M JA P R A C T I C E E S S E N TI A L S A L L ER G Y

5: Allergy and the skin:

eczema and chronic urticaria
Constance H Katelaris and Jane E Peake

he skin is commonly involved in acute allergic reactions. It is

also involved in the chronic allergic entities of eczema
(common in infancy and childhood) and chronic urticaria
(more commonly seen in adults). Here, we outline how these
conditions can be recognised and managed in practice and when to
refer for specialist advice. We also highlight some current controversies and evolving concepts.
ECZEMA
The Medical Journal of Australia ISSN: 0025Eczema
is a6papulovesicular
that occurs in 15%20% of
729X
November 2006dermatitis
185 9 517-522
infantsThe
and young
children.
of eczema
Medical
JournalThe
of onset
Australia
2006 (also known as
atopicwww.mja.com.au
dermatitis or atopic eczema/dermatitis syndrome) freMJA
Practice
Essentials
Allergy
quently
occurs
in the
first few
months
of life and usually within the
first year of life. The exact cause of eczema is unknown, but factors
that may precipitate or aggravate the condition include food and
environmental allergens/irritants, heat or cold, stress, and genetic
predisposition. Often dismissed as a trivial disorder, severe eczema
can cause significant morbidity and have major social, emotional
and financial impacts on children and their families.1

Making the diagnosis

The diagnosis of eczema is made clinically, on the basis of the
distribution of skin involvement and symptoms. The hallmarks are
pruritus and inflammation. In infants, there is usually involvement
of the extensor surfaces, face, neck and trunk (Box 1). As the child
gets older, eczema more commonly involves the flexural surfaces,
but can be widespread and also affect the hands, feet, face and
trunk. In acute lesions, there are usually erythematous papules on
a background of erythematous skin and pruritus, and sometimes
vesiculation and ooze, but, over time, excoriation, scaling, lichenification and thickened plaques may develop (Box 2). The clinical
course can be quite varied, often with periods of remission and
exacerbation due to a variety of factors.
Eczema should be differentiated from other common forms of
dermatitis, such as contact dermatitis and seborrhoeic dermatitis.
Distribution often provides the clues. Seborrhoeic dermatitis,
which is also common in infants, primarily involves the scalp,
axillae and nappy area. Contact dermatitis, more common in older
patients, often involves a sudden flare-up of short-lived dermatitis
in exposed areas. Apart from history-taking, patch testing can help
confirm the cause. Psoriasis should also be considered in the
differential diagnosis, especially in older children and adults.
Eczema is not a single entity; rather, it is a group of inflammatory disorders of the skin involving a genetically determined skin
barrier defect. Recent data suggest that, as for other diseases such
as asthma, there are different forms of eczema. Eczema associated
with IgE antibodies is called atopic eczema and eczema without
IgE antibodies is called non-atopic eczema.2,3 Attempts to further
delineate the different types of eczema will have important
implications for management and prognosis of the disease.
Atopic eczema is associated with other atopic diseases such as

ABSTRACT
Eczema is common, occurring in 15%20% of infants and
young children. For some infants it can be a severe chronic
illness with a major impact on the childs general health and
on the family. A minority of children will continue to have
eczema as adults.
The exact cause of eczema is not clear, but precipitating or
aggravating factors may include food allergens (most
commonly, egg) or environmental allergens/irritants, climatic
conditions, stress and genetic predisposition.
Management of eczema consists of education; avoidance of
triggers and allergens; liberal use of emollients or topical
steroids to control inflammation; use of antihistamines to
reduce itch; and treatment of infection if present. Treatment
with systemic agents may be required in severe cases, but
must be supervised by an immunologist.
Urticaria (hives) may affect up to a quarter of people at
some time in their lives. Acute urticaria is more common in
children, while chronic urticaria is more common in adults.
Chronic urticaria is not life-threatening, but the associated
pruritus and unsightly weals can cause patients much distress
and significantly affect their daily lives.
Angioedema coexists with urticaria in about 50% of patients.
It typically affects the lips, eyelids, palms, soles and genitalia.
Management of urticaria is through education; avoidance of
triggers and allergens (where relevant); use of antihistamines
to reduce itch; and short-term use of corticosteroids when
antihistamine therapy is ineffective. Referral is indicated for
patients with resistant disease.
MJA 2006; 185: 517522

SERIES EDITORS: Andrew Kemp, Raymond Mullins, John Weiner

food allergy, allergic rhinitis and asthma, which may become

evident at a later stage.
Management
Management of eczema principally involves explanation to patients
and parents of the chronic nature of the disease, advice on avoiding
irritants, and symptom control (Box 1). Irritants such as soaps,
perfumes, sand, extreme temperatures and some clothing fabrics
should be avoided. As soap strips oils from the skin, adding oils to
the bath and using aqueous creams as soap substitutes often works
well. Bacterial infection, especially with Staphylococcus aureus, can
often cause exacerbations of eczema. This can be difficult to
diagnose clinically, and empirical treatment with antibiotics may be
justified.
Pharmacological therapy

Oral antihistamines: Oral antihistamines may be useful in reducing

pruritus in some patients. Older, sedating antihistamines should not

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1 Case scenario*
A 12-month-old boy presented with severe eczema. The eczema had
started at 6 weeks of age; flare-ups of the condition were common and
were becoming more severe. Itch was a major problem, waking him
frequently at night.
On examination, widespread generalised eczema was noted. There
were some inflammatory plaques, and the skin was excoriated and
infected in some areas (see Figures). The baby was otherwise quite well.
The patients history revealed that various treatments had been applied
over the preceding months, with limited success. Oatmeal was regularly
added to his bath, and moisturiser was applied twice daily.
Methylprednisolone aceponate ointment was used when severe
exacerbations occurred, and pimecrolimus cream had been used
mainly on his face and legs.
The child was still being breastfed, but had slowly been introduced to
solids with a few vegetables, fruits and rice. Goats milk and baby
yoghurt had been found to cause welts all over his face. The mother
had tried eliminating milk from her diet, but continued eating other
dairy products. The father was prone to allergic rhinitis, and members of
the extended family were subject to eczema and asthma.
Skin prick testing showed a significant response to egg, cows milk, beef
and house dust mite. It was suggested to the mother that she eliminate
all dairy products, egg, potato and beef from her diet until weaning and
that these foods not be introduced into the childs diet. Cows milk
allergy implies allergy to all dairy products and usually also to goats
milk. Advice on house dust mite control was also given. Other

be used, especially in young children, as there have been reports of

severe and even life-threatening side effects.4
Emollients: There have been very few randomised controlled trials
of the use of emollients in eczema, but those that have been done
confirm their usefulness.5 Moisturising the skin improves its barrier
function and reduces itch and irritation. There are a huge number of
bathing and moisturising products available for treating eczema, and
patients will often try many before finding one that suits. Products
should not be continued if they cause burning, stinging or increased
itching. Soft white paraffin is one of the more suitable moisturisers
and is best applied immediately after getting out of the bath, while
the patient is still wet and warm. Wet wraps may be effective in
patients with moderate to severe eczema and provide a partial
barrier to scratching.
Topical steroids: Inflammation needs to be controlled, and topical
steroid creams and ointments are effective for this purpose.5 A
moderate to potent steroid should be applied at the initial signs of
inflammation. As the inflammation subsides, steroid use should be
tapered off to prevent rebound. This will generally provide better
resolution and require a lower total dose of steroid than if a low
potency steroid is used alone for a prolonged period. Parental
concern about the effects of steroid use, including thinning of the
skin, can lead to problems with compliance. However, if steroids are
used appropriately for short periods, there is little evidence to
support this concern.6
Topical calcineurin inhibitors: More recently, the topical calcineurin
inhibitors pimecrolimus cream and tacrolimus ointment (the latter
currently only available in Australia at certain hospital and compounding pharmacies) have become available as alternatives to
topical steroids to suppress inflammation.
Tacrolimus ointment has been found to be safe and effective in
patients with moderate to severe eczema.7 Transient burning and
518

recommendations were to add cottonseed oil to the bath; wash with

aqueous cream and moisturise liberally with soft white paraffin; apply
wet wraps twice daily; apply steroid cream twice daily to the limbs and
trunk; and continue pimecrolimus cream treatment on the face.
Cetirizine and a course of oral cephalosporin were also prescribed. The
child was referred to a dietitian to ensure adequate nutrition.
On review a few weeks later, the childs skin had improved significantly.
He still had some eczema on the limbs, but this was restricted to the
cubital and popliteal fossae, hands and feet. He was now sleeping
through the night and was considerably less irritable. He had started to
be weaned onto soy milk and was eating chicken and lamb without any
obvious adverse effect on the skin.
* This is a fictional case scenario based on similar real-life cases.

pruritus can occur when the ointment is initially applied. Pimecrolimus is similar in action to tacrolimus but has only been assessed
in mild to moderate disease. It can be used to prevent flaring of
eczema,8 and may be useful in body areas where there is concern
about applying steroids (eg, on the face, around the eyes and around
the groin).
Safety concerns about topical calcineurin inhibitors have been
raised with respect to increased risk of skin malignancy (on the basis
of animal studies), but a review of the literature suggests that black
box warnings are not indicated.9 Nevertheless, calcineurin inhibitors should not be used in clinically infected areas. Further, there are
few studies assessing the effectiveness of these newer agents compared with appropriate strength topical steroids.7
Treatment-resistant disease

For patients who fail to respond to topical therapy, systemic therapy

may be considered. Long-term treatment with oral steroids cannot
be justified, because of side effects. Other treatment options such
as narrow-band ultraviolet B therapy, systemic immunosuppressive
drugs or intravenous gammaglobulin therapy are reserved for
very severe disease and should only be given under the guidance of
a specialist with experience in their use.
When to refer

Referral to a specialist is indicated for any young infant with severe

eczema and for those in whom food allergy is suspected of playing a
role. A specialist should also be consulted if systemic immunosuppressive drugs are being considered.
Controversies and evolving concepts
Food allergy

The role of food allergy in causing or exacerbating eczema is

controversial, perhaps because many studies of food avoidance

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have used an unselected population of chilprognosis for eczema has been shown to
2 Chronic eczema in a 10-year-old child
dren with and without sensitisation to
correlate with its severity and the presence of
foods. Also, foods used in the control group
atopic sensitivity.19 Patients with chronic,
(eg, soy instead of cows milk) may themsevere eczema and their families need adeselves have elicited reactions. Recently,
quate support.
numerous double-blind, placebo-controlled
food studies have demonstrated that about
CHRONIC URTICARIA
35%40% of children with moderate to
severe eczema have food allergy, and that
Urticaria (hives) is characterised by traneliminating the causative food from their
sient eruptions of pruritic weals or patchy
diet can bring about significant improveerythema on the skin. It probably affects up
ment in the severity and extent of eczema
to 25% of people at some time in their lives.
(Box 3).11-14 However, eczema is often mulIt affects people of all races and is about twice
tifactorial, and elimination of allergenic
as common in women as in men. Acute
foods does not provide complete resolution
urticaria is more common in children, while
in all infants. Food allergy is rare in adultchronic urticaria (defined as recurring epiOver time, with continued inflammation and
onset eczema.
sodes that last for over 6 weeks) is more
scratching, the skin becomes very thick.

Allergy to egg is the most common food

common in adults. The incidence of chronic
allergy associated with eczema. Other comurticaria is unknown, but it is thought to
monly associated foods include milk, soy,
occur in 0.1%3% of the population.
wheat and peanuts. Thus, food allergy screening tests such as skin
The significance of chronic urticaria is sometimes trivialised
prick tests and radioallergosorbent tests should be performed in
because it is a non-life-threatening disease. However, the unrelentyoung infants with severe eczema. False negative tests are uncoming pruritus and disfiguring, random occurrence of unsightly weals
mon, but false positive tests may occur, particularly in older
can cause patients great misery. Chronic urticaria has a major impact
children.15 Food challenges are more accurate; reactions may be
on quality of life, with impact on activities of daily living similar to
immediate or delayed. Food allergens from the maternal diet may be
that experienced by patients with heart disease.20
16
excreted in breastmilk and cause eczema in a breastfed infant. A
trial of restriction of maternal diet may be useful if an infant is shown
Making the diagnosis
to be allergic to a particular food.
Urticaria
Care should always be taken with any recommendations for
Urticaria is characterised by transient weals that last less than 24
dietary restriction in young infants. When special diets are used, it is
hours and then disappear without sequelae. It is associated with
imperative that adequate nutrition be maintained, particularly in
intense itch. If these two key features are not present, the diagnosis
young infants, and consultation with a dietitian is advisable.
needs to be reconsidered.
Environmental allergens
The three main types of chronic urticaria are papular urticaria,
Patients with eczema may have sensitisation to environmental
urticaria with a physical cause, and urticarial vasculitis. They can be
allergens such as house dust mite (HDM) or pet dander. There is
distinguished from chronic idiopathic urticaria by weal appearance
strong circumstantial evidence that HDM is an important precipitant
and characteristic history.
for atopic eczema. However, there are relatively few randomised
Papular urticaria: Papular urticaria is a reaction to bites from grass
controlled trials looking at the role of HDM eradication in treatment
mites, fleas and other arthropods. It most commonly occurs in
of eczema. The limited studies suggest that there is some benefit if a
children and during the warmer months. Lesions, typically seen on
5
very low level of HDM can be achieved.
the extremities, are intensely itchy, leading to marked excoriation
and often secondary infection that results in scarring. Lesions often
Dietary supplements
occur in clusters and may last for days.
Based on the concept that probiotics, which are normal commensal
Urticaria with a physical cause: A physical cause for chronic
bacteria of the healthy human gut, play a role in the development of
urticaria is probably present in about 20% of cases (Box 4, Box
normal immune tolerance and may be immunomodulatory, recent
5). Dermatographism and cholinergic urticaria are the most
studies have looked at probiotics in the treatment and prevention of
common forms of urticaria with a physical cause and have
allergy.17,18 These studies look promising, but further work is
characteristic appearances. Various types
required to clarify whether these agents
of urticaria may coexist in the same
should be recommended and which is most
3 Evidence-based practice tips*
patient. However, once the typical history
effective. There is currently no evidence for
Patients with atopic eczema have a higher
is elicited, no further investigations are
the use of other dietary supplements such as
likelihood of developing other atopic
required.
evening primrose oil, fish oils or omega-3
diseases such as asthma and allergic
fatty acids.
Urticarial vasculitis: An atypical appearrhinitis (Level III-2).
ance, long-lasting lesions or a lack of respon Removal of an identified allergenic food
Prognosis
siveness to antihistamine treatment suggests
from the diet can significantly improve
urticarial vasculitis, a rare condition seen in
For most infants and children, eczema is a
eczema in an individual patient (Level III-2).
less than 1% of people with chronic urticaria.
mild disease that will resolve during child* Based on National Health and Medical Research
Patients suspected of having this condition
hood, but for some patients, the condition is
10

Council levels of evidence.

require further investigation (Box 6).
severe and may continue into adulthood. The
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4 Physical forms of chronic urticaria

Type

Comments

Symptomatic
dermatographism

Commonest form of physical urticaria. May accompany other forms. Linear weals with wide flares at site of scratching or
stroking. Treatment usually not required.

Cold-induced

Rapid onset of pruritus, erythema and swelling following exposure to cold. Reaction confined to site of exposure. May be lifethreatening if whole body exposed (eg, swimming in cold water).
Various forms exist: localised cold urticaria, systemic cold urticaria and cold-induced dermatographism.

Cholinergic or
heat-induced

Characteristic 12 mm weals with marked flare occurring after exercise, sweating, showering, emotional stress or fever.

Exercise-induced
anaphylaxis

Large weals often accompanied by angioedema, wheeze and/or hypotension after exercise.

Pressure-related

Swelling occurs 46 hours after pressure applied (typically, swelling of hands after manual work, swelling of feet after
standing, or swelling under areas of tight clothing).

Food-dependent and food-independent subtypes have been described.

Solar

Prompt onset of pruritus followed by weals 15 minutes after exposure. Lesions last 13 hours. Severity may lessen with tanning.

Aquagenic

Small weals develop on contact with water of any temperature. This is a rare condition.

Angioedema

Angioedema (typically affecting the lips, eyelids, palms, soles or

genitalia) coexists with urticaria in about 50% of patients. If it occurs
as a recurrent condition in isolation, causes other than urticaria
should be considered, such as medication (eg, angiotensin-converting enzyme inhibitors) or rare conditions such as hereditary
angioedema or acquired deficiency of C1-esterase inhibitor.
Management
The first step in managing urticaria is to try to find a cause, but this
is easier said than done. There is little role for extensive laboratory
testing, as this rarely helps to identify a cause.
Discussion with patients and parents about minimising bites and
trigger factors is useful. Non-specific stimuli that may trigger an
episode of urticaria include increasing body heat; alcohol ingestion;
and taking certain medications, particularly aspirin and non-steroi5 Cold urticaria: the ice cube test

The ice cube test is performed by holding ice on the skin for 5 minutes
and then removing it. Wealing occurs as the skin rewarms.

520

dal anti-inflammatory drugs, which may exacerbate chronic urticaria in 60% of cases. Some women prone to urticaria note a
premenstrual worsening in their condition.
Pharmacological therapy

The primary goal of therapy for urticaria is to relieve pruritus, as this

is the symptom that impairs the patients quality of life and causes
sleep disturbance. It is important that the patient understand that,
despite taking medication, urticarial lesions may still occur.
Oral antihistamines: Oral antihistamines remain the mainstay of
treatment of chronic urticaria. They are best taken prophylactically,
as various stimuli can cause mast cell degranulation, resulting in
histamine release. While older antihistamines are cheaper and their
sedative effect may be useful for sleeping at night, they are undesirable for long-term use because of other side effects.
Addition of a tricyclic antihistamine such as doxepin may be very
effective for night-time discomfort and sleep disturbance due to itch.
Doxepin is a potent antihistamine, with H1- and H2-histamine
blocking activity, as well as having an anti-anxiety effect. However,
its sedative side effect is a limitation, especially in older patients.
Some years ago, there were reports that addition of an H2 antagonist
could help control chronic urticaria. The benefit is small, but the
treatment may be worth trying, as it may help selected patients.21 A
number of studies have demonstrated benefit from the use of newer,
non-sedating antihistamines over that derived from placebo.22-25
Leukotriene inhibitors: Theoretically, there may be a use for leukotriene antagonists in the treatment of chronic urticaria. However,
randomised controlled trials comparing the use of an antihistamine
alone with use of a combined treatment (antihistamine plus montelukast) have shown conflicting evidence of efficacy.23,26 Currently,
montelukast is not listed for use in chronic urticaria and is an
expensive treatment.
Oral corticosteroids: Oral corticosteroids are often used for shortterm relief of symptoms of chronic urticaria when antihistamine
therapy is ineffective. In this circumstance, patients are grateful for
temporary relief. But, unfortunately, corticosteroids cannot be a
long-term option, as the risk of side effects will outweigh the benefit.
Doctors must be responsible for warning their patients of the longterm consequences of corticosteroid use so that the medication is
not taken indiscriminately.

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not an elimination diet was used before challenging, which food

additives were included in the challenge battery, the dosages of food
additives used, and whether medication was ceased before challenging (and if so, for how long). Based on the few rigorous studies that
have been performed, food additives appear to be a distinctly
uncommon cause of chronic urticaria.29

6 Urticarial vasculitis*
Suspicious features

Lesions lasting longer than 24 hours in the one place

Condition painful rather than itchy
Bruising or scarring after occurrence of lesions
Presence of arthralgia or arthritis

Helicobacter pylori

Presence of constitutional symptoms

Lack of response to antihistamines

Investigations when urticarial vasculitis is suspected

Skin biopsy to demonstrate vasculitic changes in postcapillary

venules (leukocytoclastic vasculitis)

Full blood count and erythrocyte sedimentation rate

Urinalysis
Antinuclear antibodies to extractable nuclear antigens
Complement studies

* Seen in less than 1% of people with chronic urticaria.

The question of whether Helicobacter pylori infection is a cause of

chronic urticaria remains controversial. A link between the two, first
described in the European literature, has not been confirmed by
other studies.30 Reports of improvement in chronic urticaria after
eradication of H. pylori infection have added to the debate.31
Although H. pylori seropositivity is not higher in patients with
chronic urticaria than in other patients, eradication of the infection
where it coexists appears worthwhile. Patients presenting with a
history of reflux and urticaria may be considered for investigation for
H. pylori and appropriate treatment if found.
Thyroid autoimmunity

When to refer

In cases of acute severe urticaria and angioedema with no obvious

trigger, or where there is a presumed food or drug trigger, specialist
evaluation is required to identify the trigger, if at all possible.
Patients with chronic urticaria and/or angioedema who do not
respond to the therapies listed above or who are suspected of having
an underlying condition should be referred to a specialist.
In cases of recurrent angioedema, specialist evaluation may be
appropriate to exclude hereditary or acquired C1-esterase inhibitor
deficiency.
Controversies and evolving concepts
Malignancy

There has been concern, based on anecdotal reports, that chronic

urticaria may be an indicator of an underlying malignancy, particularly in older patients. A very large Swedish epidemiological study
has shown that there is little evidence to support this fear.27 However,
acquired angioedema associated with C1-esterase inhibitor deficiency is associated with malignancy, particularly lymphoma.27
Diet

Ingestion of certain foods may produce a generalised acute allergic

reaction that includes urticaria. The patient often makes the connection
between food ingestion and an acute episode of urticaria, but may fail
to consider the possibility of a hidden ingredient in the food, such as
nuts. In this circumstance, skin prick tests or in-vitro measurement of
specific IgE may suggest that a particular food is the likely cause, but
food challenges may be the only way to establish a definite relationship. Attributing chronic urticaria to food allergy, rather than some
other possible cause, is another common pitfall, with most patients
believing a particular food to be the cause of their problem at some
stage. Skin prick testing or in-vitro testing for food allergy may relieve
the patient from unnecessary avoidance of certain foods.
Idiosyncratic reactions to food additives have been suggested as an
important cause of chronic urticaria, but this area suffers from a lack
of rigorous placebo-controlled studies and also from the inherent
problem of challenging patients with chronic urticaria and then
trying to interpret the results. Early studies reporting reactions to
tartrazine and benzoates in patients with chronic urticaria were not
placebo-controlled.28 Other complicating factors include whether or

A link between chronic urticaria and thyroid autoimmunity has been

known of for more than 20 years.32 Kikuchi et al33 reported that
patients with chronic urticaria had an increased prevalence of IgG
antithyroid antibodies (usually antithyroid peroxidase) compared
with controls (10%13% v 3%5%). They demonstrated that
antithyroid antibodies are definitely associated with the presence of
antibodies to the IgE receptor, and concluded that antithyroid
antibodies and antibodies to the IgE receptor are associated immune
abnormalities, rather than one being the cause of the other.
The use of thyroxine to treat patients with chronic urticaria and
thyroid autoimmunity in the absence of thyroid disease remains
controversial. Some investigators have reported improvement in
chronic urticaria symptoms with thryoxine treatment.34 In a recent
study that included both euthyroid and hypothyroid women, 16 of
20 women with chronic urticaria who were given thyroxine to
suppress thyroid-stimulating hormone showed improvement in
chronic urticarial symptoms after 12 weeks.35
Is chronic urticaria an autoimmune disease?

In the past decade, 35%45% of patients with chronic urticaria have

been found to have an autoimmune basis for their condition. An IgG
antibody directed to the alpha subunit of the IgE receptor has been
demonstrated in 35% of patients, and a functional anti-IgE antibody
has been found in a further 5%10%.36 Measurement of these
antibodies is confined to research laboratories. However, an intradermal skin test with autologous sera can induce a delayed weal
with a macroscopic and microscopic appearance similar to that seen
in chronic urticaria. The stimulus for this autoantibody production
is unknown.
The notion that chronic urticaria may be an autoimmune disease
opens up the possibility of using immunomodulatory treatment
when antihistamines have failed to control the condition. There is
one controlled trial demonstrating a positive effect from the use of
hydroxychloroquine.37 Cyclosporin A has been shown to be an
effective treatment, but its use should be restricted and requires
careful monitoring because of its potential to cause renal and other
side effects.38 Plasmapheresis or administration of intravenous gammaglobulin or low-dose tacrolimus have also been tried, with some
benefit, in small numbers of patients with autoimmune chronic
urticaria.

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Fact or fiction true or false?

1. All eczema is allergy-based (T/F)
2. Food allergy plays no role in eczema (T/F)
3. Food allergy is an important cause of chronic urticaria (T/F)
4. Five per cent of the population suffers from dermatographism (T/F)
1. False. About 20% of people with eczema are not atopic and allergy does not
play a role in their disease.
2. False. 35%40% of children with moderate to severe eczema have food
allergy.
3. False. Approximately 5% of patients with chronic urticaria may have food
intolerance. Food allergy is more likely to be associated with acute urticaria.
4. True. This does not require treatment, but antihistamines are useful if the

condition causes embarrassment.

Prognosis
Fifty per cent of patients who experience chronic urticaria will be
symptom free at the end of 1 year, but 20% will continue to have
problems for many years. Approaches based on the concept of
chronic urticaria as an autoimmune disease offer promise to patients
who have severe long-term disease.
Competing interests
None identified.

Author details
Constance H Katelaris, MB BS, PhD, FRACP, Senior Consultant
Physician1
Jane E Peake, MB BS, FRACP, Senior Lecturer and Paediatric
Immunologist and Allergist2
1 Allergy and Immunology Services, Westmead Specialist Medical
Centre, Sydney, NSW.
2 Department of Paediatrics and Child Health, University of Queensland,
Brisbane, QLD.
Correspondence: [email protected]

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Allergy Clin Immunol 2005; 116: 1067-1072.
3 Johansson SG, Bieber T, Dahl R, et al. Revised nomenclature for allergy for
global use: report of the Nomenclature Review Committee of the World
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4 Starke PR, Weaver J, Chowdhury BA. Boxed warning added to promethazine
labeling for pediatric use. N Engl J Med 2005; 352: 2653.
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(Received 12 Apr 2006, accepted 20 Sep 2006)

MJA Volume 185 Number 9 6 November 2006