• Anaphylaxis is a serious, life-threatening, systemic allergic reaction that is rapid in onset and is a result of mast cell and basophil activation and degranulation.
  • Skin and mucosal symptoms such as flushing, itching, urticaria, or angioedema are present in 80–90% of patients with anaphylaxis. However, absence of skin findings does not exclude anaphylaxis.
  • In fatal anaphylaxis, initial signs and symptoms may include respiratory distress without urticaria resulting in delayed diagnosis and treatment.


  • Rate of occurrence appears to be increasing.
  • Estimated to be fatal in 0.7–2% of cases

Risk Factors


There are few studies of genetic factors in human anaphylaxis; however, individuals with a previous history of anaphylaxis or a history of atopy are at increased risk for future anaphylaxis episodes.


  • In anaphylaxis, mast cells and basophils are activated via an IgE-mediated (most common) or non–IgE-mediated mechanism releasing preformed and newly generated mediators of inflammation.
    • Mediators include histamine, tryptase, proteoglycans, leukotrienes, prostaglandins, platelet-activating factor, and cytokines.
    • Local or systemic effects can include increased vascular permeability, vasodilation, smooth muscle contraction, complement activation, and coagulation.
  • IgE-mediated anaphylaxis occurs when IgE is synthesized in response to allergen exposure (sensitization) and becomes fixed to high-affinity IgE receptors located on the surface of mast cells and basophils. Subsequent allergen exposure results in receptor-bound IgE aggregation and cell activation.
  • Non–IgE-mediated anaphylaxis generally results from nonimmune stimulation of mast cells or basophils. Rarely, IgG and complement can be implicated.


  • IgE-mediated:
    • Foods (peanut, tree nuts, fish, shellfish, milk, egg, wheat, soy)
    • Medications (antibiotics especially β-lactams, NSAIDs, biologic products)
    • Venoms (usually from stinging insects including fire ants)
    • Latex (direct exposure to natural rubber or ingestion of cross-reacting foods)
    • Other (vaccines, occupational allergens, and rarely inhaled allergens)
  • Non–IgE-mediated:
    • Radiocontrast media (can also trigger IgE-dependent anaphylaxis)
    • Medications (opiates, NSAIDs, dextrans, vancomycin, polymyxin B)
    • Physical stimuli (exercise, cold, heat, sunlight/UV radiation)
    • Ethanol
  • If no identifiable trigger is found, anaphylaxis may be idiopathic in origin.

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