fers to a sudden, potentially life-threatening, systemic condition mediated by highly reactive molecules released from mast cells and basophils. Mediators include histamine, platelet-activating factor, and products of arachidonic acid metabolism (Fisher, 1987). Release of mediators depends typically upon the interaction of antigen with specific antibodies of the IgE class that are bound to the mast cells and basophils. Antibodies of other immunoglobulin classes are thought to mediate anaphylaxis on occasion. By definition, the antibodies are formed by prior exposure to the same or a closely related antigen. Anaphylaxis results from widespread release of mediators that enter the circulation, and thus, anaphylaxis is an expression of allergy that is systemic. At a cellular level, the reaction begins within seconds of exposure to the inciting antigen. However, depending upon the degree of sensitization (IgE antibody formation), and presumably upon the rate with which the antigen enters the circulation, localized or systemic symptoms may not be expressed for minutes or a few hours (Dolovich et al., 1973; Pearlman and Bierman, 1989). In proposed changes to the Vaccine Injury Table, which is used by the Vaccine Injury Compensation Program to determine eligibility for compensation for vaccine-induced injuries, the time frame for the onset of anaphylaxis/anaphylactic shock following vaccination has been set at 4 hours (U.S. Department of Health and Human Services, 1992). Classic symptoms include pallor and then diffuse erythema, urticaria and itching, subcutaneous edema, edema and spasm of the larynx, wheezing, tachycardia, hypotension, and hypovolemic shock (Kniker, 1988; Pearlman and Bierman, 1989). These symptoms are due to leaking of fluid from blood vessels, constriction of smooth-muscle in certain viscera, and relaxation of vascular smooth muscle. If death occurs, it is most commonly from airway obstruction caused by laryngeal edema or bronchospasm, or from cardiovascular collapse from arterial smooth-muscle relaxation and transudation of fluids from the intravascular space (Pearlman and Bierman, 1989). Tissues at autopsy show primarily widespread edema.

Less severe manifestations of immediate hypersensitivity that do not qualify as anaphylaxis under the above definition occur commonly. These may be expressed as urticaria and generalized pruritus, wheezing, or more alarming symptoms such as facial and other edemas. However, hypotension, shock, and collapse do not occur either because the reactions are naturally less severe or because they are aborted by intervention with epinephrine or antihistamines.

The clinical presentation of anaphylaxis can also be produced by intravascular antigen-antibody reactions that activate the complement system. In this case, the antibodies may be of the IgG or IgM class. Peptides that are split from activated complement components act on mast cells and basophils to induce the release of the same mediators (Kniker, 1988). This reaction is recognized most clearly after intravenous administration of anti-



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