Atopic eczema: clinical features and diagnosis

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Vol 2
September 2010
Clinical Pharmacist
CLINICAL FOCUS
Atopic eczema can have a substantial impact on a patient’s daily living. Assessment should focus
on both physical and quality-of-life aspects of the disease to ensure optimal management
Atopic eczema
clinical features and diagnosis
A
topic eczema is an inflammatory skin condition that
affects all age groups, but usually starts in childhood.
It is the most common form of eczema, affecting up
to 20% of children and 2–10% of adults in the UK.
Moreover, there has been a steady increase in the
prevalence of atopic eczema over the past 30 years.1
There are many clinical variants of eczema (see Box 1,
p286) but the common features are red, itchy, sore and
inflamed skin. The terms “eczema” and “dermatitis” are
now used interchangeably (see Box 2, p289).
Atopic eczema can have a substantial negative impact
on quality of life for both the sufferer and his or her
family — an Australian study showed that caring for
children with moderate-to-severe atopic eczema was more
stressful than caring for children with type 1 diabetes.2
Inability to sleep due to severe itching means that
schoolwork and home life are disrupted and, for some
people, eczema affecting the hands also interferes with
their ability to work. Additionally, the erroneous belief
that eczema is contagious can prompt negative reactions to
the condition from other people.
The epidermal barrier
The skin has two main layers: the dermis and the
epidermis.
The dermis is 3–5mm thick and contains blood vessels,
hair follicles and sweat glands.
The epidermis is the surface layer which varies in
thickness from about 0.06mm on the eyelids to 0.8mm on
the palms and soles of the feet. The epidermis is composed
of four layers of densely packed keratinocytes (skin cells).
Keratinocytes are continually formed in the basal layer and
gradually move upwards to the stratum corneum. As they
move they change progressively from plump, nucleated
cells to flattened, dead cells that are shed. This process
takes about 28 days.
Several factors contribute to the formation of the
epidermal barrier. The uppermost layer of the epidermis
(stratum corneum) can be visualised as a brick wall where
the cells (now known as corneocytes) are the bricks. They
Christine Clark is a freelance journalist and chairman
of the Skin Care Campaign, a UK organisation
representing the interests of people with skin diseases.
E: [email protected]
SUMMARY
Atopic eczema (or atopic dermatitis) is an inflammatory, itchy skin
condition that follows a relapsing and remitting course. It usually starts in
early childhood and is often caused by a genetic defect that leads to a
breakdown of the skin barrier.
Trigger factors, such as irritants and allergens, can precipitate flares of
eczema or make the condition worse. Although atopic eczema is often not
considered to be a serious medical condition, it can have a substantial
impact on quality of life for patients and carers.
are held together by mortar made up of intercellular lipids
that are extruded from the maturing cells (see Figure 1,
p286).
Also contributing to cell compaction in the epidermis is
a protein called filaggrin. Filaggrin is broken down to form
smaller units (filaggrin monomers) that bind to keratin.
Further breakdown of filaggrin releases amino acids that
are constituents of natural moisturising factor (NMF).3
NMF enhances the epidermal barrier by ensuring water is
held in the cells — cells with a high water content swell
and press tightly against each another, with no gaps.
Finally, the cells are linked by protein bridges known as
corneodesmosomes. Corneocytes are shed from the
uppermost surface when the corneodesmosomes are
cleaved by skin proteases.
Thus, although cells are continuously shed from the
upper surface of the stratum corneum, the deeper layers
are held together firmly through the combined actions of
barrier lipids, NMF and corneodesmosomes. This is
Soap should be avoided by people with eczema
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By Christine Clark, PhD, FRPharmS
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September 2010
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Intercellular lipids
Natural moisturising factor
Corneocyte
Corneodesmosome
inflammatory cytokines. The problems are further
exacerbated by scratching, which relieves itching
temporarily but further damages the skin and can itself
trigger further release of inflammatory mediators, thereby
increasing inflammation and itching and perpetuating the
cycle (the “itch-scratch cycle”).
Diagnosis
A diagnosis of atopic eczema is made with the presence of
an itchy rash plus three or more of the following:6
● Visible flexural dermatitis (or visible dermatitis on
the cheeks or outer aspects of the limbs in children)
● Personal history of flexural dermatitis (or dermatitis
on the cheeks in children under 10 years of age)
● Personal history of dry skin in the past 12 months
● Personal history of asthma (or history of atopic
disease in a first-degree relative for children)
● Onset of signs and symptoms under the age of two
years (this criterion should not be used in children
under four years of age)
Figure 1: Representation of the brick-like structure of the epidermal barrier
known as the epidermal barrier and it serves to prevent
excessive water loss from healthy skin and to prevent the
entry of allergens and irritants.
Pathophysiology
Atopic eczema appears to be caused by genetically
determined defects in the epidermal barrier of the skin,
which increase the susceptibility of the skin to damage
from environmental factors. Such damage allows the entry
of allergens and irritants that trigger immune and
inflammatory responses. Therefore, some experts have
described eczema as the result of a gene-environment
interaction.
In atopic eczema, the intercellular lipids are not formed
normally, which reduces the effectiveness of the
epidermal barrier.4 There is increased water loss from the
stratum corneum causing the corneocytes to shrink; cracks
then open up between the cells. The result is dry skin,
which can neither retain water effectively nor prevent the
incursion of irritants or allergens.
Two genetic variations have been identified recently
that go some way towards explaining these changes. The
first is a genetic filaggrin deficiency which leads to a
poorly formed stratum corneum that is prone to water loss.
It is estimated that filaggrin gene defects are present in one
in 10 Europeans.5
Another genetic defect leads to high levels of a skin
protease called stratum corneum chymotryptic enzyme —
this is also associated with atopic eczema. Furthermore,
raising the skin pH from 5.5 to 7.5, for example (as happens
when washing with soap), results in a doubling of protease
activity.4
Similar changes can also be seen in normal skin when
some of the epidermal lipids are removed by repeated use
of surfactants or solvents. The use of soap not only
removes natural oils from the skin, making it feel dry, it
also increases shedding of skin cells.
People with atopic eczema are more sensitive to the
detrimental effects of soap than people without the
condition. The absence of visible eczema in a particular
area does not alter this — a lower threshold for irritation
remains even if the skin appears “normal”.
Current thinking suggests that when irritants and
allergens penetrate the weakened epidermal barrier they
trigger immune responses, including the release of pro-
Minor changes to the diagnostic criteria for children
were made in the 2007 National Institute for Health and
Clinical Excellence guidance for atopic eczema in
children.7
Acute eczema can be accompanied by exudation and
crusting, while chronic eczema lesions are dry, lichenified
and fissured.
Other dermatological conditions can be mistaken for
eczema. Scabies can look like eczema and the severe itching
that accompanies established scabies infestation adds to the
confusion. Scabies and head lice can also precipitate local
flare of eczema. Psoriasis can sometimes look like eczema,
but psoriasis plaques are usually found on extensor
(outside) surfaces whereas eczema, in adults, more
commonly affects flexor (inside) surfaces. Fungal infections
and rosacea can also mimic the appearance of eczema.
Box 1: Other types of eczema
TYPE OF ECZEMA
DETAILS
Irritant contact
Triggered by contact with irritant substances (eg,
shampoo, detergents)
Allergic contact
Triggered by contact with allergens (eg, chromate,
nickel, perfumes, preservatives)
Seborrhoeic
Typically affects scalp, eyebrows and ears, but can
also affect axillae. Characteristic greasy yellow scales.
Associated with Pityrosporum spp overgrowth
Gravitational (varicose)
Associated with oedematous legs. Skin is fragile and
can ulcerate if scratched
Asteatotic
Occurs on the legs of elderly patients where the skin is
very dry. Appear as fine, red, superficial fissures
Pompholyx
Presents with vesicles or large blisters on the palms,
fingers or soles of the feet
Discoid
Multiple coin-shaped, itchy lesions, typically found in
middle-aged men. Thought to be stress-related.
Chronic hand
Erythema, vesicles, papules, scaling, fissures, itching
and pain affecting the hands. Can be incapacitating
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Parents should be warned of the dangers of contact with
anyone who has H simplex or cold sores.
The atopic march
Assessment
Atopic eczema often develops as part of a wider pattern of
atopic conditions — this is known as the “atopic march”.
Gastrointestinal symptoms (commonly due to an allergy
to milk and eggs) occur in the first few months of life. This
is followed by atopic eczema, often starting within the first
three months. Later during childhood, asthma develops
and then allergic rhinitis. The factors responsible for the
atopic march are not fully understood but it is thought that
the defective skin barrier seen in atopic eczema could play
a key role.9
Experts recommend that assessment of a patient with
eczema should embrace both the physical aspects of the
condition and its impact on quality of life. The NICE
guideline for the management of atopic eczema in
children7 outlines a severity grading scheme, incorporating
both physical and quality-of-life assessments (see Box 3).
Clinicians should always conduct both physical and
quality-of-life assessments because even mild eczema can
affect a patient’s well-being.
Course of disease
Atopic eczema commonly starts in early childhood, but it
can also start later in life. Like other inflammatory skin
diseases it runs a relapsing and remitting course with the
severity often varying from day to day. The “International
study of life with atopic eczema” (ISOLATE)8 showed that,
on average, patients experienced nine flares per year, each
lasting for 15 days. Overall, patients spent an average of
136 days per year experiencing flares.
References
Complications
St Bartholomew’s Hospital | SPL
A common complication of atopic eczema is bacterial
infection with Staphylococcus aureus, leading to impetigo.
Eczematous skin is almost always colonised with S aureus
but treatment is only required when there is evidence of
infection (eg, worsening inflammation, weeping, pustules,
crusting, eczema failing to respond to treatment, rapidly
worsening eczema or, in severe cases, fever and malaise).
People with eczema are more susceptible to infection
with viruses, such as those causing warts and molluscum
contagiosum.
Infants and young children with eczema can develop
widespread lesions if infected with Herpes simplex (see
Figure 2). This condition, known as eczema herpeticum,
requires urgent referral for medical attention because it
can be life-threatening. It is associated with:
Figure 2: Eczema herpeticum affecting wrists and hands
1
National Institute for Health and Clinical Excellence. Clinical Knowledge
Summaries: atopic eczema. www.cks.nhs.uk/eczema_atopic#-323502
(accessed 13 August 2010).
2
Su JC, Kemp AS, Varigos GA, et al. Atopic eczema: its impact on the
family and financial cost. Archives of Disease in Childhood
1997;76:159–62.
3
Sandilands A, Sutherland C, Irvine AD, et al. Filaggrin in the frontline:
role in skin barrier function and disease. Journal of Cell Science
2009;122:1285–94.
4
Cork MJ. The importance of skin barrier function. Journal of
Dermatological Treatment 1997;8:S7–13.
5
Palmer CN, Irvine AD, Terron-Kwiatkowski A, et al. Common loss-offunction variants of the epidermal barrier protein filaggrin are a major
predisposing factor for atopic dermatitis. Nature Genetics 2006;38:441–6.
6
Williams HC, Burney PG, Hay RJ, et al. The UK Working Party’s
Diagnostic Criteria for Atopic Dermatitis. British Journal of Dermatology
1994;131:383–96.
7
National Institute for Health and Clinical Excellence. Atopic eczema in
children. December 2007. www.nice.org.uk/cg57 (accessed 13 June 2010).
8
Zuberbier T, Orlow SJ, Paller AS, et al. Patient perspectives on the
management of atopic dermatitis. Journal of Allergy and Clinical
Immunology 2006;118:226–32.
9
Leung DY, Boguniewicz M, Howell MD, et al. New insights into atopic
dermatitis. Journal of Clinical Investigation 2004;113:651–7.
Box 3: Assessment of atopic eczema4
GRADE
PHYSICAL ASSESSMENT
IMPACT ON QUALITY OF LIFE
Clear/none
Normal skin; no evidence of
atopic eczema
No impact
Mild
Areas of dry skin; infrequent
itching (with or without small
areas of redness)
Little impact on everyday
activities, sleep and social wellbeing
Moderate
Areas of dry skin; frequent
itching; redness (with or without
excoriation and localised skin
thickening)
Moderate impact on everyday
activities and psychosocial wellbeing; frequently disturbed sleep
Severe
Widespread areas of dry skin;
Severe limitation of everyday
incessant itching; redness (with activities and psychosocial
or without excoriation, extensive functioning; nightly loss of sleep
skin thickening, bleeding,
oozing, cracking and altered
pigmentation)
289
CLINICAL FOCUS
The terms eczema and dermatitis are interchangeable
Atopic eczema is the most common form of eczema
The common clinical feature is red, itchy, inflamed skin
Eczema can have a significant impact on quality of life
The severity of eczema often varies from day to day
Acute eczema can be accompanied by exudation and crusting, while
chronic eczema lesions are dry, lichenified and fissured
Clinical Pharmacist
● Areas of rapidly worsening, painful eczema
● Possible fever, lethargy or distress
● Clustered blisters that look like early-stage cold
sores
● Uniform, punched-out erosions (usually 1–3mm
diameter) which may coalesce
Box 2: Key points about atopic eczema
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September 2010