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These diseases result from IgE-dependent release of mediators from sensitized basophils and mast cells upon contact with an offending antigen (allergen). Associated disorders include anaphylaxis, allergic rhinitis, urticaria, asthma, and eczematous (atopic) dermatitis. Atopic allergy implies a familial tendency to the development of these disorders singly or in combination.


IgE binds to the surface of mast cells and basophils through a high-affinity receptor. Cross-linking of this IgE by antigen causes cellular activation with subsequent release of preformed and newly synthesized mediators including histamine, prostaglandins, leukotrienes (C4, D4, and E4, collectively known as slow-reacting substance of anaphylaxis—SRS-A), acid hydrolases, neutral proteases, proteoglycans, and cytokines (Fig. 167-1). These mediators have been implicated in many pathophysiologic events associated with immediate-type hypersensitivity, such as vasodilatation, increased vasopermeability, smooth-muscle contraction, and chemotaxis of neutrophils and other inflammatory cells. The clinical manifestations of each allergic reaction depend largely on the anatomic site(s) and time course of mediator release.

FIGURE 167-1

Bioactive mediators of three categories generated by IgE-dependent activation of murine mast cells can elicit common but sequential target cell effects leading to acute and sustained inflammatory responses. LT, leukotriene; PAF, platelet-activating factor; PGD2, prostaglandin D2; IL, interleukin; GM-CSF, granulocyte-macrophage colony-stimulating factor; INF, interferon; TNF, tumor necrosis factor.



May occur together or separately. Urticaria involves only the superficial dermis and presents as circumscribed wheals with raised serpiginous borders and blanched centers; wheals may coalesce. Angioedema involves deeper layers of skin and may include subcutaneous tissue. The classification of urticaria-angioedema focuses on mechanisms that elicit clinical disease and can be useful for differential diagnosis (see Table 167-1).



Characterized by massive edema formation in the dermis (and subcutaneous tissue in angioedema). Presumably the edema is due to increased vasopermeability caused by mediator release from mast cells or other cell populations.


History, with special attention to possible offending exposures and/or ingestion as well as the duration of lesions. Vasculitic urticaria typically ...

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