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Table 1 Epidemiology and patient risk factors

From: 2015 update of the evidence base: World Allergy Organization anaphylaxis guidelines

Epidemiology [ 7 16 ]
Hospitalization rates for anaphylaxis continue to increase year-on-year [912].
Anaphylaxis fatality rates have remained stable or decreased slightly. Fatalities are age-, co-morbidity-, and trigger-related [1214].
The highest hospital admission rates for food-induced anaphylaxis occur in very young children age 0–4 years; however, the rate of increase in the age groups 5–14 years and 15–29 years is accelerating [11].
Patient risk factors and amplifying co-factors [ 17 37 ]
Data from an anaphylaxis registry of more than 5000 patients with systemic allergic reactions indicated that although monotherapy with beta-blockers and to a lesser extent, ACE inhibitors, increased the risk of severe anaphylaxis, the risk was further increased by concurrent use of a drug from each class [26].
In an experimental model, although a beta-blocker (metoprolol) given alone had a modestly aggravating effect and an ACE inhibitor (ramipril) given alone had no significant effect, anaphylaxis was exacerbated and mediator release was increased when these medications were given concurrently [26].
In vitro, FcεRI-mediated mast cell histamine release was not increased by metoprolol or ramipril given alone, but was synergistically increased when the drugs were given together. This three-part study provides epidemiologic and experimental evidence that ACE inhibitors and beta-blockers aggravate anaphylaxis partly as a result of direct mast cell priming and decreasing the threshold for mast cell activation [26].
In a prospective study of co-factors that amplify anaphylaxis, wheat-dependent, exercise-induced anaphylaxis occurred when plasma gliadin levels were elevated by ingestion of higher gluten doses, gluten and exercise, or gluten and acetylsalicylic acid plus alcohol [36].
  1. ACE angiotensin-converting enzyme inhibitor