Abstract
Anaphylaxis, often explosive in onset, is one of the most serious emergencies in medical practice. It is usually attributed to the antigen-induced release of biologically active substances by IgE-sensitized mast cells, but identical clinical manifestations can be induced by activation of the complement pathway, as well as the arachidonate–prostaglandin pathway. Certain agents may act directly on the mast cell, with similar pharmacologic effects.1 The sites of clinical expression of such mast cell–mediated reactions include the skin, the respiratory and gastrointestinal tracts, and the cardiovascular system. Urticaria–angioedema, respiratory obstruction due to laryngeal edema or bronchospasm, and hypotension may occur singly or . . .