Anaphylaxis
PREVALENCE AND RISK FACTORS
Published incidence and prevalence data are likely inaccurate because anaphylaxis is underdiagnosed and underreported. It is estimated that up to 1000 fatalities caused by anaphylaxis occur every year in the United States. In-hospital anaphylaxis complicates roughly one of every 5000 admissions, and anaphylaxis occurs more frequently in community than in health care settings. Risk factors affecting the incidence of anaphylaxis have been identified (Box 1).
PATHOPHYSIOLOGY
The clinical symptoms of anaphylaxis derive from the mediators (Table 1) released by the activation of sensitized mast cells and basophils. Anaphylactic reactions are triggered by the cross-linking of the high-affinity IgE receptor by receptor-bound IgE that recognizes antigens such as food, drug, or insect venom. Complement protein anaphylatoxins such as C3a and C5a can also trigger anaphylaxis, and nonsteroidal anti-inflammatory agents can trigger anaphylaxis by altering arachidonic acid metabolism. These mediators directly contribute to increased airway resistance, fall in PO2, and vasodilation with hypotension seen during anaphylaxis.
Table 1 Relevant Mediators Released by Mast Cells and Basophils in Anaphylaxis
| Mediator | Action |
|---|---|
| Arachidonic Acid Metabolites | |
| Cysteinyl leukotrienes Prostaglandins Platelet activating factor | Bronchoconstriction, coronary vasoconstriction, increased vascular permeability, mucus hypersecretion, eosinophil activation and recruitment |
| Chemokines | |
| IL-8 MIP-1α | Neutrophil chemotaxis, inflammatory cell recruitment, activation of NADPH oxidase |
| Cytokines | |
| GM-CSF IL-3, -4, -5, -6, -10, and -13 TNF-α | Eosinophil chemotaxis and activation; inflammatory cell activation and recruitment, induction of IgE-receptor expression, induction of apoptosis |
| Proteases | |
| Chymase Tryptase | Cleavage of complement proteins and neuropeptides, inflammatory-cell chemoattractant, conversion of angiotensin I to angiotensin II, activation of protease-activated receptor-2 |
| Proteoglycans | |
| Chondroitin sulfate Heparin | Anticoagulation, complement inhibition, eosinophil chemoattractant, kinin activation |
| Other | |
| Histamine | Vasodilation, bronchial and gastrointestinal smooth muscle contraction, mucus hypersecretion |
| Nitric oxide | Vasodilation, increased vascular permeability |
GM-CSF, granulocyte-macrophage colony-stimulating factor; NADPH, reduced nicotinamide adenine dinucleotide phosphate; TNF-α, tumor necrosis factor α.
The most common antigenic triggers of anaphylactic reactions are listed in Box 2. Food-triggered anaphylaxis can occur from any food at any age. Patients allergic to eggs might have an increased frequency of reactions to the egg-containing influenza vaccine, so patients with egg-induced anaphylaxis should not receive the influenza vaccine unless under the guidance of an allergy specialist. Egg-allergic children are not at increased risk for anaphylaxis with the measles–mumps–rubella (MMR) vaccine because sensitivity to this vaccine is likely triggered by sensitivity to gelatin.
