• The age group most affected by AR is late teens to early twenties.
• Risk factors: cigarette exposure, family history of atopy, higher socioeconomic status, first born or only child, elevated total IgE level before age of 6
• Atopy: predisposition to produce IgE laden response to environmental antigen
• Manifestations include eczema, food allergy, rhinitis, asthma
• Atopic march: tendency for topic patients to present with eczema and food allergy in infancy, with food allergy decreasing in incidence sharply and eczema incidence on a slower downtrend; asthma follows, with peak incidence between ages of 5 and 7, then incidence decreasing into adolescence; allergic rhinitis hits peak in early teens and remains the most prevalent manifestation of atopy throughout life
• Incidence of allergic and autoimmune disease is noted to be increasing over the last 50 years, whereas the incidence of infectious disease has been falling over the same time period, largely believed due to hygiene improvements.
• Allergic disease is more prevalent in higher socioeconomic groups, firstborn and only children. Each of higher socioeconomic groups, firstborn and only children are protective factors for infection.
• The theory is that early exposure to antigen associated with infection (such as endotoxin), and consequent mounting of regular healthy immune responses, may be protective against development of the dysregulated immunity seen in allergy.
• allergic disease has genetic predisposition, 26% of children with one parent affected by asthma develop the disease.
• Heredity is complex and multifactorial; genes and environmental influence play a role.
• Ongoing studies commonly find certain genes with positive association with atopy (eg, IL 4, IL 13, TNF, high-affinity IgE receptor).
EVALUATION OF THE ALLERGIC PATIENT
History: Establish Primary Complaints: Itching, Sneezing, Runny Nose, Obstruction
• Duration: since childhood or recent onset?
• Frequency: intermittent or persistent?
• Alleviating and exacerbating factors
• Associated symptoms
• History of other atopic associated complaints: eczema, asthma, food allergy
• Family history
• Medication use
• Impact on quality of life
• Social history: smoke, smoke exposure, job or environmental change
• Include questions about triggers: pets, gardens, certain buildings, chemicals
Physical Exam
• Eyes: injection, chemosis, allergic shiners (edema or appearance of bruising under lower lid), Dennie-Morgan lines (skin folds on lower lids)
• Nose: large turbinates, boggy and/or bluish mucosa, rhinorrhea, transverse nasal crease (allergic salute: wiping away rhinorrhea, bending the tip of the nose upward)
• Ears: TM retraction, middle ear effusion
• Skin: stigmata of pruritis (signs of scratching), dry, scaly skin (characteristic of eczema), angioedema
• Hyperreactivity of the nasal respiratory mucosa to allergen
• Mediated by IgE which recognizes allergen and binds to eosinophils, basophils, and mast cells, causing inflammatory factor and histamine release, resulting in manifestations of allergic disease
• Early allergic response: tingling, pruritus, sneezing, rhinorrhea, nasal congestion
• Edema, inflammation, and rhinorrhea of AR are significant factors in the development and severity of other allergy related diseases, such as nasal congestion, sleep disordered breathing, eustachian tube dysfunction (ETD), and chronic rhinosinusitis.
• Medical treatment focused on AR should be considered in all cases of these diseases; often adequate treatment of AR will resolve or greatly improve symptoms.
• AR is a risk factor for developing asthma.
• See Chapter 12.
• Hyperreactivity of the lower airways; inflammatory mediators promote smooth muscle contraction, vascular permeability, mucus secretion, and airway remodeling
• IgE mediated sensitivity (atopy) to airborne allergens is currently the strongest identifiable risk factor for the development of asthma.
• The unified airway: paradigm gaining acceptance; states that, given the similar pathophysiologic mechanisms of AR and asthma, they should be considered different manifestations on the continuum of the same disease process (see Chapter 31)
• Any patient undergoing evaluation for asthma should also be evaluated for AR and vice versa; treating one disease often improves symptoms of the other.
• Often the first disease to manifest in an atopic patient, causing dysfunction of epidermal barrier of skin and possibly predisposing to sensitization to allergens
• Theorized that adequate treatment of eczema may prevent the rest of the atopic march
• Up to 20% of children affected, and 2% to 10% of adults
• Characterized by dry, flaky skin and pruritis, with polymorphic features including vesicles, papules, and plaques
• Often resolves during childhood or early adolescence
• Should be differentiated from food aversion and food intolerance
• Food intolerance is nonimmune mediated, and may be metabolic, pharmacologic, or toxic (lactose intolerance is the most common).
• Oral tolerance: normal ability of the immune system to suppress response to food antigen processed through digestive system; process fails in food allergy
IgE Mediated Food Allergy
• Manifestations: urticaria, anaphylaxis, oral allergy syndrome
• Reproducible upon exposure
• Small quantities of food cause severe reactions
• Oral allergy syndrome: one manifestation of food allergy, fast onset reaction limited to oral cavity and oropharynx, tingling, pruritis, angioedema
Non-IgE Mediated/Cell Mediated
• Most commonly, celiac disease, contact dermatitis
• Allergic conjunctivitis, drug allergy, insect allergy, urticaria, and angioedema
• An allergen is an antigen that, upon exposure can induce a type I hypersensitive immune response in atopic individuals.
• Epitope: site of an antigen actually recognized by antibody; each antigen may have multiple epitopes
• Antigens may share epitopes, leading to cross-reactivity, where sensitization to one antigen predisposes an individual to hypersensitive reaction to another similar antigen.
• Most antigens are proteins with 10 to 40 kDa molecular weight.
• Size effects: larger airborne allergens typically filtered by the nose, with greatest impact on nasal mucosa; smaller allergens may reach and impact smaller airways in lungs
• The terminology traditionally referred to as “seasonal” and “perennial” AR is based on sensitivity to outdoor versus indoor allergens; this paradigm is shifting to “intermittent” and “persistent” disease.
• Dust mite: common sensitization in patients with persistent allergic rhinitis; most common allergen in asthmatic children; exists on small particles capable of reaching lower airways
• Mites found in beds, pillows, drapes; survive on shed human skin
• Two species: D. pteronyssinus (allergens Der p1, Der p2), D. farinae (allergens Der f1, Der f2)
• Allergens are mite feces and shed mite skin, averaging 10 microns in size, with moderate cross-reactivity between species.
• Cockroach: allergen associated with asthma and persistent allergic rhinitis, common allergen in urban settings; 10 to 200 microns; significant cross-reactivity between species
• Pet Dander: Fel d1 is a major cat allergen, produced in the salivary and sebaceous glands, that flakes off with old skin; Can f1 is a major dog allergen. Both show minor cross-reactivity between species.
• Mold: many varied allergens with regionally based species
• Common molds: alternaria, aspergillus, cladosporium, helminthosporium, penicillium
Pollen
• Male germinal cell of plants; major source of outdoor antigenicity
• Common clinically significant allergens seen in North America by season are listed in Table 29–2. It is important to note that, in addition to those listed, there are many allergens that are regionally significant; one should be aware of regionally important allergens when performing testing.
• Evaluation and testing for allergen sensitivity should be tailored to high-yield allergens on a regional basis.
• History remains the most important means of diagnosing allergy, but laboratory and skin testing can be useful adjuncts to confirm diagnosis, identify clinically significant allergens, and quantitate the degree of sensitivity. Positive testing results should always be correlated to clinical symptoms when considering treatment.
• The basic dichotomy of testing for allergy is in vivo skin testing versus in vitro serological testing.
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