Atopic eczema or atopic dermatitis in children, along with the other atopic diseases,
asthma & hay fever (allergic rhinitis), has considerably increased in Western
population over the last 30 years (almost tripled). The prevalence is about 10-20%
of children under the age of 14 years, and 2-10% in adults. This very common condition
has a significant emotional, social and economic impact on the sufferer and his/her
family, and thus it is important for all healthcare clinicians to be familiar and
up-to-date with the disease and its therapeutic management based on "Evidence".
Stedman’s medical dictionary defines Eczema as:
Generic term for inflammatory conditions
of the skin, particularly with vesiculation in the acute stage, typically erythematous,
edematous, papular, and crusting; followed often by lichenification and scaling
and occasionally by duskiness of the erythema and, infrequently, hyperpigmentation;
often accompanied by sensations of itching and burning; the vesicles form by intraepidermal
spongiosis; often hereditary and associated with allergic rhinitis and asthma.
This definition, like most definitions of eczema, to a large extent is defining
atopic eczema, which will also be the focus of this paper, but for completeness
and to assist in differentiating AD from the other types of eczema, the other types
of eczema will be mentioned in the differential diagnosis of Atopic Eczema towards
the end of this paper as well.
Some writers use the classification of endogenous eczema to mean atopic eczema and
exogenous to include irritant and allergic contact dermatitis. Others classify the
patients with AD who are allergic as extrinsic and those without as intrinsic eczema.
"Atopy" is defined as a form of allergy in which there is a hereditary or constitutional
tendency to develop hypersensitivity reactions. This tendency to produce specific
IgE responses to allergens is associated with "atopic" eczema, but up to 40% of
individuals with the disease phenotype may not be atopic. This makes continued use
of the term atopic eczema somewhat problematic. A more useful nomenclature of Atopic
eczema / dermatitis syndrome (AEDS), which was proposed by the European Academy
of Allergology and Clinical Immunology (EAACI) Nomenclature Task Force in 2001 has
been updated by the World Allergy Organization in 2004.( Ref Johansson et al, JACI,
2004). The new nomenclature is based on the mechanisms that initiate and mediate
The term "eczema" is proposed to replace the
provisional term Atopic eczema / dermatitis syndrome (AEDS). The term ‘atopy’ should
not be used until an IgE sensitization has been documented by IgE antibodies in
the blood of a person or a positive skin prick test to common environmental allergens
such as dust mites, pollens , or cat. The term eczema can therefore be split into
‘atopic eczema’ and non-atopic eczema’.
This WAO nomenclature further classifies contact eczema as follows:
Delayed hypersensitivity caused by close contact with low-molecular–weight chemicals
(like nickel) which provoke a predominantly TH1 lymphocyte-mediated
The non-allergic variety can also be described by terms like
Intrinsic vs Extrinsic Atopic Dermatitis
Frequency of AD
Age of onset
Association with other atopic disease (asthma, hay fever)
Serum IgE level
Skin prick tests or RAST to
Foods & aeroallergens
Atopic hereditary is less predictive for AD than sensitization to common food and
inhalant allergens in early childhood.
Case 1: Atopic Eczema secondary to egg allergy
Cade developed eczema on cheeks at 6 weeks while he was being breast-fed. Mom suspected
that he was reacting to her breast milk since she thought at times he was very unsettled
after feeding. At 2 months he had his first attempt at a cow’s milk formula and
spat it out and developed peri-oral urticaria. Mother assumed a cow’s milk allergy
and decided to breast-feed only. Despite exclusive breast-feeding the eczema progressively
got worse. It required twice daily hydrocortisone creams and intermittent locoid
cream to keep it moderately controlled.
At 6 months when he came to see me, he had chronic eczema on his cheeks in his flexures
and also few small urticarial plaques on his trunk.
Skin Prick Test:
Milk=4mm, Egg=12mm, wheat=0, soy=0, peanut=6mm
House dust mites=0, cat=0, dog=0.
Management and Progress
Mother was told to eliminate eggs and peanut from her diet as well as the milk which
she had been eliminating for the last 4 months. Weaning onto a hypoallergenic formula
was recommended, but mom preferred to continue breast-feeding (with omission of
milk and eggs from her diet) for another 3 months.
In 2 weeks she was able to reduce the hydrocortisone to alternate days and the skin
was free of eczema.
Case 2: Contact Dermatitis to several agents used to treat eczema, masquerading
as atopic eczema
Glenys is a 51 yr-old non-atopic female who developed eczema for the first time
2 years prior to her consulting me. The rash started on her hands and then gradually
spread to limbs, then trunk then involved entire body, including her face.
She has seen numerous doctors and alternative practitioners and tried several topical
steroids including Locoid, which she though made the rash much worse. She also tried
several antihistamines and several different herbal creams and supplements. She
had moderate benefit from a 2 month course of prednisone. At one stage was prescribed
fluoxetine, which she took for 3 months and thought that it gave the best relief
to the intense itching.
A herbal cream containing tea tree oil.
Multivitamins and flaxoil which she has been on for 18 months.
Of significance, she was also using a shampoo containing chamomile.
On Examination: patches of chronic lichenified eczema on legs,
and trunk. There was evidence of excoriations especially on legs.
Skin Prick Test: were negative to 20 common environment and food
Patch Test: Positive to fragrance 1, tea tree oil and compositae
at 48 hrs and 72 hrs and weak positive reactions to budesonide hydrocortisone butyrate
and tixocortal pivolate at 72 hrs.
Extended steroid patch test showed that she was tolerant to mometasone.
Diagnosis: Allergic contact dermatitis to tea tree oils, fragrances
Management: her eczema improved after stopping her herbal cream
and using mometsone ointment and a fragrance-free moisturizer.
Pathogenesis of Atopic Dermatitis (AD)
The hallmarks of atopic dermatitis are a chronic, relapsing inflammation
of the skin, and the current thinking is that this is due to a defect in the epidermal
barrier function that leads to dry skin, and IgE-mediated sensitization to foods
One of the most exciting recent developments in our understanding of atopic eczema
has been new research suggesting that the primary defect in AD is with the (physical)
barrier function of the epidermis, leading to the secondary immunologic and inflammatory
changes instead of the primary defect being immunologic.
Genetics of Atopic dermatitis
Atopic dermatitis is a complex genetic disease that arises from gene-gene-environment
interactions. The concordance rate for AD is 15% for dizygotic twins, but as high
as 77% among monozygotic twins.
Atopic Dermatitis: A Skin Barrier Disease
Barrier Function of the skin
An intact epidermis is a prerequisite for the skin to function as a physical and
chemical barrier. The barrier is the stratum corneum, which forms a brick and mortar-like
structure of the upper epidermal layer. An alteration of the barrier that causes
increased transepidermal water loss is the hallmark of atopic dermatitis.
For a long time efforts to understand the etiology and pathophysiology of atopic
dermatitis concentrated on the immune system. Due to very important recent discoveries
in the last few years increasing attention has been paid to the barrier-forming
The innate immune system in Atopic dermatitis
The epithelial cells are the first line of defense between the skin and the environment.
The epithelial sensing structures for pathogens are abnormal in AD, which is one
of the reasons bacterial, viral and fungal infections are more common in patients
Triggers for atopic eczema
In understanding the pathogenesis (hopefully leading to better management) of atopic
eczema it is important to remember that it is a multifactorial disease with multiple
triggers. The triggers also vary depending on the genetics, age, environment and
even the psyche (mindset) of the individual. Therefore,
not every patient will
react to every trigger.
The most important triggers based on evidence
based medicine include:
Dry skin (almost universal due to defective barrier function):
- Climate: winter, excess sweating
- long frequent hot showers.
- Staph infection (and other microbes)
- Food allergy in infants*
- soaps, detergents, wet work
- cigarette smoke
- clothing: wool, synthetic fibers
- habitual scratching.
- Environmental allergens (house dust mites, pollens, pets)
- Emotional stresses (school exams, work pressures, relationship problems)
- Iatrogenic - Irritant or allergic contact dermatitis to topical treatment
- Hormonal: Pregnancy and menstrual cycle.
Atopic Dermatitis stands at the frontier between allergy and autoimmunity
About 25% of adults with AD have IgE antibodies against self-proteins. It is believed
that scratching damages skin cell, releasing autoantigens that induce IgE autoantibodies.
Evidence based medicine on what causes Worsening of Eczema
Food allergy in children suffering from atopic eczema
There should no longer be any controversy in the fact that food is a significant
trigger for eczema in infancy.
Studies showing prevalence of food allergy (proven by DBPC food
challenges) in children with eczema:
Food Allergy (%)
Sampson & McCaskill
Burks et al
Niggeman et al
Eigenman & Calza
Staph Aureus and Atopic Eczema
S. aureus rarely colonises normal skin. Only 2% of adolescents and adults are colonized
in non-specialized skin sites, although this increases to 35% in the anterior nares
and 5-15% in the axillae, perineum and toe webs. This is in contrast with almost
universal colonization among atopic dermatitis patients.
Super antigens in AD.
Numerous studies have shown that superantigens produced by staph aureus play a central
pathogenic role in AD. These enterotoxins are more potent than most antigens at
stimulating the immune system.
Superantigens trigger mast cell degranulation directly and amplify IgE-mediated
- Superantigens induce dermatitis on application to skin by patch testing.
The importance of s aureus colonization in AD is supported by the observation that
not only patients with impetiginised AD, but also AD patients without superinfection,
show a synergistic clinical response to combined treatment with antistaphylococcal
antibiotics and topical steroids.
House dust mites and aeroallergens causing eczema
Three provocation studies suggest an association between exposure and flares, and
this evidence is also supported by 2 patch test studies.
Stress causing eczema
Kimata studied the impact of road traffic, video games and ringing mobile phones
on wheal response and neuropeptides in eczema (not eczema severity) in 2 provocation
case control studies. In all 3 groups, increased wheal responses, substance P, VIP,
and nerve growth factor were increased in the eczema group but not in controls.
Effect of UV radiation on atopic eczema
Deguchi H et al felt that sun exposure is an aggravating factor responsible for
the recalcitrant facial erythema in adult patients with atopic dermatitis, however
the result of this study of sun exposure on an unselected group of patients with
recalcitrant facial eczema is unclear.
Atopic eczema or atopic dermatitis is a common inflammatory, chronically relapsing,
extremely pruritic skin disease. It has a wide spectrum of dermatologic manifestations.
There is no definitive ‘gold standard’ for the diagnosis of atopic eczema. and uniformity
in the use of diagnostic criteria is lacking From a systematic review looking at
several sets of criteria the UK Diagnostic Criteria were found to be the most extensively
validated. However, there is room for improvement in methodological design for future
intervention studies, but I think it is probably the best we have at present.
A carefully taken history using the UK Diagnostic criteria followed by a full examination
of the patient should diagnose most cases of true atopic eczema.
The UK Diagnostic Criteria for Atopic Dermatitis
Must have an itchy skin condition over the past
12 months, PLUS 3 or more of the following:
- Onset below the age of 2
History of flexural involvement (around the eyes, around the neck, front of elbows,
behind knees, front of ankles)
- Generally dry skin
- Personal or (in children under 4 years) allergic disease in parents or siblings
Visible flexural dermatitis (around the eyes, around the neck, front of elbows,
behind the knees, front of ankles).
Clinical Features of Atopic Dermatitis (AD)
AD usually begins early in life; 45% of al cases begin within the first 6 months
of life, 57% of cases begin by age 2 years, and 87% of cases by the age of 5 years
The principal feature of AD is pruritus, which is universally present (almost 100%
negative predictive value), and scratching is a major factor in the pathogenesis
of the acute and chronic lesions. "If it does not itch its probably not eczema"
Early lesions of AD are erythematous and dry with small papules, mild scaling, and
areas of excoriation.
Lesions that are moist and oozing or those with intense erythema suggest the possibility
of superficial secondary infection.
Chronically affected areas show accentuated skin lines and thickening of the skin
(lichenification) and post-inflammatory pigment abnormalities are common (especially
in dark skin).
The pattern of distribution of AD lesions changes with age. Areas affected in infants
include the cheeks, trunk and extensor surfaces of the extremities. The area around
the nose is never involved, and this "headlight "sign is characteristic of AD.
During childhood and adolescence, the distribution shifts to the flexures and the
The severity of AD tends to decrease after childhood, although occupational eczema
and increased skin sensitization is common.
Other types of eczema that is often confused with AD
Eczema in the broadest sense (inflammation of the epidermis and dermis) is a component
of many skin diseases. Despite this, eczema can be very easily diagnosed visually.
The real problem is usually in differentiating the different types of eczema. Some
find it easy to classify eczema (dermatitis) into those diseases that are caused
by external factors (exogenous dermatitis), namely irritant contact dermatitis and
allergic contact dermatitis, and those that do not require external induction or
endogenous eczema, the commonest examples being atopic eczema and seborrheic dermatitis.
Classification of Eczema: Differential Diagnosis of Atopic Eczema
- Irritant contact dermatitis
- Allergic Contact dermatitis.
- Atopic Eczema
- Dishidrotic Dermatitis or Pompholyx
- Neurodermatitis or lichen simplex chronicus
- Nummular eczema
- Unclassified Eczema or Nonspecific Endogenous Eczema.
Contact dermatitis is the term for the type of eczema resulting from exposure to
allergens (allergic contact dermatitis) or irritants (irritant contact dermatitis).
Contact dermatitis accounts for at least 60% of occupational skin diseases.
Seborrheic dermatitis is a common, inflammatory skin condition that causes flaky,
white to yellowish scales to form on oily (sebum rich) areas such as the scalp,
inside the ear, the sides of the nose, between the eyebrows and the midsternal area.
It can occur with or without erythema.
Dishidrotic Dermatitis or Pompholyx
- Other synonym is vesicular palmoplantar eczema.
It causes small vesicles on the palms and sides of the fingers and soles of the
- Intense burning or itching.
- Excessive sweating in affected areas.
- stress, female gender
- hot weather
- Pre-existing atopy and contact dermatitis
- Smoking, oral contraceptives, aspirin.
Neurodermatitis or Lichen simplex
These are types of eczema that are thought to be self-induced by habitual scratching,
and are usually localized. Common areas affected include, the lower legs, scrotum
and vulvae. They are usually very difficult to treat and sometimes require intralesional
injection of steroids and psychotherapeutics.
Nummular (meaning "coin-shaped") dermatitis is a form of eczema, characterized by
round-to-oval erythematous plaques most commonly found on the arms and legs. Lesions
start as papules, which then coalesce into plaques. Early lesions may be studded
with vesicles containing serous exudates. They are usually very pruritic. Very little
is known about the pathogenesis, except an increased amount of mast cells is usually
found in these lesions, compared to non-lesional skin.
Ichthyosis is the term used to describe continual and widespread scaling of the
skin. The skin is very dry, thickened and scaled. It is associated with increased
wrinkling of the palms and soles and increased skin infections. It comes from a
Greek root "Ichthy", meaning fish. It may be inherited (genetic) or acquired during
life. The inherited forms are rare and are generally present from infancy and are
usually lifelong conditions. Acquired Ichthyosis can develop at any age due to a
number of medical problems, such as kidney disease.
Unclassified Eczema (UE) or Nonspecific Endogenous Eczema
The term nonspecific endogenous eczema (dermatitis) is preferred because a major
criterion for diagnosis is the exclusion of exogenous contact factors. These are
patients with eczema that does not fit any of the distinct patterns above.
Unclassified eczema is a common type of eczema with a very poor prognosis. This
is a diagnosis of exclusion. The diagnosis is made after atopic eczema, allergic
contact dermatitis, seborrhoeic dermatitis and the other well defined forms of eczema
Differences between atopic eczema, seborrhoeic dermatitis and allergic contact
Probably the conditions that are most often confused with AD are allergic contact
dermatitis and infantile seborrhoeic dermatitis.
In one study 2% patients tested were allergic to topical steroids and also equally
(2%) to propylene glycol.
Allergens associated with medications used to treat eczema include:
Allergic contact dermatitis
< 3 months
Distribution of rash
Spares nappy area
May involve nappy area
Localized depending on cause
Family history of atopy
Skin test or RAST
Positive in about 75%
Patch test positive
Usually clears once trigger found
Allergy to Corticosteroids
- The incidence of contact allergy to corticosteroids has increased dramatically
since the late 1980’s.
Allergic Contact dermatitis due to:
- fragrance in moisturisers
- Vehicles in creams
Propylene glycol is present in Elide, cetaphil, and some topical
An irritant reaction (burning, stinging, itching or redness within
20 minutes of applying the cream) occurs in >56% of children with atopic eczema
when aqueous cream is used as an emollient, compared to only 17% of children using
other emollients, according to an audit published in Pharmaceutical Journal.
Investigations in Eczema
Skin Prick Test (SPT)
Can be done to confirm atopy or to assist in the diagnosis of food allergy. A
positive test to a food only confirm sensitivity and this needs to be followed up
with an oral challenge (ideally double-blind).
Atopy Patch Test (APT)
APT using common food allergens (like milk, eggs) applied to the skin of the upper
back for 48 hours, and read again at 72 hrs, has become a very useful way of picking
up non-IgE (delayed) reactions to these foods. APT was found to be more sensitive
and specific method than skin prick test or RAST-type tests, in diagnosing delayed
food allergy in children with AD. The combination of SPT and APT significantly enhances
identification of food allergy in children with AD.
Should be considered in all cases of AD that is not responding to conventional
treatment with topical steroids and emollients, since this is the only way to diagnose
a secondary allergic contact dermatitis to the topical steroids or one of the vehicles
in the creams being used.
Oral Food Challenges (Double-blind Placebo-controlled)
This is the ‘gold standard’ for diagnosing food allergy as a trigger for atopic
eczema. One of the drawbacks to this test is that it is very time-consuming and
the flare-up of eczema can be delayed outside of the observation period.
Evidence based management of Atopic Dermatitis
"Good science demands independent replication of new ideas and results and abandonment
of accepted theories in light of more reliable evidence. Failure to comply leads
to damaging bad science. Progress of good science often requires serendipity, ‘making
discoveries by accident and sagacity of things not sought".
Science and Serendipity Mark B Pepys, Clin Med 2007;7762-78
A multifaceted Approach to the Treatment of AD
A multipronged approach is required for treatment of AD. This should include:
- Skin hydration
- Control of itching
Look for and Remove triggers / exacerbating factors
- Emotional stress
Moisturizer and emollients
Emollients and moisturizers are used interchangeably, but technically speaking,
"moisturizer" adds moisture to the skin and "emollients" soften the skin. An ideal
preparation for dry skin should have both properties.
Since we now know that defective skin barrier function is the primary
or underlying cause of atopic eczema, it is easier to understand why moisturizers
and emollients are so important in its management. It is important to emphasize
to patients that they will need to make a habit of using moisturizers daily, for
the rest of their life, regardless of whether their eczema is in remission or not.
The faulty skin barrier causes an increase in transepidermal water loss. As a result,
the corneocytes shrink and cracks open between them, permitting the penetration
of irritants and/or allergens, and causing the development of eczematous lesions.
Even in normal skin, repeated use of soaps and solvents produces eczematous reaction
in the same way because they remove the epidermal lipids.
Essentially emollients are lipid containing agents that provide a lipid film that
sits on the surface of the skin and encourages the build up of water in the stratum
corneum. They do this mostly by preventing the evaporation of water from the skin
One study has shown that emollients may reduce the need for topical
steroids by about 50%
In New Zealand there is a vast array of moisturizers / emollients to choose from,
but they all work in one or more of the following ways:
Occlusive Moisturizers: These contain oils such as liquid paraffin
(mineral oil), white soft paraffin, yellow soft paraffin, wool fat or lanoline,
coconut oil, or emulsifying wax. They all work by providing a layer of oil on the
surface of the skin, which prevents evaporation of water from the skin surface.
These oils may be mixed with varying amounts of water to produce moisturizer with
different properties, e.g. lotions, creams or ointments.
Humectant moisturizers: contain ingredient such as urea, glycerin,
lactic acid, glycolic acid, which penetrate into the stratum corneum, where they
attract and retain water. They are particularly useful in very dry skin.
Keratolytics: In chronic eczema there is a build up of a skin protein
called keratin, which makes the skin hard and scaly. At higher concentrations lactic
acid and glycolic acid act as keratolytics, which means they have the ability to
break down the keratin in hardened and thickened skin. Some of the moisturizers
will have these keratolytics added for this purpose.
Finding the most suitable emollient for an individual is a matter of trial and error,
but some basic rules apply:
Tips for choosing the best moisturizer / emollient:
The key to getting the best out of moisturizers /emollients is education.
In theory greasier oil based products are more effective but these are rarely tolerated
and are not used by people with mild to moderate eczema.
Lotions are mixtures of oil in water, and are light & non-greasy,
and have a cooling effect. They are good for mildly dry & weeping eczema. They
are also good for hairy areas, such as scalp.
Creams are also mixtures of oil in water, but slightly thicker
than lotions. They are generally non-greasy, and easily absorbed. They are therefore
more cosmetically acceptable than ointments.
Ointments are thick, occlusive oil based moisturizers that is most
suitable for very dry skin. Many patients don’t like them , as they find them too
- It is best to let children choose their favorite emollient.
Caregivers should specifically ask about skin reactions like stinging, burning,
itching or redness after using emollients before, and avoid prescribing them.
- Urea-containing emollients are of great help to patients with atopic dermatitis.
How to use emollients
- Emollients should be used directly after bath or shower.
It is important to emphasize the importance of using moisturizer at least twice
The application of moisturizer and topical steroids should be separated by at least
1 hour to avoid dilution of the steroid.
If applied several times daily to the whole body children will require at least
250g per week and adults 500g per week.
Adverse reactions to emollients and moisturizers
Allergic contact dermatitis: Apart from paraffin and water, almost
any ingredient of emollients may sensitize. Patch testing will help to identify
contact allergens. The main sensitizers are:
- Perfumes / fragrances
- Preservatives (antimicrobials)
- Propylene glycol
Glucocoticoids are the mainstay of anti-inflammatory therapy in the management of
chronic AD. Topical steroids will help majority of patients with AD, and absolute
steroid insensitivity is unusual, but a spectrum of steroid responsiveness exists.
From the observation that combined treatment of AD with antibiotics and steroids
is more effective than steroids alone, this would suggest that s. aureus secrete
products that can induce steroid insensitivity. Recently Leung et al made the discovery
that when T-cells are stimulated with superantigens, as compared to other stimuli,
they become insensitive to the immunosuppressive effects of steroids.
The main advantages of topical steroids are their proven clinical effectiveness,
low cost, and wide variety of preparations.
Topical Corticosteroids in NZ Classified by relative potencies
Group 1: Superpotent
Clobetasol propionate 0.05%
Group 2: High potency
Betmethasone diproprionate 0.05%
Group 3: Mid to high potency
Betamethasone dipropionate 0.05%
Group 4: Mid potency
Mometasone furorate 0.1%
Group 5: Mid to low potency
Hydrocortisone butyrate 0.1%
Group 6: Low to mid potency
Clobetasone butyrate 0.05%
Group 7: Low potency
Hydrocortisone 0.5%, 1%
Principles of prescribing Topical Steroids
Amount of steroids prescribed
Adult: 30 g for whole body once
- 3g for head and face
- 3g for an arm
- 6g for a leg
- 9-12g for the trunk.
Fingertip units for application of topical steroids
One fingertip unit is the amount of cream that is squeezed out of a standard 5mm
size nozzle along an adult fingertip. Two fingertip units is about the same as 1gm
of topical steroids.
Choice of Steroid class by disease severity and site
Ezcema of face
Flexural eczema in babies
Eczema elsewhere in children and flexures
Seborrhoeic dermatitis of trunk
Eczema of palms and soles
Adverse effects of topical steroids
The local side effects of using potent steroids for long period of time (such as
striae, skin atrophy, telangiectasia, perioral dermatitis, erythema, acne, glaucoma
and cataract) are well described, and well known to all of us and will not be discussed
Probably what is not so well known is the increasingly recognized side effect of
allergic contact dermatitis to the steroid molecule. Contact allergy
to topical corticosteroids is sufficiently common to justify their inclusion for
patch testing in the standard series and tixocortol pivalate and budesonide have
been recommended as contact allergy markers.
Rational approach to treating staph infection in AD
Staph colonization rates are lower in clinically uninvolved skin than in lichenified
or inflamed skin, and highest in acute weeping lesions, with the density of colonization
being roughly proportional to the severity of eczema.
Staph Infection & AD
- Staph is found on 90% of AD skin vs 5% of non-AD skin
- The majority of AD staph produce superantigens, which induces inflammation
- T-cells activated by superantigens are steroid insensitive
Combination of antibiotics/corticosteroid therapy is more effective than either
Oral Antibiotics in Eczema
Signs of bacterial infection in atopic eczema include:
- Pustules or cellulitis
- A sudden worsening of the eczema.
In these cases oral antibiotics should be prescribed. In New Zealand flucloxacillin
and dicloxacillin are commonly prescribed. In case of penicillin allergy erythromycin
Swabs for bacteriology are always a good idea, but are particularly useful if patients
do not respond to treatment, in order to identify antibiotic resistant strains of
S. aureus or to detect additional streptococcal infection.
Dietary treatment of childhood atopic eczema (EBM)
In a systematic review Fiocchi et al looked at 14 prospective studies looking at
dietary intervention in the management of childhood AD. Allergenic food exclusion
claimed efficacy in 13 of the 14 studies and was most useful n infants, in patients
with elevated IgE levels and/or multiple food sensitization and in patients with
a diagnosis of food allergy.
Topical Immunomodulators (Tacrolimus and pimecrolimus (elidel®)
Tacrolimus (which is not currently available topically in NZ) is
probably as strong as betamethasone valerate (potent steroid). NICE guideline recommends
tacrolimus for moderate to severe eczema that has not responded to appropriate potency
®): is less potent
than tacrolimus. There is some evidence that it prevents flares of atopic eczema.
It is useful for head and neck eczema.
Despite the concerns expressed by the US FDA about their potential to cause malignancies,
to date there are no data supporting an increased incidence of cutaneous malignancies
or lymphoma in patients treated with these drugs.
In New Zealand Elidel® is recommended for short-term or intermittent long-term
treatment of AD in patients >= 3 months when topical steroids are ineffective, intolerable
or inappropriate. My personal experience is that it is not very effective for treating
flare-ups, but better at preventing eczema of the face and neck (part of the maintenance
Do oral antihistamines stop the itch of AD? The Evidence
There are no good studies investigating the efficacy of oral antihistamines in AD.
The evidence to date is that it does not relieve the itch, but can be useful if
they have sedating properties.
Infants with eczema that is being triggered by food allergy will often have
superimposed urticaria with their eczema and can have dramatic improvement from
oral non-sedating antihistamines.
Systemic Treatment of Severe Atopic Eczema:
Cyclosporine usually leads to prompt relief of symptoms within 2 weeks of starting
treatment. However, following cessation of therapy, relapse within 6 weeks is common.
Adverse effects include renal toxicity, hypertension, nausea and abdominal pain.
2 small RCT looked at systemic steroids in children. Unfortunately no data was identified
for prednisone, which would be the standard systemic steroids in NZ. Anecdotally,
the big problem with systemic steroids in treating atopic eczema is the frequent
rebound on stopping.
Azothiaprine can be very effective in treating severe AD, but is a slower acting
medication (4 – 6 weeks), and has the potential to cause bone marrow suppression,
hepatotoxicity, squamous cell carcinoma and lymphomas.
This drug can lead to improvement in AD after 8 and 12 weeks of treatment.
Phototherapy has an anti-inflammatory effect on the cells of the immune system.
Types of UV therapy that have been used successfully in treating AD include psoralen
and UVA (PUVA), combination of broadband UVA/UVB, broadband UVA, broadband UVB,
narrowband UVB (311nm), and UVA1 (340-400nm). Adverse effects include premature
aging of the skin and increased likelihood of squamous cell carcinoma and melanoma.
Prevention of Atopic Dermatitis (AD)
In the case of primary prevention (preventing AD in high risk individuals), there
is no evidence that exclusive breastfeeding, infant avoidance of allergens, mother
avoidance of certain foods or aeroallergens will prevent the development of AD.
There are some conflicting reports of treatment with probiotics, particularly Lactobacillus,
during pregnancy or infancy may delay the onset of AD in infants and children.
Education in evidence based management of AD
Some recent studies have shown that patient education through a nurse practitioner
may be able to improve patient concordance and, as a consequence, can reduce the
unnecessary use of topical steroids in atopic eczema. The studies showed that the
education requires time, that is often not available in a busy clinic.
Basic education in management of atopic dermatitis should include:
- Skin barrier function is abnormal and Importance of daily emollients for life
- Control vs cure
- Identify the individual triggers including foods
- Signs of infection
- Provide written individual treatment plan
- Offer educational websites or support groups.
Advice against career choices that may exacerbate AD or lead to hand eczema:
- Cook or cleaner
- Factory worker (wet work).
Identify and discuss hidden concerns (what patients / parents often aren’t telling
- They are looking for a cure
- arents fear that the child will be permanently scarred
They have steroid phobia and does not like long-term use of antihistamines and therefore
compliance is an issue
- They are concerned about food allergy being a cause
- They are keen to try or are trying alternative therapies.
Consider a therapist /counseling if there is:
- Significant family distress or dysfunction
- Excessive absence from school (especially if out of proportion to AD severity
- Poor coping skills (family or child)
Evidence of depression, obsessive-compulsive disorder, or neurotic scratching /
Unconventional Treatment of AD and evidence for using them (or not):
Immunotherapy for Atopic Eczema
It has been shown that reduction of the house dust mite allergen load is effective
as preventative and therapeutic measure in atopic Eczema. Furthermore, recent data
indicate that specific immunotherapy with house dust mite allergen is effective
in patients with atopic eczema.
"Wet wrap" bandages
Wet wraps can occasionally be a helpful treatment in infants and young children
where limb scratching is a major problem. It involves the application of a weak
topical steroid, like 1% hydrocortisone ointment or just emollients under an inner
wet and an outer dry layer of cotton tubular bandage or garment. At present clear
evidence for wet wraps is very limited. There is some concern about side effects,
with regards to applying steroids under occlusion in children.
From my clinical experience, wet wraps with 1% hydrocortisone is particularly helpful
to break the itch-scratch cycle in kids who have developed habitual scratching.
Alternative Medicines in Atopic Dermatitis
Alternative medicine has been termed as a means of therapy or examination that has
no scientific basis, and no effective or diagnostic reliability validation has been
demonstrated. The use of such medicine is increasing, without the benefit of controlled
trials on the subject. Alternative medicines for treating eczema are very popular
in New Zealand.
Some of the alternative remedies used in New Zealand to treat eczema include:
- Chinese Herbs
Evening primrose oil – Studies have failed to show benefit Dietary restriction without
scientific testing (Alternative testing).
Chinese herbal creams
Parents consider herbal remedies as natural products that are usually derived from
plants, and therefore should be harmless. Some of these products are also very effective
in clearing stubborn eczema. In 1999 Keane et al analyzed 11 herbal creams obtained
from children attending dermatology outpatient clinics in the UK. Eight of the 11
creams contained dexamethasone at concentrations inappropriate for use on the face
of children. In 2003 the Ministry of Health’s Medicines Safety Authority in New
Zealand, (Medsafe) recalled a herbal cream that illegally contained potent steroids
(clobetasol propionate ) and ketaconazole. Again in 2005 herbal products were recalled
for containing betamethasone.
Summary of Treatment options for Atopic Eczema
Recommendations for referral for Specialist care
← Access Severity and look for triggers at every visit →
← Emollients and Education →
Mild Potency topical
Potent topical steroids
Phototherapy (UV-B and/or UVA)
• Oral steroids
- Uncertainty of the diagnosis
If severe infection with herpes simplex (eczema herpeticum) is associated with systemic
symptoms urgent referral is recommended
If secondarily infected eczema is not responding to appropriate oral antibiotics
plus adequate potency topical steroids
- If food allergy is suspected in infancy
- If eczema is causing significant social or psychological problems
- If contact dermatitis is suspected and confirmation is required by patch testing.
Checklist for recalcitrant eczema: Why is the eczema not improving?
- Lack of Compliance due to steroid phobia
- Food Allergy in infants
- Secondary infection (staph, viruses, fungi)
Iatrogenic Dermatitis due to
- Co-existence of a contact dermatitis related to creams being used
- Irritant dermatitis.
- Emotional / Psychological stresses causing habitual scratching
- More education needed: especially on the important role of emollients.
Some Key References:
Brenninkmeijer EE et al.
Diagnostic Criteria for Atopic Dermatitis: A Systematic
Br J Dermatol. 2008;158(4): 754-765
Rance F et al Food allergy in children suffering from atopic eczema
Pediatr Allergy Immunol 2008: 19: 279-284
Williams HC, Burney PG et al.
The UK working Party’s Diagnostic Criteria
for Atopic Dermatitis I. Derivation of a minimum set of discriminators for atopic
Br J Dermatol 1994;131:383-96
Eigenmann PA et al
Prevalence of IgE-mediated food allergy among children
Schmitt J et al Systemic Treatment of Atopic Eczema: A Systematic review.
Acta Derm Venerol 2007;87: 100-111
B Li L-f et al Prognosis of unclassified eczema: a follow-up study.
Arch Dermatol. 2008;144(2): 160-164
Sichere SH et al
Food hypersensitivity and AD: pathophysiology, epedimiology,
diagnosis, and management.
J Allergy Clin Immunol 1999;104: S114-S122
Ottens S et al
More than 50% of positive challenge with foods are associated
with late eczematous reactions in AD
Allergy Clin Immunol Int 2006
Tupker RA et al Induction of eczema by inhalation of dust mite.
J Allergy Clin Immunol 1996; 97:1064-70
Wanukul S et al
Eczematous skin reaction from patch testing with aeroallergens
in atopic children with and without atopic dermatitis.
1993; 10: 209-13
Hoare C, Li Wan Po A et al., Systematic review of treatment for atopic eczema.
Southampton National Coordinating Centre for HTA, 2000 (Health Technology Assessment;
Wolkerstorfer A, et al
Efficacy and safety of wet wrap dressing in children
with severe atopic dermatitis: influence of corticosteroid dilution.
J Dermatol 2000;143: 999-1004
Novak N, Bieber T. Allergic and non-allergic forms of atopic diseases.
J Allergy Clin Immunol 2003;112:252-262
Burden AD, Beck MH. Contact Hypersensitivity to topical steroids.
Br J Dermatol. 1992 Nov;127(5):497-500
Wanukul S et al
Eczematous skin reaction from patch testing with aeroallergens
in atopic children with and without atopic dermatitis.
1993; 10: 209-13
Cork ML et al
An audit of adverse drug reactions to aqueous cream in children
with atopic dermatitis.
The Pharmaceutical Journal. Nov. 2003. Vol.271