Anaphylaxis is a sudden-onset, immediate reaction that implies a risk of death. Think of a “rule of 2's” for anaphylaxis implying that reactions usually begin within 2 minutes to 2 hours after injection, infusion, ingestion, contact, or inhalation. Fatalities can be from
asphyxiation from laryngeal or oropharyngeal swelling, collapse from hypotensive shock, cardiac arrest, or acute severe bronchoconstriction causing respiratory failure and arrest. When there is activation of mast cells and basophils in anaphylaxis, chemical mediators are detectable. The preformed
mediators from mast cells include histamine, tryptase, carboxypeptidase A, and proteoglycans (heparin and chondroitin sulfates). Newly synthesized mediators include prostaglandin D2, leukotriene D4, and platelet-activating factor. Crucial actions of the mediators include
an abrupt increase in vascular permeability, vascular smooth muscle relaxation, and bronchial smooth muscle contraction. Anaphylaxis can be classified into immunologic, nonimmunologic, or idiopathic based on the associated mechanism. For example, immunologic causes of anaphylaxis are those
mediated by IgE antibodies acting through the FcεR I (foods, insect venom, and beta-lactam antibiotics) whereas non-IgE immunologic anaphylaxis is mediated without presence of antiallergen IgE antibodies or via FcεRI activation (radiographic contrast material). Nonimmunologic
anaphylaxis involves mast cell mediator release such as occurs with exercise, cold temperature exposure, or from medications such as opioids or vancomycin. Idiopathic anaphylaxis involves mast cell activation (acutely elevated urine histamine or serum tryptase) and activated lymphocytes. Because
anaphylaxis is a medical emergency, the drug of choice is epinephrine, not H1-receptor antagonists.
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Allergy and Asthma Proceedings
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