Abstract
Anaphylaxis is a severe, systemic allergic reaction characterized by multisystem involvement, including the skin, airway, vascular system, and gastrointestinal tract. Severe cases may result in complete obstruction of the airway, cardiovascular collapse, and death. The term classic anaphylaxis refers to hypersensitivity reactions mediated by the subclass of antibodies immunoglobulins IgE and IgG. Prior sensitization to an allergen has occurred, producing antigen-specific immunoglobulins. Subsequent reexposure to the allergen provokes the anaphylactic reaction. Many anaphylactic reactions, however, occur without a documented prior exposure. Anaphylactoid or pseudoanaphylactic reactions display a similar clinical syndrome, but they are not immune-mediated. Treatment for the two conditions is similar. The inciting allergen binds to antigen-specific IgE that has accumulated on previously sensitized basophils and mast cells. These cells almost immediately release a series of mediators, including histamines, leukotrienes, prostaglandins, thromboxanes, and bradykinins. When released locally and systemically, these mediators cause increased mucous membrane secretions, increased capillary permeability and leak, and markedly reduced smooth muscle tone in blood vessels (vasodilation) and bronchioles. Any antigen capable of activating IgE can be a trigger for anaphylaxis. In terms of etiology, researchers generally list the following categories of causes: pharmacologic agents, latex, stinging insects, and foods. In up to 5% of cases the antigenic agent cannot be identified.
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