C L I N I C A L F O C U S : P A I N M A N A G E M E N T, R A R E D I S E A S E S , A N D A L L E R G I E S
Optimal Treatment of Anaphylaxis: Antihistamines
Versus Epinephrine
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Stanley M. Fineman, MD
Adjunct Associate Professor,
Department of Pediatrics, Emory
University School of Medicine,
Atlanta, GA; Atlanta Allergy and
Asthma Clinic, Marietta, GA
For personal use only.
Correspondence: Stanley M. Fineman, MD,
Atlanta Allergy and Asthma Clinic,
895 Canton Road,
Building 200, Suite 200,
Marietta, GA 30060.
Tel: 770-427-1471
Fax: 770-424-2280
E-mail: sfineman@atlantaallergy.com
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DOI: 10.3810/pgm.2014.07.2785
Abstract: Anaphylaxis is a rapid, systemic, often unanticipated, and potentially life-threatening
immune reaction occurring after exposure to certain foreign substances. The main immunologic
triggers include food, insect venom, and medications. Multiple immunologic pathways underlie
anaphylaxis, but most involve immune activation and release of immunomodulators. Anaphy-
laxis can be difficult to recognize clinically, making differential diagnosis key. The incidence
of anaphylaxis has at least doubled during the past few decades, and in the United States alone,
an estimated 1500 fatalities are attributed to anaphylaxis annually. The increasing incidence
and potentially life-threatening nature of anaphylaxis coupled with diagnostic challenges
make appropriate and timely treatment critical. Epinephrine is universally recommended as the
first-line therapy for anaphylaxis, and early treatment is critical to prevent a potentially fatal
outcome. Despite the evidence and guideline recommendations supporting its use for anaphylaxis,
epinephrine remains underused. Data indicate that antihistamines are more commonly used to
treat patients with anaphylaxis. Although histamine is involved in anaphylaxis, treatment with
antihistamines does not relieve or prevent all of the pathophysiological symptoms of anaphylaxis,
including the more serious complications such as airway obstruction, hypotension, and shock.
Additionally, antihistamines do not act as rapidly as epinephrine; maximal plasma concentra-
tions are reached between 1 and 3 hours for antihistamines compared with , 10 minutes for
intramuscular epinephrine injection. This demonstrates the need for improved approaches to
educate physicians and patients regarding the appropriate treatment of anaphylaxis.
Keywords: anaphylaxis; antihistamines; epinephrine; first-line treatment
Introduction
Anaphylaxis is a rapid, systemic, often unanticipated, and potentially fatal immune
reaction occurring after exposure to certain foreign substances (ie, antigens).1,2 The
main immunologic triggers include food, insect venom, and medications; however,
the extent to which these triggers contribute to anaphylaxis varies depending on study
design, study population, and geographic area.3 In the United States and Europe, food
is typically the primary contributor and accounts for approximately 32% to 56% of
cases overall3–7; however, among older adults (ie, aged . 50 years), food-associated
anaphylaxis is much less frequent than in children and younger adults.8 In Asia and
Latin America, medications are more common triggers for anaphylaxis than foods.9,10
Less common immunologic triggers include latex, immunotherapy, and environmental
allergens.3–5 Nonimmunologic triggers, such as exercise, cold exposure, radiocontrast
materials, nonsteroidal anti-inflammatory drugs, and opioids, can also cause anaphy-
laxis.3,11 Unknown triggers are responsible for approximately 20% of anaphylactic
events.3
73
 Stanley M. Fineman
According to a recent consensus definition, which takes
into account epidemiologic, research, and clinical needs,
a diagnosis of anaphylaxis should be considered if any 1 of 3
specific criteria occurs within minutes to hours of exposure to
a foreign substance (Table 1).1 The onset and specific signs
and symptoms of an anaphylactic episode vary depending
on the sensitivity of the person exposed and the absorption
rate, route, and quantity of the allergen.12 The majority of
reactions are immediate and occur within minutes of expo-
sure; however, a small proportion of reactions may also be
biphasic,13 whereby the initial symptoms wane for a period of
time and then recur.14–18 Additionally, because of the diversity
of immune mediators involved in anaphylaxis, several organ
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systems can be affected, including the skin, respiratory tract,
gastrointestinal tract, cardiovascular system, and central
nervous system.3,19,20
Multiple factors contribute to the difficulty of differ-
entially diagnosing anaphylaxis in the clinic. Diagnosis
can be especially challenging during an initial episode;
if the trigger is a novel agent; if noncutaneous symptoms
predominate; or if anaphylaxis occurs in an infant, young
child, or unconscious individual.21–24 Certain clinical situa-
tions, such as an asthmatic event, hemodialysis, and under-
For personal use only.
going anesthesia while in surgery, can also complicate the
diagnosis.25–28 Furthermore, anaphylaxis can occasionally
be confused with septic or other forms of shock, airway
obstruction due to a foreign body, or panic attack.29 In
most cases, given the emergency nature of anaphylaxis, a
diagnosis is based on clinical symptoms and patient history.19
Table 1. Consensus Definition of Anaphylaxis
Anaphylaxis should be considered if any 1 of the following 3 criteria
occurs within minutes to hours of exposure to a foreign substance:
1. Acute onset of illness with cutaneous and/or mucosal involvement
AND at least 1 of the following:
a. Respiratory compromise (eg, dyspnea, bronchospasm, stridor, hypoxia)
b. Cardiovascular compromise (eg, hypotension, collapse)
2. Two or more of the following:
a. Involvement of skin or mucosa (eg, generalized hives, itch, flushing,
swelling)
b. Respiratory compromise
c. Cardiovascular compromise
d. Persistent gastrointestinal symptoms (eg, abdominal cramping,
vomiting)
3. H ypotension: age-specific low blood pressure or . 30% decline from
baseline
Reprinted from Sampson HA, Muñoz-Furlong A, Campbell RL, et al. Second
symposium on the definition and management of anaphylaxis: summary report—
second National Institute of Allergy and Infectious Disease/Food Allergy and
Anaphylaxis Network symposium. Ann Emerg Med. 2006;47(4):373–380 with
permission from Elsevier.
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However, laboratory tests can also aid in proper diagnosis in
specific circumstances, including uncertain presentations of
symptoms.20,30–33 Although plasma histamine levels increase
during anaphylaxis, evaluating serum histamine for the diag-
nosis of anaphylaxis is impractical, given that levels only
remain elevated for 30 to 60 minutes.21,34
Evaluating serum tryptase is likely more realistic because
levels peak 60 to 90 minutes after onset and remain elevated
for up to 5 hours.29,34 Measurement of total tryptase concentra-
tions in serum or plasma is currently the most widely used
laboratory test for the diagnosis of anaphylaxis. Elevated
levels are not commonly found in individuals with food-
induced anaphylaxis; thus, low levels of tryptase do not rule
out a diagnosis of anaphylaxis.21,35 Serial tryptase measure-
ments may be helpful to improve sensitivity of detection
of an anaphylactic reaction, particularly in patients whose
tryptase levels are only moderately elevated (ie, patients who
are experiencing reactions to drugs or insect venom).36,37
Finally, some patients with anaphylaxis have increased levels
of histamine or tryptase but not both.29
Although studies assessing the incidence of anaphylaxis
are limited, often imprecise, and likely underestimate the
actual prevalence, most concur that the incidence has at
least doubled across age groups during the past few decades,
with an estimated lifetime prevalence ranging from 0.05%
to 2% in North America, Europe, and Australia.3,7,38–40 Over
the last decade, this increase may be as high as 350% for
food-induced cases and 230% for non–food-induced cases
in some countries.41 Up to 20% of individuals with anaphy-
laxis have a second episode, and between 5% and 13% have
a third episode.5,40 In the United States alone, an estimated
1500 fatalities per year are attributed to anaphylaxis42; in the
United Kingdom and Australia, the rates of fatal anaphylactic
reactions have been estimated at 0.33 per million per year
and 0.64 per million per year, respectively.43
The increasing incidence and potentially life-threatening
nature of anaphylaxis coupled with diagnostic challenges
make appropriate and timely treatment critical. Clinical
evidence and guideline recommendations indicate that
epinephrine should be the first-line therapy for anaphy-
laxis19,20,44–48; however, data indicate that other treatments,
including antihistamines, corticosteroids, and bronchodi-
lators, are often more commonly used than epinephrine
to treat patients with anaphylaxis.44 This review focuses
on the misuse of antihistamines as a first-line therapy for
anaphylaxis; they are frequently selected for treatment
because of the role of histamine in anaphylaxis.44 However,
a thorough examination of anaphylaxis pathophysiology

and the respective mechanisms of action of antihistamines
and epinephrine provide a strong, evidence-based rationale
for the use of epinephrine versus antihistamines for optimal
treatment of anaphylaxis.
Pathophysiology of Anaphylaxis
Anaphylaxis is a multifactorial response in which multiple
immunologic mechanisms may be involved in a single
episode.21 The typical pathway/mechanism of anaphylaxis
results from immunoglobulin E–mediated activation of
mast cells and basophils.3,21,38 Exposure to allergens causes
cross-linking of immunoglobulin (Ig) E molecules and acti-
vation of the FcεR1 receptors on the surface of mast cells
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and basophils.38 Upon activation, mast cells and basophils
release various preformed immunologic mediators such as
histamine, heparin, tryptase, chymase, carboxypeptidase A3,
tumor necrosis factor-α, and cathepsin G as well as newly
formed immunologic mediators including platelet-activating
factor (PAF); prostaglandin D2; leukotriene C4; cytokines
such as interleukin (IL)-5, IL-6, IL-8, IL-13, and granulocyte-
macrophage colony-stimulating factor; and chemokines
such as macrophage inflammatory protein-1α and -1β, and
monocyte chemoattractant protein-1 (Figure 1).21 In addi-
For personal use only.
tion, activated mast cells can trigger a complement cascade
via release of trypsin and kallikrein.38 Interestingly, some
allergens (eg, nonsteroidal anti-inflammatory drugs/aspirin
or radiocontrast materials) can activate the complement cas-
cade directly.21 Of note, individuals with elevated numbers of
mast cells are more prone to anaphylaxis or anaphylaxis-type
symptoms.21 More severe anaphylaxis (eg, presenting with
hypotension, hypoxia, and symptoms involving $ 3 organ
systems) has also been linked to the use of antihypertensive
medications such as β-blockers and angiotensin-converting
enzyme inhibitors.49
Histamine plays a key role in the pathophysiology of
anaphylaxis.3,38,50,51 Following allergen exposure, histamine
levels are higher than most other allergen-stimulated immune
modulators, and the effects of histamine are mediated by
various histamine receptors. Currently, 4 subclasses of
histamine receptors have been identified. Coronary vaso-
constriction and bronchial constriction occur through the H1
receptor; systemic vasodilation, gastric acid secretion, and
cardiac contractility are mediated by the H2 receptor; neu-
rotransmission is regulated by the H3 receptor; and immune
cell activation occurs via the H4 receptor.3,50 Both the H1 and
H2 receptors regulate hypotension, tachycardia, flushing,
and headache, and the H1 and H3 receptors modulate nasal
congestion and cutaneous itch.51
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Epinephrine and Antihistamines for Anaphylaxis
However, histamine is not the only immune factor to play
an important role in anaphylaxis.3,38 Of the newly formed
immunologic mediators, PAF has recently been shown to
play a major role in anaphylaxis. A study demonstrated that
mean serum PAF levels are significantly higher in patients
with anaphylaxis than in control patients (P , 0.001) and
also differ by grade of anaphylaxis reaction.52 The proportion
of patients with elevated PAF levels increased from 4% in
control patients to 20% in those with grade 1 anaphylaxis
(acute allergic reactions with cutaneous involvement only),
71% in those with grade 2 anaphylaxis (mild-to-moderate
manifestations of anaphylaxis, including decrease in
systolic blood pressure), and 100% in those with grade 3
anaphylaxis (severe manifestations of anaphylaxis, including
life-threatening respiratory and cardiovascular signs;
P , 0.001).52 Data also suggest that PAF may mediate an
amplification loop for mast cell activation in anaphylaxis.38
Other factors involved in anaphylaxis include tryptase,
immune aggregates, IgG, IgM, platelets, and T cells.38 As
described previously, determining serum tryptase levels can
be a useful diagnostic tool to identify anaphylaxis.30,31,33
Antihistamines: Inadequate for
Treatment of Anaphylaxis
Because histamine plays a key role in the pathophysiology
of anaphylaxis, H1-antihistamines (eg, diphenhydramine,
fexofenadine, hydroxyzine, cetirizine) and H2-antihistamines
such as ranitidine are frequently used for the treatment
of anaphylaxis.44 In a national study of 12.4 million US
emergency department visits for anaphylaxis from 1993 to
2004, H1-antihistamines were prescribed in 59% to 62%
of cases, and H2-antihistamine prescriptions increased
from 7% to 18%.53 Another retrospective study found that
72% and 61% of patients with anaphylaxis who visited an
Australian emergency department were treated with H1- and
H2-antihistamines, respectively.54 In a pediatric study of
patients presenting to an Australian emergency department,
51% and 5% of children were found to be treated with H1- and
H2-antihistamines, respectively.55 Data from the anaphylaxis
registry of German-speaking countries reveal that antihis-
tamines were the most frequently used (50%) emergency
therapy for anaphylaxis in children and adolescents between
2006 and 2010.56 However, H1- and H2-antihistamines do not
target all of the underlying mechanisms of anaphylaxis, and
although they are assumed to be effective on the basis of theo-
retical reasoning and misconceptions in popular culture, their
efficacy for the treatment of anaphylaxis is not supported by
randomized controlled clinical trials. A Cochrane systematic
75
 Stanley M. Fineman

Figure 1. Mast cells and basophils generate several products upon activation during anaphylaxis.
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For personal use only.

Reprinted from Simons FE, Frew AJ, Ansotegui IJ, et al. Risk assessment in anaphylaxis: current and future approaches. J Allergy Clin Immunol. 2007;120(1 suppl):S2–S24 with
permission from Elsevier.
Abbreviations: GM-CSF, granulocyte-macrophage colony-stimulating factor; IgE, immunoglobulin E; IL, interleukin; MIP-1α, macrophage inflammatory protein 1α; TNFα,
tumor necrosis factor α.

review of 2070 studies found no high-quality evidence from
randomized controlled trials without methodological issues
to support the use of H1-antihistamines in anaphylaxis.57 In
addition, a systematic review on the use of H2-antihistamines
for the treatment of anaphylaxis failed to identify any ran-
domized controlled trials that could be used to support their
use as first-line agents.58
As described above, histamine is not the only regulator
of anaphylaxis, and data show that the use of antihistamines
is inadequate to fully control the array of symptoms, some
life-threatening, associated with an anaphylactic response.
H1-antihistamines may help to relieve itching, flushing, hives,
and nasal symptoms (Figure 2)44,51,59; however, they do not
relieve or prevent the more serious complications of anaphy-
laxis, such as airway obstruction, hypotension, or shock.44
H2-antihistamines, which are only used in combination with
H1-antihistamines for anaphylaxis, may be effective at reduc-
ing hives and tachycardia but have no significant effect on
itching or other symptoms.44
In addition to limited effectiveness, there are
pharmacokinetic considerations that make the use of anti-
histamines in anaphylaxis inadequate. H1-antihistamines
have a slow absorption and relatively long time of onset
of action. The average maximal plasma concentration of
H1-antihistamines does not occur until 1 to 3 hours after oral
administration.51,60,61
Epinephrine:The Optimal Initial
Therapy for Anaphylaxis
Epinephrine is a direct-acting α- and β-adrenergic agonist
with multiple systemic actions mediated by various recep-
tors.62 On the basis of its mechanism of action, there are
multiple physiologic benefits of epinephrine in anaphylaxis
(Figure 3).62,63 For example, epinephrine can stimulate
α-adrenoceptors, leading to increased peripheral vascular
resistance, which in turn improves blood pressure and
coronary perfusion and decreases angioedema. Epinephrine
also targets β1-adrenoceptors, leading to improvement in

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 Epinephrine and Antihistamines for Anaphylaxis

Figure 2. H1- and H2-antihistamines relieve some symptoms of anaphylaxis by antagonizing the H1- and H2-receptors, respectively.
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Abbreviations: Ca, calcium; NF-κB, nuclear factor kappa-B.

cardiac contractility and heart rate. Additionally, activation
of β2-adrenoceptors via epinephrine causes bronchodilation
and increased intracellular cyclic adenosine monophosphate
production in mast cells and basophils, which can reduce
mediator release.
For personal use only.
cohort and survey studies; and nonsystematic clinical
observations) and expert opinion. Furthermore, evidence
from fatalities due to delayed use or no use of epinephrine
during an anaphylactic event is considered particularly strong
support for the early use of epinephrine in cases of severe

Not only does epinephrine target the underlying
pathophysiology of anaphylaxis, available treatment guide-
lines from the American Academy of Allergy, Asthma,
and Immunology, the American College of Allergy, Asthma,
and Immunology, the European Academy of Allergy and
Clinical Immunology, the Australasian Society of Clinical
Immunology and Allergy, and the World Allergy Organiza-
tion (WAO) published in indexed peer-reviewed journals
unanimously recommend epinephrine as first-line therapy
for anaphylaxis on the basis of human experience and
expert opinion (Table 2).19,20,44–47 Understandably, there is
reluctance to perform randomized controlled trials in ana-
phylaxis patients because of ethical, clinical, and logistical
considerations. As with antihistamines, 2 systematic reviews,
including a Cochrane analysis, did not find any adequate,
controlled clinical trials to support any new recommendations
in addition to the current recommended use of epinephrine
as first-line therapy for anaphylaxis.64,65 However, even
without randomized controlled trials, the evidence base for
epinephrine use in anaphylaxis is stronger than that for other
medications, such as antihistamines.65 First-line treatment
with epinephrine for acute anaphylaxis is firmly recom-
mended on the basis of other types of studies (eg, prospective,
nonrandomized, uncontrolled studies; retrospective studies;
analyses of emergency department visits; population-based
anaphylaxis. This includes analyses reporting the use of
epinephrine in only 14% of patients before circulatory or
respiratory arrest, and a lack of epinephrine administration
in a majority of patients immediately after or within an hour
of onset of symptoms.35,66,67
Individuals who experience severe anaphylaxis require
immediate pharmacologic assistance, and all available
guidelines are in agreement that treatment with epinephrine
should not be delayed.19,20,44–47 The median time to respiratory
or cardiac arrest after exposure to an allergen may be 5 to
30 minutes depending on the type of allergen.66 Therefore,
the most commonly recommended route of epinephrine
administration is intramuscular injection because of its rapid
absorption.68–70 Furthermore, peak plasma concentrations of
epinephrine injected intramuscularly into the thigh have been
shown to be significantly higher (P , 0.01) than those of
epinephrine injected subcutaneously or intramuscularly into
the upper arm.70 The rapid absorption time of epinephrine is in
stark contrast to the time antihistamines need to reach maxi-
mal plasma concentration (1–3 hours).51,60,61 A recent study
reviewing electronic records of children presenting with ana-
phylaxis to an urban pediatric emergency department (PED)
between 2004 and 2008 demonstrated that administration of
epinephrine before arrival to the PED was associated with
a lower rate of hospitalization compared with administration

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 Stanley M. Fineman
Figure 3. Epinephrine is a direct-acting α- and β-adrenergic agonist.
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of epinephrine in the PED (P = 0.05).22 This study highlights
the benefit of early treatment with epinephrine. The majority
of individuals who die from anaphylaxis have not received an
epinephrine injection, and delay in epinephrine injection can
result in mortality or increased hospital stay.22,35,66,71–75
In addition to being effective, intramuscular administration
of epinephrine is generally safe and associated with a low risk
of major complications or serious adverse events. Most adverse
events associated with epinephrine occur after overdose or with
intravenous administration.63 Intravenous injection should be
reserved for patients with unresponsive anaphylaxis and should
only be administered by specialists trained in dose titration
of vasopressors.44,63 Frequent and appropriate monitoring of
blood pressure, heart rate, respiratory status, and oxygenation
is also recommended.20 Importantly, there are no contraindi-
cations to intramuscular epinephrine use in anaphylaxis.62
Additionally, unintentional injection of epinephrine produced
no long-term sequelae,76 suggesting the risk associated with
intramuscular administration of epinephrine is far lower than
the potentially life-threatening risk of not using epinephrine
during an anaphylactic reaction.
Despite the scientific evidence and support from guide-
lines, the data suggest that epinephrine is both underused by
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patients and underprescribed by physicians in the treatment
of anaphylaxis. Multiple factors have been cited by patients
as reasons for the underuse of epinephrine, including lack of
affordability or access, substitution with other medications
(eg, antihistamines), one’s first experience with anaphylaxis
was mild or it resolved without epinephrine, fear of injection,
and not knowing when it is appropriate to use epinephrine.77
Additionally, a national survey revealed poor overall pre-
paredness for future anaphylactic reactions among patients
with a history of anaphylaxis: 34% of patients reported that
their plan for future anaphylactic episodes included use of
an epinephrine autoinjector, 37% of patients planned to take
an antihistamine, and 42% of patients had no anaphylaxis
emergency plan.40 This survey also reported that 50% of
patients with a history of anaphylaxis had never been pre-
scribed an autoinjector, highlighting the underprescribing
of epinephrine by physicians.40 In a national study of US
emergency department visits for anaphylaxis, epinephrine
prescriptions actually declined from 19% to 7% from
1993 to 2004.53 In the anaphylaxis registry of German-speak-
ing countries (described above), epinephrine was used in only
13% of cases between 2006 and 2010, and intramuscular
epinephrine was used in only 3.9% of cases.56
 Epinephrine and Antihistamines for Anaphylaxis

Table 2. Treatment Guidelines: Epinephrine as First-Line Therapy for Anaphylaxisa,b

Guidelines Use of Epinephrine
United States IM or SCc 1:1000 dilution; adult dose, 0.2–0.5 mg; repeat at 5-min intervals; IV infusion
United Kingdom IM 0.01 mg/kg; adult dose, 0.5 mg; repeat at 5-min intervals; IM route has greater margin of safety than IV route, which should
be used only by experienced specialists
Australia IM 0.01 mg/kg, to a maximum of 0.5 mg; repeat at 3- to 5-min intervals; IV infusion per hospital protocol only if cardiac arrest
is imminent; nebulization (in addition to injected epinephrine) for persistent stridor
EAACI (pediatric) IM 0.01 mg/kg, to a maximum of 0.5 mg, repeat at 5- to 10-min intervals; IV infusion (restrictions apply); nebulization
(restrictions apply)
WAO IM 0.01 mg/kg, to a maximum dose of 0.5 mg (0.3 mg in children), repeat at 5- to 15-min intervals
a
The rationale for selecting the guidelines listed in this table is that they are published in indexed peer-reviewed journals and used beyond the countries in which they
were developed; for example, the US guidelines are used throughout North America and Latin America, the UK guidelines are used in other European countries, and the
Australian guidelines are used throughout southeast Asia.
b
Different systems of grading the quality of the evidence and the strength of the recommendations are used in the US, UK, Australian, and EAACI guidelines.
c
The participants at the Second National Institute of Allergy and Infectious Disease/Food Allergy and Anaphylaxis Network Symposium stated that available evidence
indicated intramuscular administration is preferred over subcutaneous injection.
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Adapted from Simons FE. Pharmacologic treatment of anaphylaxis: can the evidence base be strengthened? Curr Opin Allergy Clin Immunol. 2010;10(4):384–393. Reprinted
with permission from Lippincott Williams & Wilkins, Inc.
Abbreviations: EAACI, European Academy of Allergy and Clinical Immunology; IM, intramuscular; SC, subcutaneous; WAO, World Allergy Organization.

Conclusion
Anaphylaxis is a rapid and potentially life-threatening reac-
tion that requires immediate pharmacologic intervention.
Multiple physiologic pathways underlie anaphylaxis, but
most involve immune activation and release of immuno-
modulators. Epinephrine is universally recommended as
For personal use only.
Acknowledgments
Editorial assistance was provided, under the direction of the
author, by Todd Parker, PhD, Charlene Rivera, PhD, and
Jennifer Rossi at MedThink SciCom, with support from
Mylan Specialty LP.

the first-line therapy for anaphylaxis, and early treatment is
critical to prevent a potentially fatal outcome.
Despite the body of evidence and guideline recommenda-
tions supporting the use of epinephrine for first-line treatment
of anaphylaxis, the data suggest that epinephrine is under-
used. Conversely, even though there is a lack of evidence for
the use of antihistamines for the treatment of anaphylaxis,
these agents are still commonly used in patients with ana-
phylaxis. In addition to not addressing all of the underlying
symptoms of anaphylaxis, prompt treatment of anaphylaxis is
not achieved with the use of antihistamines because maximal
plasma concentrations are reached between 1 and 3 hours for
antihistamines compared with , 10 minutes for intramuscu-
lar epinephrine injection. This suggests the need for improved
educational approaches to increase adherence to anaphylaxis
guidelines and to enhance physicians’ understanding of the
mechanisms of anaphylaxis and the reasons why epinephrine
should be considered the only first-line treatment. Improved
physician education will enable physicians to communicate
optimal anaphylaxis management strategies to their patients,
which include establishing straightforward anaphylaxis
emergency plans, emphasizing the importance of always car-
rying an epinephrine autoinjector, and appropriately training
patients on the use of epinephrine autoinjectors to address
patients’ feelings of uncertainty or fear.
Conflict of Interest Statement
Stanley M. Fineman, MD, has received research support from
Genentech, Meda, Shionogi, and Sunovion, and has served
on speakers’ bureaus for and/or has received consulting fees
from AstraZeneca, Genentech/Novartis, Meda, Mylan, and
Sunovion.
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Food Allergy and Anaphylaxis Network symposium. Ann Emerg Med.
2006;47(4):373–380.
2. Simons FE, Sheikh A. Anaphylaxis: the acute episode and beyond. BMJ.
2013;346:f602.
3. Ben-Shoshan M, Clarke AE. Anaphylaxis: past, present and future.
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