Kenji Kabashima (ed.)Immunology of the Skin10.1007/978-4-431-55855-2_26

26. Anaphylaxis

Eishin Morita¹

(1)

Department of Dermatology, Shimane University Faculty of Medicine, Enya-cho 89-1, Izumo 693-8501, Japan

Eishin Morita

Abstract

Anaphylaxis was first recognized and named in 1902 by Charles Robert Richet and Paul Portier. The definition of anaphylaxis was established with the consensus of several task forces in Europe and in the World Allergy Organization (WAO). Anaphylaxis is a rapid-onset systemic reaction involving multiple organ systems. The most frequent causes are foods, insect venom, and drugs. The mechanism of anaphylaxis is basically an IgE-mediated allergic reaction; mediators released from mast cells and basophils elicit the symptoms in various organs. The prevalence of anaphylaxis symptoms are as follows: urticaria and/or angioedema (85–90 %); flush (45–55 %); dyspnea and/or wheezing (45–50 %); swelling of the upper airways (50–60 %); vertigo, syncope, and/or hypotension (30–35 %); nausea, vomiting, diarrhea, and/or cramps (25–30 %); loss of consciousness (22 %); and rhinitis (15–20 %). In cases of food-dependent exercise-induced anaphylaxis (FDEIA), exercising and/or nonsteroidal anti-inflammatory drugs (NSAIDs) are common triggers of anaphylaxis. These triggers elicit symptoms within a few hours of eating the culprit food by enhancing allergen absorption from the gastrointestinal tract. The basic initial management of anaphylaxis is calling for assistance and injecting epinephrine intramuscularly. Lying supine with the lower extremities elevated, using supplemental oxygen and intravenous fluid resuscitation are also necessary.

Keywords

AnaphylaxisIgEIgE-mediated allergic reactionMast cellsBasophilsHistamineFood-dependent exercise-induced anaphylaxis (FDEIA)Nonsteroidal anti-inflammatory drugs (NSAIDs)

26.1 History of Anaphylaxis

The path to the discovery of anaphylaxis can be retraced to 1901 in the Principality of Monaco [1]. On the orders of Albert Grimaldi, Prince of Monaco, who had a perpetual passion for the sea, Charles Robert Richet and Paul Portier studied the adverse effects of stings by the tentacles of the gelatinous invertebrates, Physalia. They were able to confirm that Physalia tentacles contain a paralyzing poison, which they named as “hypnotoxin”. On the basis of this observation, they extended their experiment to developing a vaccine against a toxin from the sea anemone, Actinia sulcata, which was later named “actinotoxin”, by administering the toxin into dogs. The trial with dogs was astonishing, because all of the dogs collapsed and died within a few minutes after the repeat administration of doses as small as 0.1 mL/kg. In 1902, they reported their findings and coined the term “aphylaxis”, which was subsequently changed to “anaphylaxis”.

Anaphylaxis was formerly recognized as an IgE-mediated allergic reaction. However, the following definition of anaphylaxis was recently established as a result of the consensus of several task forces in Europe and in the World Allergy Organization (WAO): “a serious, life-threatening generalized or systemic hypersensitivity reaction” and “a serious allergic reaction that is rapid in onset and might cause death” [2].

26.2 Epidemiology and Symptoms of Anaphylaxis

26.2.1 Epidemiology

Anaphylaxis is not rare, and the rate of occurrence appears to be increasing [3]. Although numerous studies have estimated the occurrence rate of anaphylaxis, the true global occurrence rate from all triggers in the general population has not been established, mainly because patients are often seen by different medical specialists (e.g., emergency doctors, allergists, or other clinicians). The lifetime prevalence based on international studies is estimated to be 0.05–2 % [4]. The most frequent causes of anaphylaxis are foods, insect venom, and drugs [4]. The precise frequencies of the causes vary depending on age, geographical regions, and the data source (e.g., emergency doctors and allergists). Food allergens are the most frequent cause of anaphylaxis in children, and venom is the most frequent cause in adults. Among drugs, antibiotics, nonsteroidal anti-inflammatory drugs (NSAIDs), and biologic agents are the most common causes of anaphylaxis.

26.2.2 Symptoms

Anaphylaxis is a systemic reaction involving multiple organ systems in humans. A major characteristic of anaphylaxis is the rapid onset of symptoms, mostly within 1 or 2 h, after the allergen exposure. Symptoms involve the skin, mucosa, respiratory system, gastrointestinal tract, cardiovascular system, and central nervous system. The symptoms of anaphylaxis are summarized in Box 26.1. The prevalence of symptoms in anaphylactic reactions is as follows: urticaria and/or angioedema (85–90 %); flush (45–55 %); dyspnea and/or wheezing (45–50 %); swelling of the upper airways (50–60 %); vertigo, syncope, and/or hypotension (30–35 %); nausea, vomiting, diarrhea, and/or cramps (25–30 %); loss of consciousness (22 %); and rhinitis (15–20 %) [4]. Anaphylaxis is diagnosed on the basis of clinical findings. Box 26.2 shows the clinical criteria for diagnosing anaphylaxis established by the WAO [2].

The above-mentioned symptoms are sometimes followed by an asymptomatic period of 1 h or more and a subsequent return of symptoms without further exposure to the allergen; this is called a biphasic anaphylactic reaction. The reported incidence of the biphasic reactions ranges from 3 to 20 % in the literature [5].

26.2.3 Box 26.1: Symptoms of Anaphylaxis

Skin and mucosa
- Flushing, urticaria, angioedema, erythema, and itching (skin)
- Conjunctival erythema and tearing (eyes)
- Itching of lips, tongue, and palate, and swelling of lips, tongue, and uvula (oral mucosa)
Respiratory system
- Itching, congestion, rhinorrhea, and sneezing (nose)
- Itching and swelling (throat)
- Dyspnea sensation, cough, increased respiratory rate, wheezing, cyanosis, and respiratory arrest (chest)
Gastrointestinal tract
- Abdominal pain, nausea, vomiting, and diarrhea
Cardiovascular system
- Chest pain, tachycardia, hypotension, shock, and cardiac arrest
Central nervous system
- Vertigo, headache, and loss of consciousness

26.2.4 Box 26.2: Clinical Criteria for Diagnosing Anaphylaxis [2]

Anaphylaxis is highly likely when any one of the following three criteria is fulfilled,

Acute onset of an illness (minutes to several hours) with involvement of the skin, mucosal tissue, or both (e.g., generalized urticaria, itching or flushing, swollen lips-tongue-uvula)

and at least one of the following,

(A)

Respiratory compromise (e.g., dyspnea, wheeze-bronchospasm, stridor, reduced peak expiratory flow (PEF), hypoxemia)

(B)

Reduced blood pressure or associated symptoms of end-organ dysfunction (e.g., hypotonia [collapse], syncope, incontinence)

Two or more of the following that occur rapidly after exposure to a likely allergen¹ for that patient (minutes to several hours),

(A)

Involvement of the skin–mucosal tissue (e.g., generalized urticaria, itch-flush, swollen lips-tongue-uvula)

(B)

Respiratory compromise (e.g., dyspnea, wheeze-bronchospasm, stridor, reduced PEF, hypoxemia)

(C)

Reduced blood pressure or associated symptoms (e.g., hypotonia [collapse], syncope, incontinence)

(D)

Persistent gastrointestinal symptoms (e.g., crampy abdominal pain, vomiting)

Reduced blood pressure after exposure to known allergen² for that patient (minutes to several hours)

(A)

Infants and children: low systolic blood pressure (age-specific) or greater than 30 % decrease in systolic blood pressure³

(B)

Adults: systolic blood pressure of less than 90 mmHg or greater than 30 % decrease from that person’s baseline

26.3 Mechanisms of Anaphylaxis

The pathogenesis of anaphylaxis includes immunologic and nonimmunologic reactions; the former is categorized as IgE-mediated and non-IgE-mediated reactions [2]. Nonimmunologic mechanisms include direct mast cell activation by factors such as physical exercise, ethanol, and medications. The IgE-mediated reaction has been thoroughly investigated. Exogenous allergens recognized by antigen-presenting cells in immune systems are introduced to helper T-lymphocytes (Th) as processed allergens. The Th cells subsequently differentiate into various types of effector cells such as Th1, Th2, Th9, and Th17 cells under the influence of several cytokines, chemokines, costimulatory signals, and regulatory T-cells. The expansion of allergen-specific Th2 cells results in the production of interleukin (IL)-4 and IL-13, which induce immunoglobulin class switching to IgE as well as the clonal expansion of naïve and IgE+ memory B-lymphocyte populations. The production of allergen-specific IgE is genetically influenced; this constitution is called atopic diathesis.

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