Allergy

447 Pages·2006·43.92 MB·English

by  Stephen T. Holgate

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First published 2006
First edition 1993
Second edition 2001
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ISBN-13: 978-0-323-03227-8
ISBN-10: 0-323-03227-3
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List of Contributors
Mitsuru Adachi,MD Thomas Bieber,MD,PhD Virginia L Calder,BsC,PhD
First Department of Internal Medicine Professor and Chairman Lecturer in Immunology
Showa University School of Medicine Director of the Department of Dermatology Division of Clinical Ophthalmology
Shingawa-ku,Tokyo University of Bonn Institute of Ophthalmology
Japan Bonn,Germany University College London
London,UK
N Franklin Adkinson Jr.,MD Stephan C Bischoff,MD
Thomas B Casale,MD
Professor of Medicine Professor of Medicine
Professor of Medicine
Clinical Immunology Unit Department of Clinical Nutrition and
Chief,Division of Allergy/Immunology
Johns Hopkins Asthma & Allergy Center Prevention
Creighton University
Baltimore,MD University of Hohenheim
Omaha,NE
USA Stuttgart,Germany
USA
Mariana Castells,MD,PhD
Neil Alexis,MD David H Broide,MB,ChB
Assistant Professor of Medicine,
Assistant Professor Professor of Medicine
Harvard Medical School
Department of Pediatrics Division of Allergy and Immunology
Brigham & Women’s Hospital
Division of Immunology and Infectious University of California - San Diego
Boston,MA
Disease La Jolla,CA
USA
US EPA Human Studies Facility USA
University of North Carolina at Ernest N Charlesworth,MD
Chapel Hill Roger J Buckley,MA,FRCS,FRCOphth, Associate Professor of Medicine
Chapel Hill,NC HonFCOptom Department of Allergy & Immunology
USA Bausch & Lomb Professor of Ocular University of Texas Medical Branch
Medicine at Galveston
Andrew J Beavil,BsC,PhD Department of Optometry and Galveston,TX
Senior Lecturer in Asthma Ophthalmic Dispensing USA
King’s College London School of Applied Sciences
Martin K Church,MPharm,PhD,DSc
MRC & Asthma UK Centre in Allergic Anglia Ruskin University
Professor of Experimental
Mechanisms of Asthma Cambridge,UK;
Immunopharmacology
New Hunt’s House Honorary Consultant Ophthalmologist
Division of Infection,Inflammation and
Guy’s Hospital Moorfields Eye Hospital
Repair
London,UK London,UK
University of Southampton
Southampton General Hospital
Rebecca L Beavil,BSc,PhD William W Busse,MD
Southampton,UK
Research Fellow Professor of Medicine
King’s College London Allergy and Immunology,Department of Julian Crane,MBBS,FRCP,FRACP
The Randall Division of Cell and Medicine Professor of Clinical Epidemiology
Molecular Biophysics University of Wisconsin - Madison Department of Medicine
New Hunt’s House Medical School Wellington School of Medicine and
Guy’s Hospital Madison,WI Health Sciences
London,UK USA Wellington,New Zealand
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List of Contributors • vii
Adnan Custovic,MSc,DM,MD,PhD Respiratory Medicine Donald W MacGlashan Jr,MD,PhD
Professor of Allergy Division of Asthma Allergy & Lung Biology Professor of Medicine
North West Lung Centre Guy’s,King’s and St Thomas’ School of Johns Hopkins Asthma and Allergy Center
Wythenshawe Hospital Medicine Division of Clinical Allergy and
Manchester,UK London,UK Immunology
Baltimore,MD
Graham DevereuxMA,MD,PhD,FRCP(Ed) David J Hendrick,MSc,MD,FRCP USA
Senior Clinical Lecturer Professor of Occupational Respiratory
Department of Environmental and Medicine,Newcastle University Piero Maestrelli,MD
Occupational Medicine Consultant Physician Professor of Occupational Medicine
University of Aberdeen Department of Respiratory Medicine Department of Environmental and
Aberdeen,UK Royal Victoria Infirmary Public Health
Newcastle upon Tyne,UK University of Padova
Stephen R Durham,MA,MD,FRCP
Padova,Italy
Professor of Allergy and Respiratory Melanie Hingorani,MA,MBBS,
Medicine MD,FRCOphth
Sohei Makino,MD,PhD
Head,Allergy and Clinical Immunology Consultant Ophthalmic Surgeon
Professor of Medicine
National Heart and Lung Institute Eye Department
Department of Medicine
Imperial College School of Medicine Hinchingbrooke Hospital
Dokkyo University School of Medicine
and Royal Brompton Hospital Huntingdon,UK
Mibu,Tochigi
London,UK
Japan
Stephen T Holgate,MD,DSc,FRCP,
Leonardo M Fabbri,MD FRCPa,F Med Sci
Jean-Luc Malo,MD
Professor of Respiratory Medicine MRC Clinical Professor of
Professor
Department of Respiratory Diseases Immunopharmacology
Université de Montréal School of
University of Modena and Reggio Emilia University of Southampton
Medicine
Modena,Italy Southampton General Hospital
Montréal,Quebec
Southampton,UK
Anna Feldweg,MD Canada
Instructor of Medicine Patrick G Holt,DSc,FRCPath,FAA
Harvard Medical School Deputy Director Charles McSharry,MD,PhD,MRCPath
Brigham and Women’s Hospital Division of Cell Biology Principal Clinical Immunologist
Boston,MA Telethon Institute for Child Health Department of Immunology
USA Research Glasgow Biomedical Research Centre
Perth,Western Australia University of Glasglow
Anthony J Frew,MA,MD,FRCP Glasgow,Scotland
Professor of Allergy and Respiratory Alexander Kapp,MD,PhD
Medicine Professor of Medicine Natalija Novak,MD
Department of Respiratory Medicine Department of Dermatology and Head of Allergy Unit
Brighton General Hospital Allergology Department of Dermatology
Brighton,UK Hannover Medical School University of Bonn
Hannover,Germany Bonn,Germany
Peter S Friedmann,MD,FRCP,FMedSci
Professor of Dermatology M Thirumal Krishna PhD,MRCP(UK),
Paul M O’Byrne,MB,FRCPI,FRP(C)
University of Southampton MRCPath,DNB
EJ Moran Campbell Professor of
Dermatopharmacology Unit Consultant Immunologist and Honorary
Medicine
Southampton General Hospital Senior Clinical Lecturer
McMaster University
Southampton,UK Department of Immunology
Hamilton,Ontario,Canada
Birmingham Heartlands Hospital
David BK Golden,MD Birmingham,UK
Hans Oettgen,MD,PhD
Associate Professor of Medicine
Clinical Director
Johns Hopkins University Lawrence M Lichtenstein,MD,PhD
Division of Immunology
Baltimore,MD Professor of Clinical Immunology
Children’s Hospital
USA Johns Hopkins University
Associate Professor of Pediatrics
School of Medicine
Clive E Grattan,MA,MD,FRCP Baltimore,MD Harvard Medical School
Consultant Dermatologist USA Boston,MA
Dermatology Centre USA
Norfolk and Norwich University Hospital Susan Lightman,PhD,FRCP,FRCOphth,
Norwich,UK FMedSci Romain A Pauwels,MD,PhD
Professor of Clinical Ophthalmology Formerly Professor of Medicine
Catherine M Hawrylowicz,PhD,BSc Department of Clinical Opthalmology Department of Respiratory Medicine
Senior Lecturer Moorfields Eye Hospital University Hospital
Department of Asthma Allergy and London,UK Ghent,Belgium
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viii • List of Contributors
David Peden,MD Glenis K Scadding,MA,MD,FRCP Editor in Chief,Respirology
Center for Environmental Medicine and Consultant Allergist and Rhinologist Director,Chimes Estate
Lung Biology Royal National Throat,Nose and Ear Clinical Professor
University of North Carolina at Hospital Curin University
Chapel Hill London,UK Perth,Western Australia
Chapel Hill,NC
USA Albert L Sheffer,MD Erika von Mutius,MD,MSc
Clinical Professor of Medicine Head
Carl G A Persson,PhD Harvard Medical School Asthma and Allergy Department
Professor Brigham & Women’s Hospital Munich University Children’s Hospital
Department of Clinical Pharmacology Boston,MA Munich,Germany
Lund University Hospital USA
Lund,Sweden Ulrich Wahn,MD
Hans-Uwe Simon,MD
Professor of Pediatrics,Director
Professor of Pharmacology and Chairman
Thomas A E Platts-Mills,MD,PhD Department for Pediatric Pneumology
Department of Pharmacology
Department of Medicine,Division of and Immunology
University of Bern
Allergy and Immunology Charité
Bern,Switzerland
University of Virginia Berlin,Germany
Charlottesville,VA
Estelle Simons,MD,FRCPC
USA Andrew J Wardlaw,FRCP,PhD
Professor
Professor of Respiratory Medicine
Department of Pediatrics & Child Health
Jacqueline A Pongracic,MD Department of Infection,Immunity &
Professor
Assistant Professor of Pediatrics and Inflammation
Department of Immunology
Medicine University of Leicester Medical School
University of Manitoba
Northwestern University Feinberg Glenfield Hospital
Winnipeg,MB
School of Medicine Leicester,UK
Canada
Chigaco,IL
USA Peter DL Sly,MBBS,MD,DSc,FRACP Thomas Werfel,MD
Professor of Medicine
Head of Division
Jay J Prochnau,MD Division of Clinical Sciences Department of Dermatology and
Staff Allergist Telethon Institute for Child Health Allergology
Department of Allergy and Asthma Research Hannover Medical School
Arnett Clinic Perth,Western Australia Hannover,Germany
Lafayette,IN
USA Geoffrey A Stewart,PhD Burton Zweiman,MD
School of Biomedical,Biomolecular Professor of Medicine and Neurology
Ilona G Reischl,PhD and Chemical Sciences Allergy and Immunology Section
Head of National Affairs The University of Western Australia Pulmonary,Allergy and Critical Care
Science and Information Division Perth,Western Australia Division
Austrian Medicines and Medical Department of Medicine
Devices Agency Philip J Thompson,MBBS,FRACP, University of Pennsylvania School of
Vienna,Austria MRACMA,FCCP Medicine
Director,Asthma and Allergy Research Philadelphia,PA
Hirohisa Saito,MD,PhD Institute Inc SCGH USA
Professor of Pediatrics Director,Centre for Asthma,Allergy and
Department of Allergy Immunology Respiratory Research
National Research Institute for Child Associate Professor of Respiratory
Health & Development Medicine
Setagaya-ku,Tokyo Department of Medicine
Japan University of Western Australia
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Preface to the Third
Edition
Allergic diseases, including asthma, rhinitis, conjunctivitis, dermatitis and food allergies
are major contributors to morbidity and sometimes cause mortality in the civilized
world. Also, their incidence and severity are still rising. Over the past decades,
genetics together with both basic and clinical immunology have made great strides in
understanding the disease processes in allergy.
In 1992, we published the first edition of an entirely new text on allergic diseases
and their mechanisms based on specifically designed, clear and informative diagrams.
This allowed us to produce a text which found a unique niche between the more
heavily referenced books and the more superficial guides. In this edition, the reader
was introduced to the individual cells that participate in the allergic response and this
information was then built on to describe the histopathological features, diagnoses
and treatment of allergic responses occurring in all major organs.
When preparing the second edition, we took note of the feedback of many clinicians
who asked us if we could put primary emphasis on the clinical manifestations of
allergy and augment this with a solid scientific background. This we attempted to do
starting with an entirely new chapter on the principles of allergy diagnosis, a skill
which is crucial to all practicing physicians. This was followed by a series of chapters
focusing on the histopathology, diagnosis and management of allergic disease in
individual organs. The Basic Mechanisms of Allergy section was been substantially
revised and updated. In our preparation of this section, we attempted to bring
together various aspects of the biology of allergic disease and combine them in
integrated chapters.
In the third edition, we have followed the same format as for the second edition.
In addition, we have recognised the importance of allergic disease in children and have
included a chapter devoted to its diagnosis and treatment. Also, it is now becoming
obvious that allergy develop very early in life, the ‘allergic march’ often starting before
birth. Consequently, we have added a chapter on the early life origins of allergy and
asthma. Finally, the great advances in our knowledge about the scientific basis of
allergic diseases, particularly the relationship between genes and the environment, has
necessitated the updating of most chapters, particularly those dealing with the
scientific basis of allergy.
Again, to make sure that each chapter had international authority, we often invited
two or more authors from different countries to work together to produce their text.
While this approach is not without its logistical problems, we believe it to have
produced a more authoritative text and we thank all the authors for their forbearance.
As readers, we hope that you will appreciate the novelty of our approach to allergy
and that you find the text enjoyable and educative to read. As we requested in the
first and second editions, please give us your feedback on the book so that we can
refine it even further in the future.
STH, MKC, LML, 2006
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1
Chapter
Definition:
Successful management
of allergic disease is
dependent on the
Principles of Allergy
accurate diagnosis of the
problem and its likely Diagnosis
causes. This chapter
describes allergy
diagnosis from taking
a history to specific
allergy tests. Stephen R Durham and Martin K Church
INTRODUCTION
This chapter focuses on the diagnosis of IgE-mediated allergy. It is important to define
terms and the following are recommendations:
• ‘Atopy’ refers to IgE hyperresponsiveness and represents a predisposition to
allergic diseases.
• ‘Allergy’, by contrast, refers to the clinical expression of atopic IgE-mediated
disease (Table 1.1).
Thus atopic individuals may or may not have clinical symptoms (Fig. 1.1). Some
30–40% of individuals in developed countries are atopic whereas only a proportion has
allergic diseases, which include asthma (5–10%), rhinitis (10–20%), and food allergy
(1–3%). In population studies allergic diseases peak at different ages. Food allergy and
atopic eczema are predominant in early childhood whereas asthma shows a biphasic
peak, and rhinitis peaks in the second or third decade (Fig. 1.2).
Allergic diseases are manifest as hyperresponsiveness in the target organ, whether
skin, nose, lung, or gastrointestinal (GI) tract. This hyperresponsiveness may have both
IgE-mediated and non-IgE-mediated components (Fig. 1.3). The situation is further
complicated because allergen exposure in allergic subjects may increase target organ
hyperresponsiveness, which results in exaggerated symptoms on exposure to non-
specific irritants (tobacco smoke, changes in temperature, etc.) in allergic subjects. Only
a proportion of atopic subjects develop disease and atopic individuals may have causal
factors in their disease independent of their atopic status (see Fig. 1.3). Furthermore,
increased non-specific responsiveness lowers the threshold for symptoms on subsequent
allergen exposure (Fig. 1.4).
Diagnosis of IgE-mediated allergy depends on the history and results of skin tests
or radioallergosorbent tests (RAST), which are occasionally supplemented by a
Table 1.1Definitions of IgE-mediated disease. Note that allergy may involve immunologic
mechanisms other than IgE,e.g. extrinsic allergic alveolitis or contact eczema
IgE-mediated Disease – Definitions
Atopy A tendency for exaggerated IgE responses,defined clinically by the
presence of one or more positive skin prick tests (or caused serum
allergens) i.e. a predispositionto develop allergy
Allergy The clinical expressionof atopic disease,including asthma,rhinitis,
eczema,and food allergy
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4 • Chapter 1 • Principles of Allergy Diagnosis
Symptom Severity Versus Time Interrelationships Between Allergy and Hyperresponsiveness
hyperresponsiveness IgE sensitivity
y
erit
v
e
s
m
o
pt
m
y
s
sensitization allergy tolerance
time
non-IgE IgE-allergic 'latent' allergy or
Fig. 1.1Positive skin tests may not be associated with clinical hyperresponsiveness hyperresponsiveness clinical tolerance
symptoms (allergy). related to age or
asthma following
rhinitis immunotherapy
conjunctivitis (SPT positive,
food/drug reaction asymptomatic)
Symptom Severity Versus Age urticaria/angioedema
anaphylaxis
Fig. 1.4Interrelationships between allergy and hyperresponsiveness,
which may have both IgE-mediated and non-IgE-mediated
y components. SPT,skin prick test.
erit
v
e
s
m
o
pt
m
y therapeutic trial of avoidance of the suspected allergen or
s
provocation testing in the target organ. These parameters are
discussed and a diagnostic approach is recommended.
0 1 2 4 8 16 32 64
age (years) ALLERGY HISTORY
eczema food asthma rhinitis Before taking an allergy history, a professional but friendly
allergy manner, the early establishment of eye contact, and the
avoidance of extraneous distractions should put patients at
Fig. 1.2Manifestations of allergy differ with age. their ease. The history need not be time consuming although
patients should be allowed to give their own accounts of
symptoms followed by structured prompts or questions to
cover points listed in Table 1.2. A recent study showed that
standardized questions put to the parents of children (aged 1–17
Hyperresponsiveness Lowers Symptom Threshold
years) by a trained interviewer werehighly predictive of answers
obtained by an experienced pediatric allergist (Table 1.3).
allergy
Patient’s account
The frequency and severity of symptoms, as well as the dominant
symptom, should be established. For example, if nasal watery
discharge is accompanied by nasal and palatal itching and
hyperresponsiveness
associated eye symptoms, this is highly suggestive of allergy and
a history of potential allergic triggers, e.g. pets, pollen, and
house dust mites. Any occupational causes should be recorded.
Trigger factors
↑threshold to subsequent antigen
Patients with mite sensitivity may complain of immediate
symptoms during activities such as bed making, dusting, and
Fig. 1.3Allergy increases target organ hyperresponsiveness,which
lowers the threshold to subsequent allergen exposure. vacuum cleaning. The symptoms are frequently worse on
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Allergy History • 5
entering damp, older buildings, and better when the subject is
Table 1.2Elucidating the history of a patient’s allergy. The outside, particularly in dry areas.
history need not be time consuming although the patient should
Are symptoms worse on exposure to pets? First, confusion
be allowed to give his or her own account of symptoms followed
may arise when there are several pets. Also the absence of known
by structured prompts or questions to cover the given points
contact with pets does not exclude sensitization to animals or
Allergy History symptoms on exposure. A recent study from Sweden confirmed
high levels of the major allergens of cat (Fel d 1) and dog (Can
Put the patient at his or her ease
f 1) on the chairs and desks in schools but not on the floors.
Listen to the patient’s account of the symptoms This suggested contamination from the clothes of children who
What is the frequency or severity of the symptoms? owned pets. Horse dander is an exquisite allergen and even
contact with the clothing or livery of owners and riders may
Are the symptoms seasonal or perennial?
frequently provoke symptoms in horse-allergic subjects.
Are there any trigger factors (allergic or non-allergic)?
Seasonal pollenosis is usually evident from the clinical history
Ask about any impact on lifestyle,i.e. work or school,leisure although it will vary according to geographic areas (Fig. 1.5).
time and sleep
Within the UK, tree pollen is predominant in March and April,
Ask about occupation and hobbies and grass pollen peaks in June and July; weed pollens are most
Ask about possible allergens in the home prevalent in late summer, and molds during the late summer
and fall months. The dominant pollens and their timing vary
Ask about food allergies and any adverse reactions to drugs
across Europe. Tree pollen occurring in April and May is the
Is there a personal or family history of asthma,rhinitis,and
dominant problem in Scandinavia; in the UK it is grass pollen
eczema?
and, following an early grass pollen season (April and May) in
Ask about the influence of prior treatment,i.e. efficacy, southern Europe, the dominant pollens are Parietaria and olive
side-effects,compliance and the patient’s concerns about
during the summer months.
treatment
Ask the patient what his or her main problem is
Allergic versus non-allergic triggers
Patients with inhalant allergies from whatever cause develop
hyperresponsiveness in the target organ. Certain features in the
history may point to either allergic or non-allergic triggers as
Table 1.3Accuracy of standardized questions put to the parentsof children (aged 1–17 years) by a trained interviewer,used for
predicting answers obtained by an experienced pediatric allergist
Accuracy of Standardized Questions
Questions Accuracy (%)
Months when symptoms are worse 94
Worse in bed at night 95
Worse in morning when awakening 96
Better when outside 95
Better when in dry area of the country 96
Worse when with dogs 97
Worse when with cats 97
Worse when vacuuming or dusting 93
Worse when blankets are shaken 96
Worse when among trees in March and April 85
Worse when in grass 97
Number of patients interviewed: 151
(True positive + True negative) x 100
Accuracy (%)
(True positive + True negative + False positive + False negative
Data modified from Murray AB,Milner RA. The accuracy of features in the clinical history for predictingatopic sensitization to airborne allergens in children.
JAllergy Clin Immunol 1995; 96:588–596.
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6 • Chapter 1 • Principles of Allergy Diagnosis
of an immediate response following either natural or experimental
Seasonal Allergens in the UK allergen exposure. Such isolated late symptoms may not
necessarily be attributed to allergen exposure several hours
earlier. In contrast, irritant triggers tend to provoke symptoms on
April May June July August September October
timothy, first exposure, require high exposure concentrations and affect
rye, the majority of exposed subjects to a lesser or greater extent.
grass cocksfoot,
pollens meadow, Irritant-induced symptoms tend only to be immediate, with
dogstail, resolution within minutes or hours. A good example is the
fescue, etc
patient with non-allergic, non-infective rhinitis who typically
birch, plane complains of symptoms on exposure to changes in temperature,
tree
pollens ash, pine tobacco smoke, pollutants, perfumes, domestic sprays, bleach,
and stressful circumstances. However, these distinctions should
weed be regarded as only a guide since there is considerable overlap.
nettle, dock
pollens There is no doubt that perennial allergens – resulting in repeated
early and late symptoms – result in increased target organ
Cladosporium, Alternaria
hyperresponsiveness with heightened sensitivity to non-specific
fungal
spores triggers. In these circumstances symptoms may become
continuous and a causal relationship between allergen exposure
and symptoms may not be evident to either the patient or the
clinician (see Fig. 1.6).
Fig. 1.5Seasonal allergens may be present for most of the year.
Pollenosis is usually evident from the clinical history although the
Quality of life
timing will vary according to geographic areas.
It is important to assess the impact of allergic symptoms on the
patient’s lifestyle, e.g. impairment of work, time off work (or
school), interference with leisure activities (including sports
and hobbies), and sleep disturbance.
Allergic Versus Non-allergic Triggers
Family history
A personal and family history of asthma, rhinitis, eczema, or
food allergy, or adverse reactions to drugs should be established
in all cases. A history of allergens in the home should be
obtained, including such details as pet ownership, presence of
Allergic Non-allergic carpets, central heating, double glazing, and nature of soft
triggers triggers
furnishings in the bedroom and living areas. Old, damp accom-
modation will favor the growth of house dust mites and molds.
Influence of treatment
The effect of previous attempts at avoidance should be
• latent interval • symptoms on first exposure
ascertained, bearing in mind that several months of vigorous
• low doses • high doses
environmental control or avoidance, or respiratory protection,
• minority affected • majority affected
• early & late symptoms • immediate symptoms may be required before any improvement may become apparent.
Similarly, the response to pharmacologic treatment including
benefit and possible associated side-effects should be noted.
Compliance with medication should be carefully assessed in
continuous every case, particularly where there has been an apparent poor
symptoms
response to treatment. Patients’ knowledge and potential fears
about their conditions and the treatments should be explored.
Fig. 1.6Features suggesting an allergic or non-allergic trigger as Useful leading questions include:
the cause of symptoms. • ‘Are you concerned about any side-effects of your steroid
inhaler/nasal spray/creams?’
• ‘Do you find it difficult to always remember to use your
inhaler?’
the dominant causes of symptoms (Fig. 1.6). In general, allergen- • ‘How often do you collect repeat prescriptions for your
induced symptoms require a period of sensitization (the latent medicines?’
interval). They may occur at very low allergen concentrations
and affect only a proportion of exposed and sensitized individuals; What is your main problem?
symptoms may be ‘early’ (i.e. from minutes to 1–2 hours) or
‘late’ (3–24 hours). Continual low allergen exposures, however, It is often helpful to ask patients at the end of the interview to
have been shown to provoke only late symptoms, in the absence recap their main problem.
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Allergy History – Special Cases • 7
Table 1.4Common examples of causes of occupational asthma
Occupational Allergy
Agent At-risk employment
Laboratory animals Scientific,animal-house
work,etc.
Flour Baking
Biological enzymes Soap powder industry work
Wood dusts Saw milling,furniture
manufacture
Latex rubber gloves Health workers
Bleaching agents,hair dyes Hairdressing
Isocyanates Paint spraying,printing industry Fig. 1.7Common allergenic foods.
Colophony (solder fumes) Electronics industry
Food allergy and intolerance
ALLERGY HISTORY – SPECIAL CASES The accurate diagnosis of food allergy is critically dependent on
a good history. Up to 20% of the population may perceive food
Occupational history as a cause of their symptoms, whereas the prevalence of true
food allergy is around 1%; food allergy tends to occur in highly
An occupational history should be obtained in all patients with atopic subjects with a strong personal and family history of
asthma, rhinitis, and eczema. In contrast to occupational asthma allergies. A clear association between ingestion (or contact)
(OA) (Table 1.4), occupational rhinitis is less well documented with the food and symptoms may be elicited. Only a limited
although likely to be very common, with or without associated number of foods commonly provoke symptoms: in children the
asthma. Knowledge of potential occupational causes is culprits are eggs, milk, and peanuts; in adults they are fish,
important. Symptoms tend to occur within the workplace or shellfish, fruit, peanuts, tree nuts, etc. (Fig. 1.7). Frequently,
during the evening following work; they may improve at more than one organ system is involved; i.e. true food allergy is
weekends and during holiday periods. OA, at least within the a rare cause of isolated asthma in adults, although severe food-
UK, is a registered and compensatable industrial disease – 5% induced allergy may provoke asthma associated with other
of adult onset asthma may be attributed to an occupational typical organ involvement, e.g. lip tingling, angioedema, nettle
cause. The associated loss of self-esteem, together with financial rash, nausea, and vomiting.
and social difficulties, may provoke symptoms of depressive This is in contrast to the typical patient presenting with non-
illness and even suicidal tendencies. Moreover, symptoms may IgE-mediated food intolerance; the symptoms tend to be non-
persist in up to 50% of cases for months or even years following specific or confined to one organ. There is often no clear history
termination of the occupational exposure. For these reasons an of provoking foods. Alternatively, atypical foods, such as yeast
occupational cause should be established early and certainly not and wheat, are perceived to be involved, with no clear association
missed. A history of all occupations since leaving school should between ingestion and exposure or delayed symptoms following
be obtained if a critical timing of exposure to a potential ingestion. Such patients are either non-atopic or the symptoms
occupational sensitizer and onset of symptoms is not to be occur independently of their atopic status; the latter patients,
missed. Allergic contact eczema (Table 1.5) may also result unlike those with typical food allergy, are unlikely to be highly
from common sensitizers in the home and workplace. atopic on the basis of their personal or family history, or via the
detection of allergen-specific IgE on skin prick testing or RAST
testing.
Non-IgE-mediated food-induced reactions may occur
Table 1.5Examples of allergic contact eczema following the ingestion of preservatives such as salicylates,
benzoates, and tartrazine. Common products containing
Allergic Contact Eczema
preservatives include meat pies, sausages, cooked ham and
salami, colored fruit drinks, confectionery, and wine (Fig. 1.8).
Agent Source
No diagnostic tests are available and diagnosis depends upon
Nickel Coins,watches,jewellery the history and observation of the effect of exclusion diets and,
Cobalt Metal-plated objects,wet cement where necessary, blinded food challenges.
Several clinically relevant cross-reactions may occur between
Fragrances Cosmetics
certain inhalant allergens and foods (Table 1.6). A common
Lanolin Cosmetics,moisturizing creams
example is oral allergy syndrome in patients with springtime
p-Phenylenediamine Hair dye,fur dye hayfever (i.e. sensitivity to birch pollen) and oral itching and lip
Epoxy resins Adhesives swelling on eating apples (particularly green apples), hazelnuts,
and stone fruits (peaches, plums, etc.). Such reactions tend not