Exercise Induced Anaphylaxis: A Brief Review

Exercise-induced anaphylaxis (EIA) represents a rare presentation of anaphylaxis in athletes triggered be exercise. A sub-type of this illness is food dependent exercise-induced anaphylaxis (FDEIA) in which food and exercise are required to trigger anaphylaxis. Anaphylaxis is a type 1 hypersensitivity reaction which either presents with hives and hemodynamic instability and/or involves two or more organ systems. Involved organ systems include dermatologic with hives being the most common presenting feature, respiratory, gastrointestinal and cardiovascular.

These diseases are relatively rare. The overall incidence of anaphylaxis in the general population is 8 - 50 cases per 100,000 person years with a lifetime prevalence of 0.05% - 2% [1]. The mortality rate of anaphylaxis is 1-2%. EIA represents approximately 5-15% of all anaphylaxis cases with FDEIA making up ⅓ to ½ of EIA cases [2]. Females are more commonly affected than females.

Patients tend to develop EIA within 30 minutes of initiating exercise and it may be triggered by exercise of any intensity level including activities as benign as raking leaves. There are no safe exercises for patients with EIA although exercise with less cardiovascular demand seems to be safer and responsible for less than 2% of EIA cases [3]. Episodes are not reliably predictable. Symptoms may not always be present or repeatable, even with the same intensity exercise in the same conditions. The frequency varies widely from a single episode to numerus with an average of 14.5 attacks per year. Most patients report symptoms become stable or decrease after the initial episode.

FDEIA represents a sub-type of EIA in which food is a cofactor in triggering the event. Wheat is most commonly implicated, although many other foods have been cited in the literature including tomatoes, cereals and peanuts. Medication use, including NSAIDS, also seems to be a facilitating factor. There are no consistent reliable environmental predictors of EIA with warm environment (64%), high humidity (32%), and cold environment (23%) noted in one study [4]. The pathophysiology of FDEIA is poorly understood. Proposed mechanisms include alterations in plasma osmolality and pH, tissue enzyme activity, blood flow redistribution, altered gastrointestinal permeability, facilitated epitope recognition/allergen binding, increased basophil, histamine release [5].

The differential diagnosis is bread and includes urticaria (cold, cholinergic), angioedema (idiopathic, hereditary), mastocytosis, scombroid, vasovagal syncope, sepsis, vocal cord dysfunction, globus hystericus, laryngospasm, exercise induced asthma, exercise induced bronchoconstriction, medication reaction and idiopathic anaphylaxis.