Hindawi Publishing Corporation

ISRN Allergy
Volume 2014, Article ID 354250, 7 pages
http://dx.doi.org/10.1155/2014/354250

Review Article
Atopic Dermatitis: Natural History, Diagnosis, and Treatment

Simon Francis Thomsen

Department of Dermatology, Bispebjerg Hospital, Bispebjerg Bakke 23, 2400 Copenhagen NV, Denmark

Correspondence should be addressed to Simon Francis Thomsen; [email protected]

Received 24 February 2014; Accepted 18 March 2014; Published 2 April 2014

Academic Editors: C. Pereira and Z. Zhu

Copyright © 2014 Simon Francis Thomsen. This is an open access article distributed under the Creative Commons Attribution
License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly
cited.

Atopic dermatitis is an inflammatory skin disease with early onset and with a lifetime prevalence of approximately 20%. The
aetiology of atopic dermatitis is unknown, but the recent discovery of filaggrin mutations holds promise that the progression of
atopic dermatitis to asthma in later childhood may be halted. Atopic dermatitis is not always easily manageable and every physician
should be familiar with the fundamental aspects of treatment. This paper gives an overview of the natural history, clinical features,
and treatment of atopic dermatitis.

1. Definition to eczema symptoms having levelled off or even having

decreased in some countries with a formerly very high preva-
Atopic dermatitis is a common, chronic, relapsing, inflamma- lence, such as the United Kingdom and New Zealand. This
tory skin disease that primarily affects young children. Atopy indicates that the allergic disease epidemic is not increas-
is defined as an inherited tendency to produce immunoglob- ing continually worldwide. Nevertheless, atopic dermatitis
ulin E (IgE) antibodies in response to minute amounts of remains a serious health concern, and in many countries,
common environmental proteins such as pollen, house dust particularly in the developing world, the disease is still very
mites, and food allergens. Dermatitis derives from the Greek much on the rise.
“derma,” which means skin, and “itis,” which means inflam-
mation. Dermatitis and eczema are often used synonymously, 2.1. Natural History. Around 50% of all those with atopic
although the term eczema is sometimes reserved for the acute dermatitis develop symptoms within their first year of life,
manifestation of the disease (from Greek, ekzema, to boil and probably as many as 95% experience an onset below
over); here, no distinction is made. Over the years, many five years of age [2]. Around 75% with childhood onset of
other names have been proposed for the disease, for instance, the disease have a spontaneous remission before adolescence,
prurigo Besnier (Besnier’s itch), named after the French der- whereas the remaining 25% continue to have eczema into
matologist Ernest Besnier (1831–1909). Allergic sensitization adulthood or experience a relapse of symptoms after some
and elevated immunoglobulin E (IgE) are present in only symptom-free years. Many with adult-onset atopic dermatitis
about half of all patients with the disease, and therefore atopic or atopic dermatitis relapsing in adulthood develop hand
dermatitis is not a definitive term. eczema as the main manifestation. In some patients, this
constitutes a serious concern as it may affect their choice of
2. Epidemiology career or employment and in some cases it may even lead to
an early exit from the labour market.
Atopic dermatitis affects about one-fifth of all individuals Around 50–75% of all children with early-onset atopic
during their lifetime, but the prevalence of the disease varies dermatitis are sensitized to one or more allergens, such as
greatly throughout the world [1]. In several so-called indus- food allergens, house dust mites, or pets, whereas those
trialised countries, the prevalence increased substantially with late-onset atopic dermatitis are less often sensitized [3].
between 1950 and 2000 so much that many refer to as However, intake of foods or exposure to airborne allergens is
the “allergic epidemic.” However, current indications point rarely the cause of exacerbations in atopic dermatitis; many
2 ISRN Allergy

patients with the disease are sensitized to foods without are protected to some extent against developing the disease
this playing a role in eczema activity. Atopic dermatitis, and against allergic diseases in general [11]. In contrast,
particularly severe disease, in a child heralds other atopic disease development is probably positively correlated with
diseases. A child with moderate to severe atopic dermatitis duration of breastfeeding [12], whereas several studies have
may have as much as 50% risk of developing asthma and 75% linked a high social position of the parents to an increased
risk of developing hay fever [4]. risk of atopic dermatitis in the child [13]. Although such
observations are not easy to interpret, they may also lend
2.2. Risk Factors. The risk of developing atopic dermatitis is support to the hygiene hypothesis or at least to the generally
much higher in those whose family members are affected. accepted theory that eczema occurs in genetically susceptible
For example, the concordance rate of atopic dermatitis in individuals who are exposed to a certain disadvantageous
monozygotic twins is around 75%, meaning that the risk of environment.
the disease in the twin sibling is 75% if the cotwin is affected
[5]. In contrast, the risk in dizygotic twins is only 30%. This 3. Pathophysiology
shows that genetic factors play a role in the susceptibility
to atopic dermatitis. However, as there is not complete Two main hypotheses have been proposed to explain the
concordance between monozygotic twins, who share all their inflammatory lesions in atopic dermatitis. The first hypoth-
genes, environmental and developmental factors must play a esis concerns an imbalance of the adaptive immune system;
role too. As such, atopic dermatitis is a complex genetic dis- the second hypothesis concerns a defective skin barrier.
ease arising from several gene-gene and gene-environment Although these two hypotheses are not thought to be mutu-
interactions. ally exclusive, they may complement each other.

2.2.1. Genetics. Many genes have been associated with atopic 3.1. Immunological Hypothesis. The theory of immunological
dermatitis, particularly genes encoding epidermal structural imbalance argues that atopic dermatitis results from an
proteins and genes encoding key elements of the immune imbalance of T cells, particularly T helper cell types 1, 2, 17,
system. A recent and interesting genetic discovery is the doc- and 22 and also regulatory T cells [14]. In the allergic (atopic
umented strong association between atopic dermatitis and dermatitis) state—particularly in acute eczema—the Th2
mutations in the filaggrin gene, positioned on chromosome differentiation of naive CD4+ T cells predominates. This
1 [6]. The filaggrin gene is the strongest known genetic risk causes an increased production of interleukins, primarily IL-
factor for atopic dermatitis. Around 10% of people from west- 4, IL-5, and IL-13, which then leads to an increased level of
ern populations carry mutations in the filaggrin gene, whereas IgE, and the Th1 differentiation is correspondingly inhibited.
around 50% of all patients with atopic dermatitis carry such
mutations. Filaggrin gene mutations give rise to functional 3.2. The Skin Barrier Hypothesis. The theory of skin barrier
impairments in the filaggrin protein and thereby disrupt the defects is more recent and has its origin in the observation
skin barrier. The clinical expression of such impairments that individuals with mutations in the filaggrin gene are
is dry skin with fissures and a higher risk of eczema. Not at increased risk of developing atopic dermatitis [6]. The
all patients with atopic dermatitis have these mutations and filaggrin gene encodes structural proteins in the stratum
other genetic variants have also been incriminated [7]. It corneum and stratum granulosum that help bind the ker-
is the combined action of all these genetic variants along atinocytes together. This maintains the intact skin barrier
with environmental and developmental risk factors that cause and the hydrated stratum corneum. With gene defects, less
atopic dermatitis. filaggrin is produced, leading to skin barrier dysfunction
and transepidermal water loss, which causes eczema. There
2.2.2. Environment. Although many different environmental is evidence to suggest that the impaired skin barrier, which
risk factors have been considered potentially causative for results in dry skin, leads to increased penetration of allergens
atopic dermatitis, only a few are consistently accepted. For into the skin, resulting in allergic sensitization, asthma, and
example, there is substantial evidence that our western hay fever [15]. Preventing dry skin and active eczema early
lifestyle leads to some of the reported increase in eczema in life via application of emollients may constitute a target
occurrence over the past years although this has not pointed of primary prevention of progression of eczema into allergic
to specific environmental risk factors or has translated airways disease.
directly into functional preventive measures [8]. Many advo-
cate the hygiene hypothesis when explaining the rapid increase 4. Histopathology
in eczema prevalence [9]. This hypothesis states that the
decrease in early childhood exposure to prototypical infec- A skin biopsy taken from a site with acute atopic eczema is
tions, such as hepatitis A and tuberculosis, has increased sus- characterised by intercellular oedema, perivascular infiltrates
ceptibility to atopic diseases [10]. The hypothesis is supported primarily of lymphocytes, and retention of the nuclei of the
by the observations that the youngest among siblings has keratinocytes as they ascend into the stratum corneum—so-
the lowest risk of atopic dermatitis and that children who called parakeratosis. Chronic eczema is dominated by a thick-
grow up in a traditional farming environment where they ened stratum corneum, so-called hyperkeratosis, a thickened
are exposed to a variety of microflora, for instance, from stratum spinosum (acanthosis), but sparse lymphocytic infil-
unpasteurized cow’s milk, livestock, and livestock quarters, trates.
ISRN Allergy 3

Table 1: Diagnostic criteria for atopic dermatitis. Table 2: Therapeutic approaches to atopic dermatitis.

Essential features Topical treatments

Itch Corticosteroids
Eczema with typical morphology and age-specific pattern Calcineurin inhibitors
Important features Phototherapy
Early age of onset Ultraviolet light A (UVA)
Atopy (personal or family history) Ultraviolet light B (UVB)
Dry skin Ultraviolet light A + Psoralene (PUVA)
Associated features Systemic treatments
Atypical vascular response (i.e., facial pallor, white Oral corticosteroids
dermographism) Azathioprine
Keratosis pilaris, palmar hyperlinearity, ichthyosis Cyclosporine A
Ocular and periorbital changes Methotrexate
Other regional findings (e.g., perioral and periauricular
lesions)
Perifollicular accentuation, lichenification, and excoriations
Modified from American Academy of Dermatology [16].
increased tension in the dermal capillaries and the ability to
sweat is reduced. There is an increased cholinergic response
to scratch, so-called white dermographism or skin-writing,
5. Diagnosis and Clinical Presentation resulting in hives at the affected site. The palms of the hands
and feet may show hyperlinearity, and the individuals’ hair
The appearance of the individual skin lesion in atopic der- is dry and fragile. Often, there is a double skinfold under-
matitis does not differ from other eczemas such as contact neath the inferior eyelid (Dennie-Morgan fold) that becomes
eczema. In its acute form, eczema is characterised by a lively exaggerated in times of increased disease activity. The eye
red infiltrate with oedema, vesicles, oozing, and crusting; surroundings may be darkened due to postinflammatory
lichenification, excoriations, papules, and nodules dominate hyperpigmentation.
the subacute and chronic form. Accordingly, the diagnostic Atopic dermatitis can be grouped into three clinical
approach builds upon other characteristics such as the dis- stages, although these may be difficult to reproduce in the
tribution of the eczema as well as associated features of the individual patient [2].
patient. The typical patient with atopic dermatitis is a person
with:
5.1.1. Atopic Dermatitis of Infancy. Infants experience eczema
an early onset of itchy eczema localised at typical sites that is often localised to the face, scalp, and extensor aspects
such as the flexures of the elbows and knees in an atopic of the arms and legs, but it can also be widespread. The lesions
patient or in a person with a familial predisposition to are characterised by erythema, papules, vesicles, excoriations,
atopic disease. oozing, and formation of crusts.
The most widely used diagnostic criteria for atopic der-
matitis were developed by Hanifin and Rajka in 1980 and 5.1.2. Atopic Dermatitis of Childhood. In toddlers and older
were later revised by the American Academy of Dermatology children, the eczema lesions tend to shift location so that they
(Table 1) [16]. are often confined to the flexures of the elbows and knees as
This set of criteria is primarily useful in clinical practice; well as the wrists and ankles, although it can occur at any site.
another set of diagnostic questions widely used in epidemio- In general, the eczema becomes drier and lichenified with
logical research was developed by the UK Working Party in excoriations, papules, and nodules.
1994 (Table 2) [17].
The severity of eczema can be graded according to several
scoring systems such as SCORAD [18] and EASI [19]. 5.1.3. Atopic Dermatitis of Adolescence and Adulthood. In
adult patients, the lesions frequently localise to the face and
5.1. Typical Manifestations. Although this description fits neck, head-and-neck dermatitis, and a considerable portion
many with the disease, the clinical presentation of atopic der- of patients, around 30%, develop atopic hand eczema, which
matitis is often more elaborate with a large variation in the may interfere with workplace activities.
morphology and distribution of the eczema combined with
various other features. However, many patients with atopic 5.2. Special Manifestations. Some patients may present with
dermatitis have a general tendency to present with dry skin several other common, benign skin conditions, for example,
(xerosis) due to the low water content and an excessive pityriasis alba, which is a condition characterised by dry, pale
water loss through the epidermis. The skin is pale because of patches on the face and upper arms, and keratosis pilaris,
4 ISRN Allergy

which manifests as small, rough keratotic papules particu- 6. Treatment

larly on the upper arms and thighs. Atopic winter feet—
dermatitis plantaris sicca—a condition usually seen in school- Atopic dermatitis is not curable, and many patients will expe-
aged children is characterised by symmetric eczema on the rience a chronic course of the disease. Accordingly, the
weight bearing areas of the soles of the feet. Earlobe eczema, treatment of atopic dermatitis aims to [21]
eczema of the nipple, and eczema around the margins of
(1) minimise the number of exacerbations of the disease,
the mouth (cheilitis) can be particularly troublesome and
so-called flares,
often involve infection with staphylococci. Keratoconus and
cataracts sometimes complicate atopic dermatitis. (2) reduce the duration and degree of the flare, if flare
occurs.
5.3. Aggravating Factors. In many patients, atopic dermatitis
The first aim relates primarily to prevention; the second
takes a chronic, relapsing course when it is not possible to
aim relates to treatment. Prevention is best attained by trying
predict periods of activity or pinpoint aggravating factors.
to reduce the dryness of the skin, primarily via daily use of
However, several exposures are well known for aggravating
skin moisturising creams or emollients along with avoidance
eczema and should be avoided. A large number of patients
of specific and unspecific irritants such as allergens and
are sensitive to woollen clothing, which aggravates itching
noncotton clothing. When dryness is reduced, the desire to
and discomfort. Hot water may also exacerbate itching, and
scratch will lessen and the risk of skin infection will decrease.
long baths should be avoided. Several infections, notably
Avoiding long, hot baths further prevents skin dryness,
staphylococci, are frequent causes of exacerbations as various
but when a bath is taken, an emollient should be applied
foods are, particularly in cases where a patient is sensitized
directly after it to secure a moist epidermis and augment the
to the food. Food avoidance should be advocated only if a
skin barrier function. Reducing the flare is warranted when
patient has documented allergy to a suspected food and not
actual eczema occurs or when mild intermittent eczema
on the basis of asymptomatic sensitization alone. Another
worsens. Management of an eczema exacerbation requires
phenomenon that can lead to the eczema worsening is contact
medical treatment often in the form of corticosteroid creams.
urticaria, which is a reaction following skin exposure to a
In addition to topical treatment, severe acute or chronic
food, for example, citrus fruits or tomatoes. The skin around
eczema often requires systemic immunosuppressant drugs or
the mouth is often the site of such a reaction. Lastly, many
phototherapy (ultraviolet, UV light).
patients report that stressful living aggravates their eczema.

5.4. Differential Diagnoses. Several diseases present with a 6.1. Emollients: Maintaining an Intact Skin Barrier. The use
skin rash that resembles atopic dermatitis. However, careful of emollients in the management of atopic dermatitis is
evaluation of the morphology and localization of the rash pivotal. They should be applied several times a day, and
combined with information about the individual patient a systematic use has been shown to reduce the need for
usually leads to a diagnosis. Diseases that sometimes resem- corticosteroid creams [22, 23]. The main reason for intensive
ble atopic dermatitis are scabies, seborrheic dermatitis, and use of an emollient is its ability to increase the hydration of
contact dermatitis. the epidermis, mainly by reducing the evaporation, as it acts
as an occlusive layer on the top of the skin. As such, emollients
5.5. Complications. Several microorganisms, such as bacte- have no direct effect on the course of the eczema. However,
ria, viruses, and fungi, can complicate the eczema (causing the appearance of the skin is enhanced and itching is reduced.
superinfections). The skin of the patient with atopic dermati- Other moisturizers have more complex modes of action as
tis is often colonised with Staphylococcus aureus, particularly they act by restoring the structural (lipid) components of
when the eczema is not well controlled. The mere presence of the outer skin layers, thereby reducing cracks and fissures.
such bacteria does not require antibiotic treatment. However, Others act by attracting water molecules from the air in order
if staphylococci become invasive, oozing crusted lesions— to moisturize the skin. The choice of emollient depends on
impetigo—can be the result, which indicates the need for the individual patient. It is generally recommended that a
topical or, preferably, oral antibiotics [20]. Some advocate thick (with a high fat content) cream or ointment is used
skin washing with antiseptic remedies, such as chlorhexidine, for the driest skin, whereas creams and lotions with a higher
as this lowers the number of bacteria on the skin; however, water content are used only for very mild eczema. Such
chlorhexidine can lead to secondary sensitization. Due to creams must be applied several times a day because of their
deficiencies in the production of antimicrobial peptides in rapid absorption into the skin. It is important to recommend
the skin, patients with atopic dermatitis also have a greater an emollient without perfume or other potential allergens
risk of several viral infections, for example, molluscum as they may provoke secondary allergic sensitization. Those
contagiosum, caused by a pox virus, which gives small, with chronic, dry eczema benefit from tar preparations in the
umbilicated, dome-shaped, pearly coloured papules. Another form of creams and occlusive bandages.
typical superinfection of the skin in atopic dermatitis patients
is herpes virus. If such a herpes infection spreads, it can cause 6.2. Topical Corticosteroids. Topical corticosteroids are the
eczema herpeticum, which is a widespread vesicular eruption, mainstay of the treatment for moderate to severe atopic
typically localised to the face, scalp, and upper chest. Eczema dermatitis, both in children and adults. Corticosteroids are
herpeticum requires systemic antiviral treatment. hierarchically grouped into different classes based on their
ISRN Allergy 5

Table 3: Topical corticosteroids. As one FTU equals roughly 0.5 g cream, the amount
needed to adequately treat an entire adult body surface once is
Mild (Class I) 20 g, whereas a 1-2-year-old child, for instance, requires about
Hydrocortisone 7 g.
Moderate (Class II)
Hydrocortison-17-butyrate 6.2.2. Proactive and Reactive Treatment. Corticosteroid
Clobetason-17-butyrate creams are used both for treating acute flares of atopic der-
Strong (Class III) matitis and for maintenance therapy; that is, prevention of
Betamethason-17-valerate disease relapses when the acute flare is under control. For
treating acute flares, one daily application is recommended
Fluticasone propionate of the cream with the lowest potency deemed sufficient to
Betamethasone clear the eczema within 1-2 weeks [24]. When the eczema
Mometasonfuroate flare is well controlled, that is, when the rash is quiescent
Desoximethasone and particularly when the itch has subsided substantially,
Fluocinonide use of the corticosteroid cream should be tapered off to two
to three weekly applications for an additional 1-2 weeks.
Fluocinolonacetonide
Another tapering approach is to use a lower potency cream
Very strong (Class IV) daily for 1-2 weeks. However, patients may find this approach
Clobetasol propionate slightly more difficult to manage. In theory, treatment could
be discontinued at the end of the tapering period if the flare
is sufficiently under control, but in many patients the eczema
Table 4: Fingertip unit. relapses, and an additional round of treatment is required. If
FTUs FTUs
this is the case, it is preferable to continue the maintenance
Area that needs treatment treatment, applying the corticosteroid cream two to three
(adults) (children 1-2 years)
times weekly on those sites—for instance, the elbow creases—
Face and neck 2.5 1.5
likely to become active again if treatment is discontinued.
One hand and fingers 1 0.5 This strategy is called the proactive treatment strategy, as
One arm, hand, and fingers 4 1.5 compared with the reactive strategy, which recommends
Chest and abdomen 7 2 intermittent use of the corticosteroid preparation according
Back and buttocks 7 3 to the activity of the eczema. The proactive treatment strategy
One leg and foot 8 2 is being increasingly advocated because the overall quantity
of corticosteroid cream used is smaller than that used with
the reactive treatment strategy; additionally, the risk of
an exacerbation of the eczema is smaller when using the
vasoconstrictory abilities. For ease, four classes are consid- proactive treatment strategy.
ered: mild, moderate, strong, and very strong preparations
(Table 3). 6.2.3. Side Effects. Patients and physicians alike fear the cuta-
neous and systemic side effects from using topical corticos-
6.2.1. How Should Corticosteroids Be Applied? Most patients teroids. However, although topical corticosteroids can cause
benefit from treatment with mild to moderate corticosteroid thinning of the skin, teleangiectasies, and stretch marks,
preparations, whereas only a small subset—those with severe when used properly, the risk of side effects is very small. It
disease—needs potent preparations; very strong preparations is essential that physicians try to reassure parents of atopic
are rarely needed. Mild and moderate corticosteroid creams children and the patients themselves and explain that this fear
are reserved for children, while adults can be treated with of side effects should not inhibit the use of corticosteroids
stronger preparations. Mild and moderate corticosteroids since insufficient use can cause worsening of the eczema.
should be used chiefly for treating eczema on body sites Including the patient (and the parents) in the treatment plan
where the skin is thin, notably in the face, axillae, groins, is paramount. Rather than dictating what is best for the child,
and anogenital area, whereas strong corticosteroids should physicians should discuss the parents’ concerns in order to
be used for treating eczema on the rest of the body. Unlike avoid disrupting the physician-patient-parent relationship,
medications used for treating asthma and allergic rhinitis, which would ultimately lead to complications for the child.
creams for atopic dermatitis are not prepared with a fixed
amount of drug release per round of usage. Instead, the “rule 6.3. Calcineurin Inhibitors. Pimecrolimus cream and tacroli-
of the fingertip unit (FTU)” must be applied. A fingertip unit mus ointment—also termed topical calcineurin inhibitors—
is the amount of cream or ointment squeezed from a standard are newer formulations used both for the treatment of acute
tube along an adult’s fingertip—a fingertip is from the very flares and for maintenance therapy of atopic dermatitis [25].
end of the finger to the distal crease in the finger. One FTU is Pimecrolimus has the potency of a mild corticosteroid cream,
sufficient to treat an area of skin twice the size of the flat of an whereas tacrolimus corresponds to a moderate to strong
adult hand with the fingers together (Table 4). topical corticosteroid. The side effects of corticosteroids, such
6 ISRN Allergy

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Conflict of Interests
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The author declares that there is no conflict of interests Working party’s diagnostic criteria for atopic dermatitis—I.
regarding the publication of this paper. Derivation of a minimum set of discriminators for atopic
dermatitis,” British Journal of Dermatology, vol. 131, no. 3, pp.
383–396, 1994.
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