on the definition and management of anaphylaxis: summary report—second National Institute of Allergy and Infectious Disease/Food Allergy and Anaphylaxis Network symposium. Ann Emerg Med. 2006;47(4):373–380, with permission.
Differential Diagnosis
Most patients with allergic rhinitis have clearly identifiable signs and symptoms consistent with a history of exposure; other etiologies should be considered, however, especially with poor response to treatment. Children experience many upper viral respiratory infections each year that can mimic allergic rhinitis. Many types of nonallergic rhinitis exist and the mechanisms responsible are unclear, although cholinergic pathways are likely involved. Vasomotor and cholinergic rhinitis often result in copious amounts of clear rhinorrhea in response to cholinergic stimuli, such as cold air (ie, skier nose) or spicy foods (ie, gustatory rhinitis). Medications such as angiotensin- converting enzyme inhibitors and nonsteroidal anti-inflammatory drugs may cause rhinitis, but this usually occurs in adults and older children. Similarly, hormone surges, such as during ovulation, may result in nasal symptoms. Overuse of topical decongestants containing α-agonists results in rebound rhinitis (ie, rhinitis medicamentosa). In children, foreign bodies produce unilateral nasal obstruction and often malodorous purulent discharge. Patients with a history of basilar skull fracture with cerebrospinal fluid leak may present with clear rhinorrhea.
Urticaria and angioedema have a distinct clinical presentation that is usually easy to distinguish from other skin conditions. As mentioned previously, numerous possible etiologies of urticaria and angioedema exist, and determining the cause of a given instance is challenging. Urticaria and angioedema may last for weeks; however, individual lesions should persist for less than 24 hours, although they can recur at 1 area. Urticarial vasculitis is a distinct form of urticaria that results from the persistence of antigens arising from collagen vascular disease, serum sickness, and neoplasia. The rash from urticarial vasculitis lasts for more than 24 hours, has a burning sensation, causes less pruritus than other forms of urticaria, and leaves an area of hyperpigmentation on resolution. Other rashes that mimic urticaria include insect bites, erythema multiforme, mastocytosis, and contact dermatitis. Anaphylaxis is usually associated with cutaneous, respiratory, cardiovascular, and systemic symptoms, such as skin rash, edema, wheezing, arrhythmia, occasionally fever, and shock. A history of an acute exposure to a potential allergen is more likely to be seen with anaphylaxis than with urticaria.
Signs and symptoms of food allergies vary. It is important to determine whether actual immune-mediated disease exists or if the patient has food intolerance. Food may contain toxic peptides, such as in scombroid fish poisoning, in which bacteria in unrefrigerated fish convert amino acids into histamine, which results in allergy-like symptoms when ingested. Patients with enzyme deficiencies, such as lactose intolerance, experience GI symptoms when eating dairy products. Alternatively, food may have pharmacologic properties, such as those found in caffeinated drinks.
Figure 95.1. Characteristic facial features in children with allergic diseases. A, Allergic shiner. B, Allergic salute. C, Adenoid facies.
Non–IgE-mediated food allergies may produce signs and symptoms similar to other disorders that can be life-threatening, such as FPIES, which often is indistinguishable from sepsis; Heiner syndrome, which shares similarities with serious diseases (eg, pulmonary hemosiderosis); and Wegener granulomatosis. These conditions must be ruled out during the evaluation of these forms of food allergies.
Most patients with symptoms associated with foods do not have an immune-mediated reaction but have food intolerances. Some manifestations have well-defined mechanisms, such as in lactase deficiency or galactosemia, whereas others, such as gustatory rhinitis, are less clear.
Evaluation
History and Physical Examination
Allergic Rhinitis and Conjunctivitis
The child with possible allergic rhinitis has a history of sneezing, itching, nasal discharge, and nasal blockage. The eyes, ears, palate, and throat may itch. The child may also have a history of mouth breathing and snoring at night, sleep disturbances, and daytime fatigue from nasal obstruction. Other signs include sinusitis, postnasal drip, halitosis, cough, and morning sore throat. Symptoms may be seasonal or associated with a specific stimulus. Additionally, systemic symptoms of fatigue, headache, anorexia, and irritability may be present.
The history should also include a search for other manifestations of allergies (eg, wheezing, atopic dermatitis). Approximately 40% of children who present with allergic symptoms also have asthma, 50% have atopic dermatitis, and about 30% have allergic rhinitis. It is also important to obtain an environmental history of allergen exposure, including pets and tobacco smoke, as well as a family history of atopy.
The physical examination should be thorough. The skin should be inspected for atopic dermatitis and the lungs for evidence of asthma. The nasal mucosa should be examined with an otoscope. In the child with allergic rhinitis, the nasal mucosa is swollen, pale, and sometimes cyanotic with copious clear discharge. Nasal polyps, if present, should be noted. Although polyps are most often present on an allergic basis, they may occur with cystic fibrosis. A transverse crease across the nose (ie, allergic crease) can occur from repeatedly using the palm of the hand in an upward thrust on the nares to relieve itching and open the nasal airway (ie, allergic salute). Dark circles under the eyes (ie, allergic shiners) may be present from chronic periorbital edema and venous stasis. Morgan fold (ie, Dennie-Morgan fold), a wrinkle just beneath the lower eyelids, is present from early infancy and is associated with atopic dermatitis and allergic rhinitis. Adenoid facies (ie, allergic gape) is secondary to chronic mouth breathing during the first several years of age and results in a characteristic pattern of maldevelopment of facial bones, causing a high-arched palate, flat maxilla, and angulated mandible with a recessed chin and dental malocclusion (Figure 95.1). If affected, the conjunctivae are erythematous with a clear discharge and may have a follicular appearance. The mouth may reveal a high-arched palate from chronic mouth breathing, and hypertrophic lymphoid follicles in the oropharynx often are seen.
Classification of allergic rhinitis, although not as stringent as that of asthma, is important because it guides the choice of optimal therapy. According to the World Health Organization Allergic Rhinitis and its Impact on Asthma guidelines, allergic rhinitis is considered to be intermittent if symptoms occur fewer than 4 days a week or fewer than 4 weeks in duration, whereas persistent rhinitis is defined as symptoms occurring 4 or more days a week or 4 or more weeks in duration. Further, mild allergic rhinitis is defined as having no sleep disturbances; normal activities, sports, and leisure; normal school or work; and no troublesome symptoms. One or more of these symptoms results in classification of moderate/severe persistent allergic rhinitis (Table 95.1). Thus, allergic rhinitis may be classified as mild intermittent, moderate/severe intermittent, mild persistent, and moderate/severe persistent.
Complications of chronic allergic rhinitis may be evident on physical examination, including chronic serous otitis, recurrent otitis media, hearing loss secondary to otitis, sinusitis, nasal polyps, sleep apnea, or dental malocclusion.
Urticaria and Angioedema
Because the most common causes of urticaria and angioedema in children are foods, medications, supplements, and viral infections, questions should focus on recent exposures to drugs, dietary changes, new soaps or detergents, environmental agents, and recent viral illnesses. Consideration should also be given to other serious conditions, such as collagen vascular disease and neoplasm. Laboratory tests usually are not required unless the history and physical examination are suggestive of a potential etiology; for example, a patient with urticaria, joint swelling, pallor, and fatigue requires testing for evidence of systemic lupus erythematosus and malignancy.
Anaphylaxis
In the patient with anaphylaxis, the history is focused on identifying an acute exposure to a foreign antigen (eg, medication, food, venom). Although most patients react within minutes to hours after exposure to the causative agent, anaphylactic reactions occurring many hours to days after exposure have been reported. Therefore, the history must be inclusive of this time frame.
Hemodynamically, patients have reduced peripheral resistance resulting from vasodilation and capillary leak. This results in warm skin and flushing. Compensatory increases in cardiac output result in tachycardia and bounding pulses. Patients often feel a sense of doom. Hypotension ensues if shock is untreated. Respiratory symptoms include airway edema with upper airway obstruction and stridor, and smooth muscle constriction results in wheezing and respiratory distress. Some patients have GI symptoms, including vomiting, abdominal discomfort or pain, and diarrhea. Most patients with anaphylaxis have skin manifestations (typically urticaria).
The most common cause of death from anaphylaxis is respiratory compromise followed by hemodynamic collapse.
| Table 95.1. Classification of Allergic Rhinitis | ||
| Frequency | Severity | |
| Not applicable | Mild: No sleep disturbances No impairment of activities, sports, leisure Normal school and work No troublesome symptoms | Moderate/severe (≥1 of the following): Sleep disturbance Impairment of activities, sports, leisure Abnormal school and work Troublesome symptoms |
| Intermittent (<4 days/week or <4 weeks’ duration) | Mild intermittent: same symptoms as above | Moderate/severe intermittent: same symptoms as above |
| Persistent (≥4 days/week and ≥4 weeks’ duration) | Mild persistent: same symptoms as above | Moderate/severe persistent: same symptoms as above |
Derived from Brożek JL, Bousquet J, Agache I, et al. Allergic Rhinitis and its Impact on Asthma (ARIA) guidelines—2016 revision. J Allergy Clin Immunol. 2017;140(4):950–958 PMID: 28602936 https://doi.org/10.1016/j.jaci.2017.03.050.
Food Allergies
Diagnosing food allergy is not difficult if a reaction is clearly associated with ingestion of a specific food. Timing of the reaction is usually minutes to a few hours after ingestion. Diagnosis is less clear after a meal with multiple ingredients. Maintaining an accurate diet diary helps narrow the list of potential reactive foods. Negative food allergy test results via skin or in vitro serum IgE are reliable in ruling out a food; however, positive test results have limited predictive value unless values are high (Table 95.2). Therefore, a positive test result is suggestive of a food being responsible for a reaction, and confirmation should be pursued via an elimination period followed by food challenge. The double-blind, placebo-controlled food challenge is the diagnostic standard; however, it is impractical in most community clinical settings. National food allergy guidelines recommend using open food challenges to confirm a diagnosis. An absolute exception is in the patient with a serious systemic reaction (eg, anaphylaxis), in which case a strong history and a positive skin or serum test result is sufficient for diagnosis.
Abbreviations: IgE, immunoglobulin E; NPV, negative predictive value; PPV, positive predictive value.
Adapted with permission from Adkinson NF Jr, Bochner BS, Burks AW, et al, eds. Middleton’s Allergy: Principles and Practice. 8th ed. Philadelphia, PA: Elsevier Saunders; 2013.
Laboratory Tests
The diagnosis of an allergic disease can be made with a thorough history and physical examination when there is resolution of symptoms with empiric therapy. Additional tests are performed when the diagnosis is in question, to provide optimal avoidance strategies, and if allergen immunotherapy is needed. Testing may be necessary for the diagnosis of food allergy and further evaluation of urticaria and angioedema.
History of exposure followed by symptoms can be suggestive of causative agents; however, the combination of allergy testing with history improves the positive predictive value of a specific antigen causing the symptoms. For example, a patient with year-round indoor symptoms of rhinorrhea and nasal pruritus may be allergic to dust mites, cats, dogs, cockroaches, or mold. Subsequent allergen testing will elucidate which single allergen or combination of allergens is responsible for the symptoms. This results in a more focused and effective approach to environmental control. Allergen testing is also necessary if allergen immunotherapy is being considered.
Allergy testing may be achieved with in vivo skin-prick testing or in vitro specific IgE testing. Skin tests are sensitive and accurate. A positive test result indicates the presence of an antigen-specific IgE. Although skin testing may be less reliable in infants because their skin is less reactive than that of older individuals, these tests have been performed in infants as young as 4 months. Typically, fewer allergens are tested in children younger than 2 years compared with older individuals because those younger than 2 years of age have not been sensitized to a wide range of antigens. Currently, skin-prick testing is the recommended method for skin tests. Intradermal testing involving injection of allergen under the skin is used for testing of stinging insect allergy and various medication hypersensitivity and rarely is necessary for the diagnosis of inhalant or food allergen sensitization. When evaluating food allergy, intradermal testing should not be performed because of the risk of precipitating a systemic reaction.
In vitro allergen-specific IgE concentrations (ImmunoCAP, radioallergosorbent tests) in sera, which are also available for the laboratory assessment of allergies, provide a measure of the amount of IgE specific for individual allergens. Generally, in vitro tests have similar sensitivity and specificity as skin testing but are more expensive. In vitro tests have an advantage in that they can be performed on patients who are using medications that affect skin-testing reactivity, such as antihistamines and tricyclic antidepressants. Additionally, they are the preferred test in patients with poor skin reactivity, such as the very young and very old; those who do not have skin findings, such as atopic dermatitis and dermographism; and those who may have anaphylaxis to the allergens being tested.
For inhalant allergens, in vivo and in vitro tests have good negative and positive predictive values. Both tests have good negative predictive value for food allergy but positive predictive value of approximately 50%. For certain foods, very high levels of specific IgE have good positive predictive values (Table 95.2).
Other screening tests may include a nasal smear for eosinophil counts. More than 10% eosinophils is consistent with allergic rhinitis. Although serum IgE levels are elevated in 60% of patients with allergic rhinitis and asthma, they are not sensitive or specific and have limited value. Rhinoscopy in adults and older children provides a painless method to detect pathology not visible by anterior inspection via the nares. Such pathology includes identification of nasal polyps, deviated nasal septum, adenoidal hypertrophy extending into the nares, sinusitis, vocal cord edema, and polyps and potential masses. Computed tomography is clinically quite useful because it reveals structural abnormalities and mucosal disease, including findings within sinus cavities. The need for such information must be weighed against the high doses of radiation associated with computed tomography. Plain radiography of the sinuses is rarely indicated because of the limited ability to detail nasal anatomy and the high rates of false-negative results for sinusitis along with exposure to radiation.
Management
General Principles
Avoidance of allergen triggers is a natural means of controlling allergy symptoms without medication and should be encouraged in all patients with allergic disease. Currently, avoidance of allergen triggers is the only option available to patients with food allergy and anaphylaxis.
For patients with allergic rhinitis, conjunctivitis, and asthma, allergic triggers consist of perennial and seasonal allergens. Perennial allergens usually include house dust mites, warm-blooded animals with fur (eg, cats, dogs, rodents), cockroaches, and indoor pollens (usually molds). Seasonal allergens include outdoor molds as well as pollen from trees, grasses, and weeds. Effective environmental controls for these are outlined in Box 95.3. In addition to allergic triggers, nonallergic irritant triggers, such as tobacco smoke, automobile exhaust, smog, and perfumes, should be avoided.
Although environmental controls are safe and effective, they may be labor intensive, expensive, and, in rare cases, psychologically detrimental. For instance, removal of carpeting is difficult and expensive, especially in rented housing. Dust mite-proof coverings are expensive and cumbersome to wash in hot water weekly. Removal of family pets may result in psychological issues if children have become attached. Patients are more likely to institute environmental controls if evidence exists of allergic sensitization via skin-prick or blood tests.
Currently, no therapy is available to treat patients with food allergies except avoidance of the triggering food. Food avoidance should be undertaken only after a careful history, allergy testing, and a trial of food elimination and challenge to correctly identify the trigger. A poor history and false-positive testing can result in the implication of many foods, a draconian elimination diet, and undernutrition. The patient who is truly allergic to multiple foods will benefit from consultation with a registered nutritionist or dietitian. Additionally, such patients should be taught to read food labels to avoid offending foods.
Children generally lose sensitivity to milk, soy, egg, and wheat by school age. For instance, a large study noted that 85% of milk-allergic and 66% of egg-allergic children lost their sensitivity by 5 years of age. Only approximately 20% of patients with peanut allergy lose their sensitivity, and even fewer become tolerant of fish and shellfish. Understanding the natural history of food allergies allows the clinician to liberalize the diet if retesting shows negative or reduced reactivity and a supervised food challenge is negative. The decision to challenge depends on the nutritional and social importance of a particular food.
Box 95.3. Environmental Control Strategies for Perennial and Seasonal Allergens
Dust Mites
•Cover mite reservoirs with mite-proof covers (eg, mattress, pillows, box springs, comforter).
•Wash linen in hot water once a week.
•Remove mite reservoirs, such as carpets, and if possible, stuffed toys.
•Use HEPA filter in conjunction with mite reduction strategies.
•Use vacuum cleaner that has HEPA filtration.
Pets (eg, dogs, cats)
•Do not get a warm-blooded furry pet (even if initially not allergic to cats or dogs), because children may sensitize to the pet later, at which time it will be difficult to remove the pet from the home.
•Bathing the pet once a week reduces the allergen load.
•Keep the child’s room pet free or, if possible, have an outside cat or dog.
•Use of HEPA filter may help.
•Re-home the pet, if possible. (Note: Cat dander may linger for many months, and continuous house cleaning is required even after removal of the pet.)
Cockroaches/Rodents
•Use of boric acid for cockroach control is a pesticide-free strategy.
•Cockroaches and rodents often require professional extermination.
Mold
•Repair water damage.
•Reduce humidity.
Pollens
•Use HEPA filter.
•Close windows at night (plants usually pollinate in early morning).
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