There are two methods for identifying allergen-specific IgE: in vivo skin testing and in vitro serum testing (Table 77-4).In vivo skin testing introduces allergen into the skin via a prick/puncture or intradermal injection. The allergen diffuses through the skin to interact with IgE that is bound to mast cells. Cross-linking of IgE causes mast cell degranulation, which results in a histamine release; this prompts the development of a central wheal and erythematous flare. The wheal and flare are measured 15 to 20 minutes after the allergen has been placed. Properly performed skin tests are the best available method for detecting the presence of allergen-specific IgE.
In vitro serum testing, such as immunoassays like the radioallergosorbent test (also known as RAST) and enzyme-linked immunosorbent assay (also known as ELISA), measures levels of antigen-specific IgE. Many allergists and laboratories regard the ImmunoCAP System as the method of choice. This method uses a solid phase and shows higher sensitivity,
Results available immediately Preferable to skin testing for dermatographism Widespread dermatitis Uncooperative children
From Skoner DP: Allergic rhinitis: definition, epidemiology, pathophysiology, detection, and diagnosis, J Allergy Clin Immunol 108:S2−S8, 2001.
specificity, and reproducibility. The assay uses a quantitative fluorescent immunoassay (FEIA); FEIA is more sensitive than other assays. These tests are indicated for patients who have dermatographism or extensive dermatitis; who cannot discontinue medications, such as antihistamines, that interfere with skin test results; who are very allergic by history, where anaphylaxis is a possible risk; or who are noncompliant for skin testing. The presence of specific IgE antibodies alone is not sufficient for the diagnosis of allergic diseases. Diagnosis must be based on the physician’s assessment of the entire clinical picture, including the history and physical examination, the presence of specific IgE antibodies, and the correlation of symptoms to IgE-mediated inflammation.
Diagnostic imaging has a limited role in the evaluation of allergic disease. Chest radiography is helpful with the differential diagnosis of asthma. Sinus radiography and computed tomography may be useful, but when these images are abnormal, they do not distinguish allergic disease from nonallergic disease.
Inflammatory cells (mast cells, eosinophils, T lymphocytes, neutrophils), chemical mediators (histamine, leukotrienes, platelet-activating factor, bradykinin), and chemotactic factors (cytokines, eotaxin) mediate the underlying inflammation found in asthmatic airways. Inflammation contributes to airway hyperresponsiveness (airways constricting in response to allergens, irritants, viral infections, and exercise). It also results in edema, increased mucus production in the lungs, influx of inflammatory cells into the airway, and epithelial cell denudation. Chronic inflammation can lead to airway remodeling, which results from a proliferation of extracellular matrix proteins and vascular hyperplasia and may lead to irreversible structural changes and a progressive loss of pulmonary function.