Anaphylaxis - No. 257 / Edition 1

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An interdisciplinary group of experts explore the pathophysiology of different types of anaphylactic and anaphylactoid reactions in this timely publication. Data are presented on the epidemiology of these conditions and problems concerning diagnosis, therapy and prevention are discussed. Cardiovascular and microcirculatory events are examined, including microcirculatory disturbances, anaphylaxis during anesthesia, and the role of histamine receptors in the response of the heart to anaphylaxis. There is detailed consideration of the different initiators of anaphylaxis, including food, radiographic media, insect venom, and artificial materials used in operating rooms. The book ends with a discussion of the various controversies surrounding diagnosis and therapy.

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Editorial Reviews

Doody's Review Service
Reviewer: Phil Lieberman, MD (University of Tennessee College of Medicine)
Description: This publication of the Novartis Foundation is an outgrowth of a symposium convened by the Foundation. Participants in the symposium were all recognized experts in the field of allergy/immunology, and each had a special interest in the clinical aspects or basic science phenomenon germane to the study of anaphylaxis.
Purpose: The purpose is to disseminate the opinions of experts regarding various issues that are topical and germane to the phenomenon of human anaphylaxis. The intent is to familiarize the reader with advances in our knowledge relating to this field.
Audience: Allergists/immunologists are the primary audience, but this book would make good reading for any physician interested in this area.
Features: The 15 chapters range from the basic science relative to anaphylactic events all the way to the perspective of patients suffering with such events. A particularly attractive feature is that each chapter (which corresponds to a presentation at the symposium) is followed by a lively discussion involving all participants in the symposium. The discussions themselves are unique and through them the reader becomes privy to the thoughts of a well-recognized panel of educators and research scientists working in the area of anaphylaxis. The editing of these conversations is superb and maintains the spontaneity of the discussion.
Assessment: This is a superb and unique book. There is no other publication comparable to it in scope or design. It is an essential addition to the library of individuals with a special interest in anaphylaxis and would be helpful to anyone dealing with patients experiencing anaphylactic episodes.
From the Publisher
"This is a superb and unique book. There is no other publication comparable to it in scope or design…an essential addition…" (Doody's Health Services)

4 Stars! from Doody
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Product Details

  • ISBN-13: 9780470861141
  • Publisher: Wiley
  • Publication date: 4/2/2004
  • Series: Novartis Foundation Symposia Series , #140
  • Edition number: 1
  • Pages: 306
  • Product dimensions: 6.18 (w) x 9.41 (h) x 0.76 (d)

Read an Excerpt

Anaphylaxis, No. 257

John Wiley & Sons

ISBN: 0-470-86114-2

Chapter One

History and classification of anaphylaxis

Johannes Ring, Knut Brockow and Heidrun Behrendt

Division Environmental Dermatology and Allergology GSF/TUM, Department of Dermatology and Allergy Biederstein, Technical University Munich, Biedersteiner Straße 29, D-80802 Munich, Germany

Abstract. Anaphylaxis is the maximal variant of an acute allergic reaction involving several organ systems. The phenomenon itself is old, but it was recognized and named at the beginning of the 20th century by Richet and Portier. The clinical symptoms of anaphylaxis affect various organs, most commonly starting in the skin and proceeding to the respiratory tract, to gastrointestinal involvement and to cardiovascular symptoms, and finally to cardiac and/or respiratory arrest. Anaphylaxis stricto sensu is an immunological reaction, mostly mediated by IgE antibodies, but also by IgG or IgM antibodies (immune complex anaphylaxis). There are cases with similar clinical symptomatology without detectable immunological sensitization which are called pseudo-allergic or anaphylactoid reactions. In the newer nomenclature, some authors tend to include these under the heading of 'anaphylaxis' which has then to be defined as an axcute systemic hypersensitivity reaction. The most common elicitors of anaphylaxis include drugs, foods, additives, but also other allergens as well as physical factors (cold, heat, UV radiation). The clinical outcome-theintensity of the reaction-is not only influenced by the degree of sensitization, but also by concomitant other factors: sometimes, individuals only develop anaphylaxis after simultaneous exposure to the allergen and an infection, physical exercise, psychological stress or concomitant medication (e.g. ß blockers). The term 'summation anaphylaxis' has been proposed for this phenomenon which probably underlies many cases of so-called idiopathic anaphylaxis. In patients with insect venom anaphylaxis, decreased levels of plasma angiotensin have been measured in inverse correlation to the severity of the reaction. Certain differential diagnoses have to be distinguished from anaphylaxis. Every patient with a history of anaphylaxis should undergo allergy diagnosis with the aim to detect the eliciting agent, characterize the relevant pathomechanism (e.g. IgE-mediated reaction) and to offer a tolerable alternative (in food or drug allergy). In clear-cut IgE-mediated anaphylaxis, allergen-specific immunotherapy (hyposensitization) is the effective causal treatment, with success rates of 90% in insect venom anaphylaxis.

2004 Anaphylaxis. Wiley, Chichester (Novartis Foundation Symposium 257) p 6-24

Allergic diseases have been increasing in prevalence in most countries over the last few decades (Ring et al 2001) and are often not taken seriously because they are not regarded as contributory to increased mortality rates. This rather superficial opinion has been contradicted by a variety of life-threatening emergencies in allergology (e.g. fatal asthma attack, anaphylaxis, laryngeal [angio-]oedema, severe serum sickness with vasculitis and nephritis, bullous drug eruptions like toxic epidermal necrolysis) among which anaphylaxis undoubtedly represents the most acute condition.


The phenomenon of anaphylaxis is old and has been described in ancient Greek and Chinese medical literature. The first documented anaphylactic patient might have been pharaoh Menes who died 2640BC from the sting of a wasp, as hieroglyphs tell (Wadell 1930).

The phenomenon was only clearly recognized in 1901 when Charles Richet and Paul Portier were doing their experiments on the yacht of the prince of Monaco and later on in the laboratory in Paris, trying to immunize dogs with Actinia extracts (Portier & Richet 1902). When, contrary to the expectation, after repeated injections, the animal died under dramatic circumstances, Richet-who was called by Portier into the lab-immediately recognized that there was something new ('C'est un phénoméne nouveau, il faut le baptiser!') and wanted to find a name for it. What he wanted to express was 'lack of protection' and should have been 'aphylaxis' (Greek [alpha] privativum = negation); however, for euphonic reasons, he preferred 'anaphylaxis', a term which rapidly spread all over the world; for its description Richet won the Nobel prize in 1913.

This discovery, describing an obvious damage by immunization-while earlier immunization was only connected with the positive and desired effect of protection against pathogenic organisms-subsequently led to the creation of the term 'allergy' by Clemens Freiherr von Pirquet in 1906 (von Pirquet 1906).

Later on, researchers realized that similar symptoms (Hanzlik & Karsner 1920) can be elicited by the injection of histamine in individuals or could occur in animals not previously sensitized ('anaphylactoid reactions') (Lorenz et al 1977, Kind et al 1972).


There is limited knowledge about the exact prevalence and incidence of anaphylaxis in the general population and in different age groups. Some estimates of insect-sting anaphylaxis range between 1 and 3% (Müller 2001, Yocum et al 1999). For drug-induced anaphylaxis, different incidence rates have been reported for different drugs (e.g. prevalence of penicillin allergy 2%; fatal anaphylaxis 1:50 000-1:100 000).

Clinical symptoms

Clinically, anaphylaxis represents a syndrome of different symptoms involving various organs which may develop either alone or simultaneously or subsequently, most commonly

starting in the skin (pruritus, flush, urticaria, angioedema) and the neighbouring mucous membranes (itchy palate, paraesthesia in pharynx, genital mucosa) are often the first symptoms

proceeding to the respiratory tract(sneezing, rhinorrhoea, hoarseness, dysphonia, laryngeal oedema, cough, laryngeal obstruction, bronchospasm, respiratory arrest)

abdominal symptoms (nausea, cramps, vomitus, defecation, diarrhoea, also miction and uterus cramps occur)

and cardiovascular symptoms (tachycardia, blood pressure changes-not necessarily hypotension, but also transient-type hypertension has been observed as first symptom-arrhythmia, shock, cardiac arrest). Primary cardiac manifestation in anaphylaxis has been observed in ECG-changes (T-flattening, supraventricular arrhythmia, AV block) (Pavek et al 1982, Marone et al 1995). Marked changes of central venous pressure are common. During anaphylaxis, myocardial infarction has occurred (Cistero et al 1992, Wagdi et al 1994).

Prodromi of anaphylaxis comprise paraesthesia on palms and soles, a metallic 'fishy' taste, anxiety, sweating, headache or disorientation.

Several attempts have been made to develop grading scales for severity scoring of anaphylaxis which differ in some respects (Mueller 1966, Ring & Messmer 1977, Ansell 1990). We proposed in a study describing 248 anaphylactoid reactions and observing 200 906 intravenous infusions of colloid volume substitutes, a simple scoring system from I to IV which is immediately useful with regard to acute therapy without need for long reflection (Table 1).

Although the clinical symptoms of anaphylaxis are rather characteristic, some differential diagnoses have to be considered (Table 2).


Anaphylaxis stricto sensu is an immunological reaction mostly mediated by IgE antibodies on the surface of mast cells and basophil leukocytes which, after a bridging with an at least bivalent allergen, trigger the secretion of preformed and newly synthesized mediators. In spite of our knowledge of mast cell activation and IgE antibodies, the exact mechanisms of amplification are not yet understood which allow a healthy individual to be killed by a few micrograms of an allergen within minutes.

Apart from IgE, other antibodies may also elicit anaphylaxis via immune complex formation and complement activation (immune complex anaphylaxis), (Smedegard et al 1979, Richter et al 1980, Ring 1978). Clinical examples are anaphylactic reactions to blood products, xenogeneic proteins as well as dextran (Ring & Messmer et al 1977, Hedin et al 1976).

Apart from these clear-cut immunologically mediated reaction patterns, there are cases with very similar clinical symptomatology of anaphylaxis without detectable immunological sensitization (antibodies or sensitized cells) which have been called pseudo-allergic or anaphylactoid reactions. The mechanisms of these reactions are much less well-understood (Table 3) and include direct liberation of vasoactive mediators (e.g. histamine), general mast cell or basophil activation with release of other mediators, activation of the complement or other plasma protein systems (coagulation, kallikrein-kinin) as well as neuropsychogenic reflex mechanisms. It is known that psychological stress alone can lead to increased plasma histamine levels (Irie et al 2002).

In the end phase of the anaphylactic reaction, similar pathophysiological changes occur which are relevant for the clinical symptoms with post-capillary plasma exudation, microcirculatory disturbance with decreased capillary pressure and perfusion and erythrocyte stasis (Withers et al 1998, Endrich et al 1979, Fisher 1986, Sudhakaran et al 1979). Mast cell dependent anaphylactic reactions go along with the secretion ofmast cell tryptase-preferably ß-tryptase-in the serum which still can be detected even hours (sometimes postmortem) after a reaction(Schwartz et al 1994, Brockow et al 1999).

The amount of mediator release from mast cells and basophils depends not only on the serum concentration of IgE antibodies or the concentration of allergen or other elicitors, but is influenced by non-specific factors like acute infection, physical exercise, psychological stress, concomitant medication, such as ß blockers or angiotensin-converting enzyme (ACE) inhibitors. These influences may-by the action of cytokines, like interleukin 3, 4, 13 or others-influence the 'releasability' of mediator-secreting cells and help to explain the well-known clinical fact that sometimes patients only react under certain circumstances when several eliciting factors act simultaneously (e.g. infection + allergen, exercise+ allergen; Sheffer & Austen 1980, simultaneous exposure to different relevant allergens, etc). The term 'summation anaphylaxis' or 'augmentation anaphylaxis' has been proposed for this phenomenon which seems to be much more common than previously thought and probably underlies many cases of so-called 'idiopathic anaphylaxis' (Table 4).

Recently, some authors have included the non-immunologically mediated immediate-type reactions also under the heading 'anaphylaxis'; then, anaphylaxis would have to be defined as 'acute generalized immediate-type hypersensitivity reaction' (Johansson et al 2001).

Problems in terminology arise from the fact that classifications are attempted at different levels, either coming from clinical symptoms or from pathophysiology. So the terms may have different meanings and furthermore, our knowledge, especially regarding pseudo-allergic reactions, is so limited that classifications always remain speculative in nature. It should be stressed that the term 'pseudoallergic' or 'non-immune' anaphylaxis is negatively defined in that it is not possible to detect immunological sensitization in the serum or at the cellular level. Possibly, with advanced technology, such reactions may be turned from pseudo-allergic anaphylactoid reactions into allergic anaphylactic reactions. From a clinical point of view, the broader meaning of 'anaphylaxis' seems acceptable and should not lead to confusion when the further distinction into immunologically mediated (IgE, IgG or others) or non-immunological (pseudo-allergic) is kept in mind!

During anaphylaxis, the organism has a variety of systems to counteract the untoward effects of the suprarenal hormones (stress), but also the rennin-angiotensin system. We could show that during drug-induced anaphylaxis under controlled conditions, angiotensin II concentrations sharply increase in urine together with clinical symptoms; this also could explain why sometimes initial hypertension is observed prior to hypotension in severe anaphylaxis (Rittweger et al 1994). In a series of patients with insect-venom anaphylaxis, we found significantly decreased plasma levels of components of the rennin-angiotensin system, and also in a patient with unexplained idiopathic anaphylaxis (Hermann & Ring 1993).

Allergens and elicitors

The most common elicitors of anaphylaxis are drugs, proteins, foods, aeroallergens, additives, body fluids, latex and microbial antigens, but also physical factors (Table 5). However, the total spectrum of elicitors is much broader, even anaphylaxis to ethanol has been described (Przybilla & Ring 1983). Rare cases of passive transfer by IgE antibodies via blood transfusion as well as attempted suicide (penicillin-allergic nurse) have been reported. Murder has been attempted by eliciting anaphylaxis in the detective literature. Also anaphylaxis factitia ('Munchausen's syndrome') exists (Ireland et al 1967). The eliciting agent may contact the organism via the air (fish allergens in volatile form around fish stores, latex allergens in operation theatres or rooms decorated with balloons), via the skin surface (contact anaphylaxis) (Ring et al 1986) but mostly after oral or parenteral intake.

Patient management

Every patient with a history of anaphylaxis should undergo allergy diagnosis which has to include three steps:

detection of the eliciting agent

characterization of the relevant pathophysiology

offering a tolerable alternative (Ring & Behrendt 1999).

For prophylaxis, this means abstaining from polypragmatic pharmacotherapy. Equally important are endeavours of the pharmaceutical industry to produce better and less allergenic drugs. Predictive testing for these purposes (namely, characterization of IgE-inducing allergens) has to be improved.

Knowledge of possible complications is the basis of successful therapy. This implies education of the informed patient and his surroundings as well as improved declaration laws.

In clear-cut IgE mediated anaphylaxis, allergen-specific immunotherapy is the effective causal treatment with success rates of over 90% (Przybilla et al 1987). Attempts of 'hyposensitization' in certain types of drug allergy have been successful. In only few cases, specific induction of tolerance against xenogeneic horse immunoglobulin (Ring et al 1974, Jones et al 1976) or by hapten inhibition in dextran anaphylaxis have been proven successful (Laubenthal 1986).

Treatment of the acute anaphylactic episode follows the severity of symptoms (Messmer 1983) and includes the intramuscular use of epinephrine (adrenaline) as soon as severe respiratory involvement or hypotension occurs.


Excerpted from Anaphylaxis, No. 257 Excerpted by permission.
All rights reserved. No part of this excerpt may be reproduced or reprinted without permission in writing from the publisher.
Excerpts are provided by Dial-A-Book Inc. solely for the personal use of visitors to this web site.

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Table of Contents

Chair’s introduction (Galli).

History and classification of anaphylaxis (Ring et al).

Rethinking TH2 antibody responses and allergic sensitization (Stern et al).

General discusssion I.

The high affinity receptor for IgE, FceRI (Metzger).

Effector cells of anaphylaxis: mast cells and basophils (Schwartz).

Cytokine enhancement of anaphylaxis (Strait et al).

General discussion II.

Patterns of anaphylaxis: acute and later phase features of allergic reactions (Golden).

Fatal anaphylaxis in the UK, 1992-2001 (Pumphrey).

The human heart as a shock organ in anaphylaxis (Marone et al).

General discussion III.

Food-induced anaphylaxis (Sampson).

Anaphylaxis to insect venom (Mosbech).

Anaphylaxis to anaesthetic drugs (Fisher).

General discussion IV.

The radiocontrast molecule in anaphylaxis. A surprising antigen (Lasser).

General discussion V.

Epinephrine (adrenaline) in the first-aid, out-of-hospital treatment of anaphylaxis (Simons).

New approaches for the treatment of anaphylaxis (Leung et al).

Patient’s perspective and publc policy regarding anaphylaxis (Munoz-Furlong).

Final discussion.

Index of contributors.

Subject index.

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