Overview of Allergy and Anaphylaxis

Abstract

Allergic reactions and anaphylaxis occur on a severity continuum from mild and self-limited to potentially life-threatening or fatal reactions. Anaphylaxis is typically a multiorgan phenomenon involving a broad range of effector cells and mediators. Emergency department visits for anaphylaxis are increasing, especially among children. There is a broad differential diagnosis for anaphylaxis, and the diagnosis of anaphylaxis can be aided by the use of the National Institutes of Allergy and Infectious Disease/Food Allergy and Anaphylaxis Network clinical diagnostic criteria. Risk factors for severe anaphylaxis include older age, delayed epinephrine administration, and cardiopulmonary comorbidities.

Keywords: Anaphylaxis; Diagnosis; Epidemiology; Epinephrine; Risk factors.

Fig. 1.

Severity grading system for acute allergic reactions. ^aFor patients with multiple symptoms, reaction severity is based on the most severe symptom; symptoms that constitute more severe grades always supersede symptoms from less severe grades. The grading system can be used to assign reaction severity at any time during the course of reactions; reactions may progress rapidly (within minutes) from one severity grade to another. The grading system does not dictate management decisions; reactions of any severity grade may require treatment with epinephrine. ^bPatients with severe cardiovascular and/or neurologic involvement may have urinary or stool incontinence. However, the significance of incontinence as an isolated symptom is unclear, and it is therefore not included as a symptom in the subgrading system. ^cAbdominal pain may also result from uterine cramping. (From Dribin TE, Schnadower D, Spergel JM, et al. Severity grading system for acute allergic reactions: a multidisciplinary Delphi study J Allergy Clin Immunol 2021;148(1):173–181: with permission.)

Fig. 2.

Mechanisms underlying human anaphylaxis. (From Simons FE. Anaphylaxis. J Allergy Clin Immunol 2010;125(2 Suppl 2):S161–8; with permission.)

Fig. 3.

Pathophysiological changes in anaphylaxis and mediators that have been implicated in these processes. (From Reber LL, Hernandez JD, Galli SJ. The pathophysiology of anaphylaxis. J Allergy Clin Immunol 2017;140(2):335–48; with permission.)

Fig. 4.

Summary of alpha-Gal sensitization leading to clinical symptoms of red meat allergy. The southeastern section of the United States is where most of the reactions to red meat have been reported. This region overlaps with the distribution of the lone star tick. The current hypothesis is that persons are bitten by lone star ticks carried by deer into rural and urban areas. After a period of time, IgE to alpha-Gal develops. Once IgE to alpha-Gal reaches sufficient levels, ingestion of red meat can trigger reactions. Several of the images used in this figure are licensed under a Creative Commons CC BY-NC 2.0 (Attribution-NonCommercial 2.0 Generic) license (Cow: https://flic.kr/p/adgjhp by user Plashing Vole; Deer: https://flic.kr/p/jeZwq7 by user Cherry Bream; Sheep: https://flic.kr/p/4WirD by user Lauren; Tick: https://flic.kr/p/cdnNaY by user Katja Schulz; Pig: https://flic.kr/p/N7gpc by user Anne). (From Steinke JW, Platts-Mills TA, Commins SP. The alpha-Gal story: lessons learned from connecting the dots. J Allergy Clin Immunol 2015;135(3):589–96; with permission.)