Key Points

• Symptoms of allergic rhinitis include allergic shiners, allergic salute, pale nasal mucosa, loss of taste or smell, nasal speech, eustachian tube dysfunction, and disrupted sleep.

• Ophthalmologist referral should be provided to prevent cornea complications.

• Treatment of acute rhinitis includes environmental control, medications, and immunotherapy.

• Use environmental controls such as air conditioning with change of filters, HEPA filters, and masks with microfoam filters for dust allergy.

• Wash linens in hot water, using impermeable encasings for pillows and mattresses.

• Avoid fans and cool-mist vaporizers, and remove carpets.

• Oral second-generation antihistamines provide less sedation than previous drugs.

• Medications include intranasal steroids, topical antihistamines, leukotriene modifiers, and decongestants.

• Immunotherapy is directed at specific allergens with possible resolution of allergy.

The allergic patient differs from nonallergic patients in several ways (Box 20-1). The cause is unknown, but these abnormalities clearly are associated with abnormal cytokine production (Table 20-1). The result of these abnormalities is that allergic persons suffer from diseases such as allergic rhinitis and allergic asthma.

It must always be remembered, however, that these diseases are defined by their phenotype, and for each allergic disease, there is an almost identical phenotypic expression unrelated to allergy, including allergic and nonallergic (intrinsic) asthma, allergic and nonallergic rhinitis, and IgE-mediated and non-IgE-mediated anaphylactic events. Thus, when approaching the patient, the physician must always consider the mechanism of production of the symptoms because subtle differences may exist in treatment between allergic and nonallergic forms of disease, often with significant differences in prognosis.

The most important aspect of establishing the diagnosis of each of these illnesses is the history. The distinction between the allergic and nonallergic forms can only be conclusively determined by allergy testing. The most sensitive and least expensive (per test) means of assessing the presence of allergy is the allergy skin test. In vitro testing is often helpful, however, as a screening procedure.

The other important phenomenon to recognize is that the major allergic diseases (allergic rhinitis, allergic asthma, and anaphylaxis) are all increasing in incidence. The cause is unknown, but several hypotheses have been proposed. The hygiene hypothesis postulates that the rise in allergic disease is related to infection control in infants and children (e.g., through vaccination) and improved public health (e.g., through hygienic measures). Another hypothesis is that the allergic response is the same response used to defend against parasites. With a reduction in parasitic disease in more technically developed countries, a population has arisen that is free from exposure to parasites but still maintains a vigorous antiparasitic immune response that is aberrantly directed against the normally harmless organic substances such as pollen, animal dander, and food. Regardless of the mechanism, the burden of allergic disease in developed countries has increased rapidly since the 1970s.

Table 20-1 Cytokine Production Abnormalities and Effects in Allergic Patients

Box 20-1 Abnormalities Described in Allergic Patients

Predisposition to manufacture large amounts of IgE directed against formerly harmless substances (e.g., pollen and food) Abnormalities in the autonomic nervous system Hyporesponsive beta-adrenergic system Hyperresponsive alpha-adrenergic system Hyperactive cholinergic responses in the airways Hyperreleasability of mast cells and basophils

Table 20-1 Cytokine Production Abnormalities and Effects in Allergic Patients

Cytokine

Effects

Increased production of IL-4

Enhanced IgE production

Increased production of IL-13

Enhanced IgE production

Increased production of IL-5

Enhanced eosinophil activity and

prolongation of the life of eosinophils

Increased production of IL-9

Bronchial hyperreactivity

Ig, Immunoglobulin; iL, interleukin.

Ig, Immunoglobulin; iL, interleukin.

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