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Atopic Dermatitis: Natural History, Diagnosis, and Treatment

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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.
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Review Article
Atopic Dermatitis: Natural History, Diagnosis, and Treatment
Simon Francis Thomsen
DepartmentofDermatology,BispebjergHospital,BispebjergBakke23,2400CopenhagenNV,Denmark
Correspondence should be addressed to Simon Francis omsen; simonfrancisthomsen@gmail.com
Received  February ; Accepted  March ; Published  April 
Academic Editors: C. Pereira and Z. Zhu
Copyright ©  Simon Francis omsen. is 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 inammatory skin disease with early onset and with a lifetime prevalence of approximately %. e
aetiology of atopic dermatitis is unknown, but the recent discovery of laggrin 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. is paper gives an overview of the natural history, clinical features,
and treatment of atopic dermatitis.
1. Definition
Atopicdermatitisisacommon,chronic,relapsing,inamma-
tory skin disease that primarily aects young children. Atopy
is dened as an inherited tendency to produce immunoglob-
ulin E (IgE) antibodies in response to minute amounts of
common environmental proteins such as pollen, house dust
mites, and food allergens. Dermatitis derives from the Greek
derma,” which means skin, and “itis,” which means inam-
mation. Dermatitis and eczema areoenusedsynonymously,
although the term eczema is sometimes reserved for the acute
manifestation of the disease (from Greek, ekzema, to boil
over); here, no distinction is made. Over the years, many
other names have been proposed for the disease, for instance,
prurigo Besnier (Besnier’s itch), named aer the French der-
matologist Ernest Besnier (–). Allergic sensitization
and elevated immunoglobulin E (IgE) are present in only
about half of all patients with the disease, and therefore atopic
dermatitis is not a denitive term.
2. Epidemiology
Atopic dermatitis aects about one-h of all individuals
during their lifetime, but the prevalence of the disease varies
greatly throughout the world []. In several so-called indus-
trialisedcountries,theprevalenceincreasedsubstantially
betweenandsomuchthatmanyrefertoas
the “allergic epidemic.” However, current indications point
to eczema symptoms having levelled o or even having
decreased in some countries with a formerly very high preva-
lence,suchastheUnitedKingdomandNewZealand.is
indicates that the allergic disease epidemic is not increas-
ing continually worldwide. Nevertheless, atopic dermatitis
remains a serious health concern, and in many countries,
particularly in the developing world, the disease is still very
much on the rise.
2.1. Natural History. Around % of all those with atopic
dermatitis develop symptoms within their rst year of life,
and probably as many as % experience an onset below
ve years of age []. Around % with childhood onset of
the disease have a spontaneous remission before adolescence,
whereas the remaining % continue to have eczema into
adulthood or experience a relapse of symptoms aer some
symptom-free years. Many with adult-onset atopic dermatitis
or atopic dermatitis relapsing in adulthood develop hand
eczema as the main manifestation. In some patients, this
constitutes a serious concern as it may aect their choice of
career or employment and in some cases it may even lead to
an early exit from the labour market.
Around –% of all children with early-onset atopic
dermatitis are sensitized to one or more allergens, such as
food allergens, house dust mites, or pets, whereas those
with late-onset atopic dermatitis are less oen sensitized [].
However, intake of foods or exposure to airborne allergens is
rarely the cause of exacerbations in atopic dermatitis; many
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Volume 2014, Article ID 354250, 7 pages
http://dx.doi.org/10.1155/2014/354250
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patients with the disease are sensitized to foods without
this playing a role in eczema activity. Atopic dermatitis,
particularly severe disease, in a child heralds other atopic
diseases. A child with moderate to severe atopic dermatitis
mayhaveasmuchas%riskofdevelopingasthmaand%
risk of developing hay fever [].
2.2. Risk Factors. e risk of developing atopic dermatitis is
much higher in those whose family members are aected.
For example, the concordance rate of atopic dermatitis in
monozygotic twins is around %, meaning that the risk of
the disease in the twin sibling is % if the cotwin is aected
[]. In contrast, the risk in dizygotic twins is only %. is
shows that genetic factors play a role in the susceptibility
to atopic dermatitis. However, as there is not complete
concordance between monozygotic twins, who share all their
genes, environmental and developmental factors must play a
role too. As such, atopic dermatitis is a complex genetic dis-
ease arising from several gene-gene and gene-environment
interactions.
2.2.1. Genetics. Manygeneshavebeenassociatedwithatopic
dermatitis, particularly genes encoding epidermal structural
proteins and genes encoding key elements of the immune
system. A recent and interesting genetic discovery is the doc-
umented strong association between atopic dermatitis and
mutations in the laggrin gene, positioned on chromosome
[]. e laggrin gene is the strongest known genetic risk
factor for atopic dermatitis. Around % of people from west-
ern populations carry mutations in the laggr in gene, where as
around % of all patients with atopic dermatitis carry such
mutations. Filaggrin genemutationsgiverisetofunctional
impairments in the laggrin protein and thereby disrupt the
skin barrier. e clinical expression of such impairments
is dry skin with ssures and a higher risk of eczema. Not
all patients with atopic dermatitis have these mutations and
other genetic variants have also been incriminated []. It
is the combined action of all these genetic variants along
with environmental and developmental risk factors that cause
atopic dermatitis.
2.2.2. Environment. Although many dierent environmental
risk factors have been considered potentially causative for
atopic dermatitis, only a few are consistently accepted. For
example, there is substantial evidence that our western
lifestyleleadstosomeofthereportedincreaseineczema
occurrence over the past years although this has not pointed
to specic environmental risk factors or has translated
directly into functional preventive measures []. Many advo-
cate the hygiene hypothesis when explaining the rapid increase
in eczema prevalence [].ishypothesisstatesthatthe
decrease in early childhood exposure to prototypical infec-
tions, such as hepatitis A and tuberculosis, has increased sus-
ceptibility to atopic diseases []. e hypothesis is supported
by the observations that the youngest among siblings has
the lowest risk of atopic dermatitis and that children who
grow up in a traditional farming environment where they
are exposed to a variety of microora, for instance, from
unpasteurized cow’s milk, livestock, and livestock quarters,
are protected to some extent against developing the disease
and against allergic diseases in general []. In contrast,
disease development is probably positively correlated with
duration of breastfeeding [], whereas several studies have
linked a high social position of the parents to an increased
risk of atopic dermatitis in the child []. Although such
observations are not easy to interpret, they may also lend
supporttothehygienehypothesisoratleasttothegenerally
accepted theory that eczema occurs in genetically susceptible
individuals who are exposed to a certain disadvantageous
environment.
3. Pathophysiology
Twomainhypotheseshavebeenproposedtoexplainthe
inammatory lesions in atopic dermatitis. e rst hypoth-
esis concerns an imbalance of the adaptive immune system;
the second hypothesis concerns a defective skin barrier.
Although these two hypotheses are not thought to be mutu-
ally exclusive, they may complement each other.
3.1. Immunological Hypothesis. e theory of immunological
imbalance argues that atopic dermatitis results from an
imbalance of T cells, particularly T helper cell types , , ,
and  and also regulatory T cells []. In the allergic (atopic
dermatitis) state—particularly in acute eczema—the 
dierentiation of naive CD+ T cells predominates. is
causes an increased production of interleukins, primarily IL-
, IL-, and IL-, which then leads to an increased level of
IgE, and the  dierentiation is correspondingly inhibited.
3.2. e Skin Barrier Hypothesis. e theory of skin barrier
defects is more recent and has its origin in the observation
that individuals with mutations in the laggrin gene are
at increased risk of developing atopic dermatitis []. e
laggrin gene encodes structural proteins in the stratum
corneum and stratum granulosum that help bind the ker-
atinocytes together. is maintains the intact skin barrier
and the hydrated stratum corneum. With gene defects, less
laggrin is produced, leading to skin barrier dysfunction
and transepidermal water loss, which causes eczema. ere
is evidence to suggest that the impaired skin barrier, which
results in dry skin, leads to increased penetration of allergens
into the skin, resulting in allergic sensitization, asthma, and
hay fever []. Preventing dry skin and active eczema early
in life via application of emollients may constitute a target
of primary prevention of progression of eczema into allergic
airways disease.
4. Histopathology
A skin biopsy taken from a site with acute atopic eczema is
characterised by intercellular oedema, perivascular inltrates
primarily of lymphocytes, and retention of the nuclei of the
keratinocytes as they ascend into the stratum corneum—so-
called parakeratosis. Chronic eczema is dominated by a thick-
ened stratum corneum, so-called hyperkeratosis, a thickened
stratum spinosum (acanthosis), but sparse lymphocytic inl-
trates.
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T : Diagnostic criteria for atopic dermatitis.
Essential features
Itch
Eczema with typical morphology and age-specic pattern
Important features
Early age of onset
Atopy (personal or family history)
Dry skin
Associated features
Atypical vascular response (i.e., facial pallor, white
dermographism)
Keratosis pilaris, palmar hyperlinearity, ichthyosis
Ocular and periorbital changes
Other regional ndings (e.g., perioral and periauricular
lesions)
Perifollicular accentuation, lichenication, and excoriations
Modied from American Academy of Dermatology [].
5. Diagnosis and Clinical Presentation
e appearance of the individual skin lesion in atopic der-
matitis does not dier from other eczemas such as contact
eczema. In its acute form, eczema is characterised by a lively
red inltrate with oedema, vesicles, oozing, and crusting;
lichenication, excoriations, papules, and nodules dominate
thesubacuteandchronicform.Accordingly,thediagnostic
approach builds upon other characteristics such as the dis-
tribution of the eczema as well as associated features of the
patient. e typical patient with atopic dermatitis is a person
with:
an early onset of itchy eczema localised at typical sites
such as the exures of the elbows and knees in an atopic
patient or in a person with a familial predisposition to
atopic disease.
e most widely used diagnostic criteria for atopic der-
matitis were developed by Hanin and Rajka in  and
were later revised by the American Academy of Dermatology
(Table )[].
is set of criteria is primarily useful in clinical practice;
another set of diagnostic questions widely used in epidemio-
logical research was developed by the UK Working Party in
 (Tab l e  )[].
e severity of eczema can be graded according to several
scoring systems such as SCORAD []andEASI[].
5.1. Typical Manifestations. Although this description ts
many with the disease, the clinical presentation of atopic der-
matitis is oen more elaborate with a large variation in the
morphology and distribution of the eczema combined with
various other features. However, many patients with atopic
dermatitis have a general tendency to present with dry skin
(xerosis) due to the low water content and an excessive
water loss through the epidermis. e skin is pale because of
T : erapeutic approaches to atopic dermatitis.
Topica l t r e a t ments
Corticosteroids
Calcineurin inhibitors
Phototherapy
Ultraviolet light A (UVA)
Ultraviolet light B (UVB)
Ultraviolet light A + Psoralene (PUVA)
Systemic treatments
Oral corticosteroids
Azathioprine
Cyclosporine A
Methotrexate
increased tension in the dermal capillaries and the ability to
sweat is reduced. ere is an increased cholinergic response
to scratch, so-called white dermographism or skin-writing,
resultinginhivesattheaectedsite.epalmsofthehands
and feet may show hyperlinearity, and the individuals’ hair
is dry and fragile. Oen, there is a double skinfold under-
neath the inferior eyelid (Dennie-Morgan fold) that becomes
exaggerated in times of increased disease activity. e eye
surroundings may be darkened due to postinammatory
hyperpigmentation.
Atopic dermatitis can be grouped into three clinical
stages, although these may be dicult to reproduce in the
individual patient [].
5.1.1. Atopic Dermatitis of Infancy. Infants experience eczema
that is oen localised to the face, scalp, and extensor aspects
of the arms and legs, but it can also be widespread. e lesions
are characterised by erythema, papules, vesicles, excoriations,
oozing, and formation of crusts.
5.1.2. Atopic Dermatitis of Childhood. In toddlers and older
children, the eczema lesions tend to shi location so that they
are oen conned to the exures of the elbows and knees as
well as the wrists and ankles, although it can occur at any site.
In general, the eczema becomes drier and lichenied with
excoriations, papules, and nodules.
5.1.3. Atopic Dermatitis of Adolescence and Adulthood. In
adult patients, the lesions frequently localise to the face and
neck, head-and-neck dermatitis, and a considerable portion
of patients, around %, develop atopic hand eczema, which
may interfere with workplace activities.
5.2. Special Manifestations. Some patients may present with
several other common, benign skin conditions, for example,
pityriasis alba, which is a condition characterised by dry, pale
patches on the face and upper arms, and keratosis pilaris,
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which manifests as small, rough keratotic papules particu-
larly on the upper arms and thighs. Atopic winter feet—
dermatitis plantaris sicca—a condition usually seen in school-
aged children is characterised by symmetric eczema on the
weight bearing areas of the soles of the feet. Earlobe eczema,
eczemaofthenipple,andeczemaaroundthemarginsof
the mouth (cheilitis) can be particularly troublesome and
oen involve infection with staphylococci. Keratoconus and
cataracts sometimes complicate atopic dermatitis.
5.3. Aggravating Factors. In many patients, atopic dermatitis
takes a chronic, relapsing course when it is not possible to
predict periods of activity or pinpoint aggravating factors.
However, several exposures are well known for aggravating
eczema and should be avoided. A large number of patients
are sensitive to woollen clothing, which aggravates itching
and discomfort. Hot water may also exacerbate itching, and
long baths should be avoided. Several infections, notably
staphylococci, are frequent causes of exacerbations as various
foods are, particularly in cases where a patient is sensitized
to the food. Food avoidance should be advocated only if a
patient has documented allergy to a suspected food and not
on the basis of asymptomatic sensitization alone. Another
phenomenon that can lead to the eczema worsening is contact
urticaria, which is a reaction following skin exposure to a
food, for example, citrus fruits or tomatoes. e skin around
the mouth is oen the site of such a reaction. Lastly, many
patients report that stressful living aggravates their eczema.
5.4. Dierential Diagnoses. Several diseases present with a
skin rash that resembles atopic dermatitis. However, careful
evaluation of the morphology and localization of the rash
combined with information about the individual patient
usually leads to a diagnosis. Diseases that sometimes resem-
ble atopic dermatitis are scabies, seborrheic dermatitis, and
contact dermatitis.
5.5. Complications. Several microorganisms, such as bacte-
ria, viruses, and fungi, can complicate the eczema (causing
superinfections). e skin of the patient with atopic dermati-
tis is oen colonised with Staphylococcus aureus,particularly
when the eczema is not well controlled. e mere presence of
such bacteria does not require antibiotic treatment. However,
if staphylococci become invasive, oozing crusted lesions—
impetigo—can be the result, which indicates the need for
topical or, preferably, oral antibiotics []. Some advocate
skin washing with antiseptic remedies, such as chlorhexidine,
as this lowers the number of bacteria on the skin; however,
chlorhexidine can lead to secondary sensitization. Due to
deciencies in the production of antimicrobial peptides in
the skin, patients with atopic dermatitis also have a greater
risk of several viral infections, for example, molluscum
contagiosum, caused by a pox virus, which gives small,
umbilicated, dome-shaped, pearly coloured papules. Another
typical superinfection of the skin in atopic dermatitis patients
is herpes virus. If such a herpes infection spreads, it can cause
eczema herpeticum, which is a widespread vesicular eruption,
typically localised to the face, scalp, and upper chest. Eczema
herpeticum requires systemic antiviral treatment.
6. Treatment
Atopic dermatitis is not curable, and many patients will expe-
rience a chronic course of the disease. Accordingly, the
treatment of atopic dermatitis aims to []
() minimise the number of exacerbations of the disease,
so-called ares,
()reducethedurationanddegreeoftheare,ifare
occurs.
e rst aim relates primarily to prevention; the second
aim relates to treatment. Prevention is best attained by trying
to reduce the dryness of the skin, primarily via daily use of
skin moisturising creams or emollients along with avoidance
of specic and unspecic irritants such as allergens and
noncotton clothing. When dryness is reduced, the desire to
scratch will lessen and the risk of skin infection will decrease.
Avoiding long, hot baths further prevents skin dryness,
but when a bath is taken, an emollient should be applied
directly aer it to secure a moist epidermis and augment the
skin barrier function. Reducing the are is warranted when
actual eczema occurs or when mild intermittent eczema
worsens. Management of an eczema exacerbation requires
medical treatment oen in the form of corticosteroid creams.
In addition to topical treatment, severe acute or chronic
eczema oen requires systemic immunosuppressant drugs or
phototherapy (ultraviolet, UV light).
6.1. Emollients: Maintaining an Intact Skin Barrier. e use
of emollients in the management of atopic dermatitis is
pivotal. ey should be applied several times a day, and
a systematic use has been shown to reduce the need for
corticosteroid creams [,]. e main reason for intensive
use of an emollient is its ability to increase the hydration of
the epidermis, mainly by reducing the evaporation, as it acts
asanocclusivelayeronthetopoftheskin.Assuch,emollients
have no direct eect on the course of the eczema. However,
theappearanceoftheskinisenhancedanditchingisreduced.
Other moisturizers have more complex modes of action as
they act by restoring the structural (lipid) components of
the outer skin layers, thereby reducing cracks and ssures.
Others act by attracting water molecules from the air in order
to moisturize the skin. e choice of emollient depends on
the individual patient. It is generally recommended that a
thick (with a high fat content) cream or ointment is used
for the driest skin, whereas creams and lotions with a higher
water content are used only for very mild eczema. Such
creams must be applied several times a day because of their
rapid absorption into the skin. It is important to recommend
an emollient without perfume or other potential allergens
as they may provoke secondary allergic sensitization. ose
with chronic, dry eczema benet from tar preparations in the
form of creams and occlusive bandages.
6.2. Topical Corticosteroids. Topical corticosteroids are the
mainstay of the treatment for moderate to severe atopic
dermatitis, both in children and adults. Corticosteroids are
hierarchically grouped into dierent classes based on their
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T : Topical corticosteroids.
Mild (Class I)
Hydrocortisone
Moderate (Class II)
Hydrocortison--butyrate
Clobetason--butyrate
Strong (Class III)
Betamethason--valerate
Fluticasone propionate
Betamethasone
Mometasonfuroate
Desoximethasone
Fluocinonide
Fluocinolonacetonide
Very strong (Class IV)
Clobetasol propionate
T : Fingertip unit.
Area that needs treatment FTUs
(adults)
FTUs
(children - years)
Face and neck . .
One hand and ngers  .
One arm, hand, and ngers .
Chest and abdomen 
Back and buttocks 
One leg and foot 
vasoconstrictory abilities. For ease, four classes are consid-
ered: mild, moderate, strong, and very strong preparations
(Table ).
6.2.1. How Should Corticosteroids Be Applied? Most patients
benet from treatment with mild to moderate corticosteroid
preparations, whereas only a small subset—those with severe
disease—needs potent preparations; very strong preparations
are rarely needed. Mild and moderate corticosteroid creams
are reserved for children, while adults can be treated with
stronger preparations. Mild and moderate corticosteroids
should be used chiey for treating eczema on body sites
where the skin is thin, notably in the face, axillae, groins,
and anogenital area, whereas strong corticosteroids should
be used for treating eczema on the rest of the body. Unlike
medications used for treating asthma and allergic rhinitis,
creams for atopic dermatitis are not prepared with a xed
amount of drug release per round of usage. Instead, the “rule
of the ngertip unit (FTU)” must be applied. A ngertip unit
is the amount of cream or ointment squeezed from a standard
tube along an adult’s ngertip—a ngertip is from the very
end of the nger to the distal crease in the nger. One FTU is
sucienttotreatanareaofskintwicethesizeoftheatofan
adult hand with the ngers together (Tabl e  ).
As one FTU equals roughly . g cream, the amount
needed to adequately treat an entire adult body surface once is
 g, whereas a --year-old child, for instance, requires about
g.
6.2.2. Proactive and Reactive Treatment. Corticosteroid
creams are used both for treating acute ares of atopic der-
matitis and for maintenance therapy; that is, prevention of
disease relapses when the acute are is under control. For
treating acute ares, one daily application is recommended
of the cream with the lowest potency deemed sucient to
clear the eczema within - weeks []. When the eczema
are is well controlled, that is, when the rash is quiescent
and particularly when the itch has subsided substantially,
use of the corticosteroid cream should be tapered o to two
to three weekly applications for an additional - weeks.
Anothertaperingapproachistousealowerpotencycream
daily for - weeks. However, patients may nd this approach
slightly more dicult to manage. In theory, treatment could
be discontinued at the end of the tapering period if the are
is suciently under control, but in many patients the eczema
relapses, and an additional round of treatment is required. If
this is the case, it is preferable to continue the maintenance
treatment, applying the corticosteroid cream two to three
times weekly on those sites—for instance, the elbow creases—
likely to become active again if treatment is discontinued.
isstrategyiscalledtheproactive treatment strategy, as
compared with the reactive strategy, which recommends
intermittent use of the corticosteroid preparation according
to the activity of the eczema. e proactive treatment strategy
is being increasingly advocated because the overall quantity
of corticosteroid cream used is smaller than that used with
thereactivetreatmentstrategy;additionally,theriskof
an exacerbation of the eczema is smaller when using the
proactive treatment strategy.
6.2.3. Side Eects. Patients and physicians alike fear the cuta-
neous and systemic side eects from using topical corticos-
teroids. However, although topical corticosteroids can cause
thinning of the skin, teleangiectasies, and stretch marks,
when used properly, the risk of side eects is very small. It
is essential that physicians try to reassure parents of atopic
children and the patients themselves and explain that this fear
of side eects should not inhibit the use of corticosteroids
since insucient use can cause worsening of the eczema.
Including the patient (and the parents) in the treatment plan
is paramount. Rather than dictating what is best for the child,
physicians should discuss the parents’ concerns in order to
avoid disrupting the physician-patient-parent relationship,
which would ultimately lead to complications for the child.
6.3. Calcineurin Inhibitors. Pimecrolimus cream and tacroli-
mus ointment—also termed topical calcineurin inhibitors—
are newer formulations used both for the treatment of acute
ares and for maintenance therapy of atopic dermatitis [].
Pimecrolimus has the potency of a mild corticosteroid cream,
whereas tacrolimus corresponds to a moderate to strong
topical corticosteroid. e side eects of corticosteroids, such
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as thinning of the skin, are not seen with topical calcineurin
inhibitors, and this allows daily treatment for longer periods.
Topical calcineurin inhibitors can also be used in the proac-
tive treatment strategy.
6.4. Phototherapy. Widespread eczema benets from treat-
ment with UV light. Narrowband UVB light is particularly
suitable for treating adults with recalcitrant eczema. Broad-
band UVA light and a combination of UVA light and the
photosensitizing drug psoralene canalsobeusedtotreat
severe recalcitrant eczema. Dicult-to-treat atopic dermatitis
oen clears with - months’ phototherapy three to ve times
a week, preferably combined with topical corticosteroids.
Nevertheless, as phototherapy causes premature aging of the
skin and increases the risk of skin cancer in the long run, it
should be prescribed with caution.
6.5. Systemic Immunosuppressant Treatments. Short-term
tapered treatment with oral corticosteroids is recommended
for acute ares of severe, widespread atopic dermatitis,
preferably in combination with topical corticosteroids. As
Staphylococcus infections oen trigger such ares, oral antibi-
oticsshouldbeprescribedsimultaneously.Duetotheriskof
side eects, continuing treatment with oral corticosteroids
is not recommended. Instead, tapering should be done
whileintroducingasecondimmunosuppressantdrug,for
example, azathioprine, methotrexate, or cyclosporine A, for
very severe, chronic, relapsing atopic dermatitis []. Such
treatment should be administered from specialised clinics or,
preferably, from hospital dermatology departments.
6.6. Other Medications. Specic immunotherapy in patients
with atopic dermatitis mainly has an eect on upper airway
symptoms if the patient has concomitant allergic rhinitis,
whereas the eect on the activity of the eczema is negligible.
Oral antihistamines are recommended for itching but
have no eect on the activity of the eczema. Nonsedating
antihistamines should be used, but when night-time itching
interferes with sleep, sedating antihistamines are recom-
mended.
Conflict of Interests
e author declares that there is no conict of interests
regarding the publication of this paper.
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SummaryA working party of 13 dermatologists, two family practitioners and a paediatrician was assembled, with the aim of developing a minimum list of reliable discriminators for atopic dermatitis. Each physician was asked to select 10 consecutive new cases of unequivocal mild to moderate atopic dermatitis and 10 controls with other inflammatory dermatoses. Each subject was examined by two independent observers, who were blind to the clinical diagnosis and study aim, with regard to 31 clinically useful diagnostic features for atopic dermatitis. Two hundred and twenty-four patients were studied (120 cases and 102 controls). Using the key physician's clinical diagnosis as a gold standard, the sensitivity and specificity of each of the 31 diagnostic criteria were tested. Using multiple logistic regression techniques, a minimum set of diagnostic criteria for atopic dermatitis was derived. These were: history of flexural involvement, history of a dry skin, onset under the age of 2, personal history of asthma, history of a pruritic skin condition, and visible flexural dermatitis. Adjustment for age, sex, region, social class and ethnic group did not alter the choice of final criteria. The discriminatory value of these criteria was also satisfactory when tested against a further sample of 150 patients drawn from the community, who did not have skin disease.
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The existing evidence for treatment of atopic eczema (atopic dermatitis, AE) is evaluated using the national standard Appraisal of Guidelines Research and Evaluation. The consensus process consisted of a nominal group process and a DELPHI procedure. Management of AE must consider the individual symptomatic variability of the disease. Basic therapy is focused on hydrating topical treatment, and avoidance of specific and unspecific provocation factors. Anti-inflammatory treatment based on topical glucocorticosteroids and topical calcineurin inhibitors (TCI) is used for exacerbation management and more recently for proactive therapy in selected cases. Topical corticosteroids remain the mainstay of therapy, but the TCI tacrolimus and pimecrolimus are preferred in certain locations. Systemic immune-suppressive treatment is an option for severe refractory cases. Microbial colonization and superinfection may induce disease exacerbation and can justify additional antimicrobial treatment. Adjuvant therapy includes UV irradiation preferably with UVA1 wavelength or UVB 311 nm. Dietary recommendations should be specific and given only in diagnosed individual food allergy. Allergen-specific immunotherapy to aeroallergens may be useful in selected cases. Stress-induced exacerbations may make psychosomatic counselling recommendable. 'Eczema school' educational programs have been proven to be helpful. Pruritus is targeted with the majority of the recommended therapies, but some patients need additional antipruritic therapies.