Different Types of Anaphylaxis: Causes and Severity
Anaphylaxis is an acute, allergic systemic reaction, during which all or some of the following are present: urticaria/angioedema, upper airway obstruction, bronchospasm, and hypotension. In some cases, these manifestations may be accompanied by cardiovascular and/or gastrointestinal disturbances. Anaphylaxis can be fatal without evidence of cutaneous involvement.
• Several schemes have been used to classify anaphylaxis into several broad categories.
Anaphylaxis: immunoglobulin E (IgE) antibody mediated.
Anaphylactoid: non–IgE antibody mediated.
The clinical presentations and acute treatment of both types of reactions are similar, but prevention strategies may differ.
Recently, the term anaphylactoid has been abandoned in favor of the following terminology:
Anaphylaxis immunologic: IgE (eg, from penicillin) or non-IgE (eg, infusion of aggregates of heterologous immunoglobulin that cause complement activation).
Anaphylaxis nonimmunologic (eg, radiocontrast media).
Incidence and Severity
• The incidence of anaphylaxis is likely underestimated because of misdiagnosis. It is estimated that anaphylaxis is responsible for 500 to 1000 deaths in the United States each year.
Causes of Anaphylaxis
• The principal causes of anaphylaxis are foods, drugs (antibiotics, nonsteroidal antiinflammatory drugs [NSAIDs], vaccines), insect stings, latex, exercise, and idiopathic.
- Approximately 35% to 55% of anaphylaxis cases are caused by food allergies.
- The incidence of food allergies and anaphylaxis is increasing.
- Accidental food exposures are common and unpredictable.
• Common triggers:
- Eight foods are responsible for approximately 90% of all allergic reactions to foods.
- In both children and adults, peanuts, tree nuts, shellfish, and fish are common triggers. Allergic sensitivity to these foods tends to persist throughout life.
- In children, other common triggers include milk, eggs, soy, and wheat. Sensitivity to these foods tends to disappear with advancing age.
It is a common misconception that food anaphylaxis occurs after ingestion of new foods.
However, anaphylaxis reactions occur to many foods that had been previously ingested with impunity but have induced an IgE antibody response (ie, a latent period of sensitization).
Once food anaphylaxis has developed, reingestion of that the offending food almost always results in a recurrent reaction.
Fatalities from food-induced anaphylaxis most commonly occur in patients with a history of systemic allergic reactions yet have no epinephrine available for use at the time of their reaction.
Insect Venom-Induced Anaphylaxis
- It is estimated that 0.5% to 5%, or 1.36 to 13 million,
- Americans are sensitive to one or more insect venoms of the Hymenoptera order (bees; wasps; yellow jackets; hornets; and in the southern United States, fire ants. At least 40 to 100 deaths occur each year in the United States.
- The incidence is increasing perhaps because of an increase in the population density of fire ants and Africanized bees.
- Immunotherapy is 98% to 99% effective at preventing anaphylaxis from stinging insect venom. In a patient presenting with anaphylaxis from a stinging insect, the use of epinephrine alone may not prevent fatality. Therefore, refer sensitized or susceptible adults for skin testing and immunotherapy.
- Patients at risk for anaphylaxis should carry self-injectable epinephrine and be counseled on avoidance.
• The mechanism is uncertain. There is an inconsistent relation to exercise intensity, and anaphylaxis may occur only episodically.
• There are cofactor dependent exercise-induced anaphylaxis syndromes, in which both exercise and a cofactor must be present for an episode to occur.
These include the following:
- Specific food; IgE-dependent exercise anaphylaxis: a particular food must be eaten before or during exercise.
- Nonspecific food; non-IgE dependent, postprandial exercise anaphylaxis: exercise in the postprandial state causes a reaction.
- Aspirin/NSAID-dependent exercise anaphylaxis.
• There is no associated immunologic abnormality or triggering event, but coexistent allergic disease or preexisting urticaria/angioedema are frequent.
• The number of mast cells are not increased or only mildly increased in skin, and not increased in the bone marrow. This is in contrast to systemic mastocytosis, which is associated with elevated numbers of mast cells in most tissues.
• Histamine and tryptase are increased in acute episodes but not between.
• For frequent episodes, prophylactic treatment regimens are used (eg, antihistamines, prednisone, and oral adrenergic agents).
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