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Clinical Pediatrics
http://cpj.sagepub.com
Diagnosis and Management of Common Dermatoses in Children: Atopic, Seborrheic, and Contact
Dermatitis
Alan B. Fleischer, Jr
Clin Pediatr (Phila) 2008; 47; 332 originally published online Dec 5, 2007;
DOI: 10.1177/0009922807309421
The online version of this article can be found at:
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Diagnosis and Management
of Common Dermatoses in Children:
Atopic, Seborrheic, and Contact
Dermatitis
Clinical Pediatrics
Volume 47 Number 4
May 2008 332-346
© 2008 Sage Publications
10.1177/0009922807309421
http://clp.sagepub.com
hosted at
http://online.sagepub.com
Alan B. Fleischer Jr, MD
Atopic, seborrheic, and contact dermatitis can significantly reduce the quality of life of patients and their families. Although differing in specific aspects of their
epidemiology, etiology, and pathobiology, all 3 dermatoses
are common in the pediatric population, and they share
a common treatment approach. Although effective and
widely used to manage exacerbations of pediatric dermatitis, the use of topical corticosteroid remains a concern for some physicians and parents because of its
potential for systemic absorption and adverse events
associated with prolonged use. Newer additions to the
dermatitis treatment algorithm, such as the topical
calcineurin inhibitors, may provide an effective steroidsparing treatment option. Adjuvant treatments, such as
antihistamines, antifungals, and antibiotics, also can provide benefit in appropriate circumstances. As there is no
cure for dermatitis, a comprehensive, multipronged management strategy of preventive measures, such as trigger
avoidance and periodic pharmacologic treatment, will
provide patients and caregivers with the best opportunity
to successfully control the disease.
D
also crucial to determine the appropriate therapeutic approach. This article will provide an overview of
AD, SD, and CD, with particular focus on how these
dermatoses manifest in infants and children, and
will discuss strategies to effectively manage these
disorders in the pediatric population.
ermatitis comprises a group of diseases
involving inflammation of the skin, with erythematous and papulovesicular morphology
when acute, and erythema and scaling when
chronic. The most common pediatric dermatoses
include atopic dermatitis (AD), seborrheic dermatitis (SD, cradle cap), and contact dermatitis (CD,
especially diaper dermatitis).1-3 As there is no cure
for dermatitis, a comprehensive long-term treatment
strategy based on education, prevention, and pharmacologic therapy can provide patients with the
means by which to manage their disease. In addition, considerations such as appropriately balancing
safety and efficacy in the pediatric population and
tailoring treatment to the disease site and severity are
From the Department of Dermatology, Wake Forest University
School of Medicine, Winston-Salem, North Carolina.
Editorial support provided by Novartis Pharmaceuticals
Corporation.
Address correspondence to: Alan B. Fleischer Jr, MD, Wake
Forest University School of Medicine, Medical Center Boulevard,
Winston-Salem, NC 27157; e-mail: [email protected].
Keywords: calcineurin inhibitor; eczema; skin disease;
inflammation
The Impact of Pediatric Dermatitis
Clinicians who treat dermatitis are beginning to
understand the effect these disorders have not only
on the pediatric patient but also on the child’s family. Dermatitis can be a significant source of physical, psychologic, and economic burden for patients,
siblings, and caregivers.4-7
As a result of pruritus, children with dermatitis
often experience disturbed sleep, with subsequent
diminishment of school performance and in some
cases, behavioral problems.8,9 These children also
can experience increased stress, anxiety, and low
self-esteem (due in part to bullying by other children)
and may not be able to take part in sports or other
332
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Managing Pediatric Dermatitis / Fleischer
social activities.10 Parents of children with dermatitis also experience sleep disturbance and increased
financial stress due to frequent doctor visits, lost
wages, diminished work productivity, home care,
and medications.6 Considerable emotional stress
was reported in an Australian survey of families that
included 48 children with moderate to severe AD;
caring for a child with AD was identified in this survey
as being significantly more stressful than caring for
a child with insulin-dependent diabetes mellitus.11
In addition, the annual cost to the health care system due to AD alone is significant, estimated at
between US$0.9 and US$3.8 billion.12 Thus, the
true cost of dermatitis should be understood both in
terms of the financial burden and the negative
impact on quality of life. Accordingly, effective treatment of pediatric dermatitis can benefit pediatric
patients, their caregivers, and society overall.
Atopic Dermatitis
Overview and Epidemiology
Atopic dermatitis is a chronic, highly pruritic, inflammatory skin condition and is the most common
chronic skin disease13 affecting approximately 7% to
17% of school-aged children in the United States.14
Onset of AD occurs in 45% of children by the age of
6 months, in 60% of children by the age of 1 year,15
and in 85% of children by the age of 5 years.16 As evidenced by an international comparison of 463 801
children aged 13 to 14 years, which evaluated the
relative frequency of certain conditions over a 12month period, the prevalence of AD was shown to
increase steadily in Western countries over the last 3
decades, parallel to the increase in the prevalence of
asthma.17 The AD has also been linked to the development of allergic rhinitis. On the basis of these and
other observations, it has been suggested that AD
may be the entry point for the atopic march, that is,
the progressive development of systemic allergy.18,19
333
Other conditions that also should be considered
include SD, psoriasis, and neurodermatitis, as well
as systemic illnesses such as malignancy, thyroid disorders, and hepatic or renal failure, all of which can
cause pruritus and excoriations.23 Children with AD
also may present with disease variants or associated
conditions (eg, ichthyosis vulgaris, keratosis pilaris,
nummular eczema, pityriasis alba, dermatophyte
infections, impetigo) that can confound the diagnosis (Figure 1; Table 2).22-26
Pathobiology
The etiology of AD, although not fully understood, is
hypothesized to be the result of dysregulation of the
immune system, particularly an imbalance of T
helper 1 and T helper 2 responses, dysfunction of
the skin barrier,27 and a combination of genetic and
environmental factors. Recent studies have identified a subset of the genes influencing development
of AD in certain patients. Epidermal differentiation
complex is expressed late during the maturation of
epidermal cells and has been linked to both AD and
psoriasis.28 In addition, the presence of 2 loss-offunction mutations in the filaggrin gene that result
in the development of ichthyosis vulgaris also are
considered as strong predisposing factors for AD.29
Compared with the skin of healthy patients,
both the affected and the unaffected skin of patients
with AD exhibit xerosis, a key clinical characteristic
of AD.27 Ceramides, whose concentrations are
reduced in affected patients, are the major lipid
present in the stratum corneum layer of the skin30
and are proposed to play a role in the pathobiology
of AD.31 As xerosis can enhance transepidermal
water loss, the skin of patients with AD often develops microfissures and cracks that allow entry of
pathogens, antigens, and irritants, which may exacerbate or complicate the condition. Consequently,
comprehensive, long-term management of AD
should address the immune and the skin barrier dysfunctions that are characteristic of the disease.
Diagnosis
Diagnosis of AD is based on the presence of several
essential and associated features (Table 1).20,21 Owing
to the wide variety of clinical presentations and the
multifactorial etiology of AD, diagnosis can be challenging. The differential diagnosis for AD includes
hyper-IgE syndrome, Wiskott-Aldrich syndrome,
Netherton syndrome, and juvenile dermatomyositis.22
Disease Management
Atopic dermatitis is a heterogeneous disease with a
clinical course characterized by alternating periods
of remission (during which the patient is asymptomatic) and periodic exacerbations (flares). The goals
of AD treatment are both to lengthen the time
between flares and to reduce their severity.
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Clinical Pediatrics / Vol. 47, No. 4, May 2008
Table 1.
Essential Features
Associated Features
Guidelines for the Diagnosis of Atopic Dermatitisa
Patient Must Have 3 or More Basic Features
Pruritus
Typical morphology and distribution
Flexural lichenification or linearity in adults
Facial and extensor involvement in infants and children
Chronic or chronically relapsing dermatitis
Personal or family history of atopy (asthma, allergic rhinitis, atopic dermatitis)
Plus 3 or More Minor Features
Xerosis
Ichthyosis/palmar hyperlinearity/keratosis pilaris
Immediate (type I) skin-test reactivity
Elevated serum IgE
Early age of onset
Tendency toward cutaneous infections (especially Staphylococcus aureus and herpes simplex)/impaired
cell-mediated immunity
Tendency toward nonspecific hand or foot dermatitis
Nipple eczema
Cheilitis
Recurrent conjunctivitis
Dennie-Morgan infraorbital fold
Keratoconus
Anterior subcapsular cataracts
Orbital darkening
Facial pallor/facial erythema
Pityriasis alba
Anterior neck-folds
Itch when sweating
Intolerance to wool and lipid solvents
Perifollicular accentuation
Food intolerance
Course influenced by environmental/emotional factors
White dermographism/delayed blanch
a. Reproduced with permission from Hanifin JM and Rajka G.20
Table 2.
Differential Diagnosis of Atopic Dermatitis23-26,a
Disease
Contact dermatitis
Dermatitis herpetiformis
Dermatophyte infections (including
tinea pedis/manuum)
Immunodeficiency disorder
Impetigo
Lichen planus
Neurodermatitis
Psoriasis
Scabies
Seborrheic dermatitis
Systemic diseases
Distinguishing Features
Positive exposure history, rash in area of exposure, absence of family history
Vesicles over extensor areas and associated enteropathy
Serpiginous plaques with central clearing, positive potassium hydroxide preparation
History of recurrent infection
Infection by streptococci or Staphylococcus aureus, infection often preceded by minor skin
injury (eg, insect bite), presents as small vesicles of blisters that rupture and leave behind
a crust (sometimes honey-colored) on the surface of the lesion
Eruption appears over the course of several weeks, absence of family history, may be
associated or preceded by a stressful event, most common in the 30-60 year age group
Usually, a single patch in an area accessible to itching; absence of family history
Localized patches on extensor surfaces, scalp, buttocks; pitted nails
Papules, finger web involvement, positive skin scraping
Greasy, scaly lesions, absence of family history
Findings on complete history and physical examination vary by disease
a. Adapted with permission from Correale et al.23
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Managing Pediatric Dermatitis / Fleischer
Figure 1.
335
A variety of different conditions can initially present with morphology similar to that of atopic dermatitis.
Nonpharmacologic Approaches
Education and Prevention. Education plays an important role in management of all types of dermatitis.
With respect to patient and family education, it is
important that clinicians anticipate parental anxiety
about dermatitis and its treatments. With proper
education, children and their caregivers will be able
to understand the chronic nature of the disease
and have realistic expectations about its course and
treatment.
Trigger avoidance. Although the factors that trigger
AD flares can vary between patients, conscientious
trigger avoidance and proper skin care help prevent
flares.32,33 Common triggers for AD flares include
exposure to harsh detergents or soaps, various chemicals, and toiletries containing alcohol, fragrances,
preservatives, and astringents.34 Data concerning
the significance of aeroallergens, such as dust mites
and animal dander, in AD are inconclusive and complete avoidance is not possible.34 Food allergies also
may trigger AD flares in some children, the offending
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Clinical Pediatrics / Vol. 47, No. 4, May 2008
foods most often being milk, eggs, peanuts, soy, wheat,
or fish.33 Parents should not overly restrict the diets
of children who have AD, because such practice has
resulted in malnutrition in some cases.35 Although
triggers can be difficult to pinpoint with currently
available methods, allergy testing may be of benefit
in individuals with a clear allergic trigger or with dermatitis that is difficult to manage or refractory to
treatment. Negative skin-prick or serum tests, in particular, are valuable for their predictive ability in ruling out suspected allergens.34
Proper skin care. As mentioned previously, xerosis is
characteristic of AD; thus, its prevention and treatment are essential. Bathing is generally considered
helpful because it hydrates the skin and enhances penetration of topical therapies.36,37 However, children
with AD should not be bathed too frequently, as water
evaporation after bathing can dry the epidermal barrier and exacerbate xerosis. Lukewarm water and mild
cleansers are recommended; it is best to avoid highly
fragranced soaps and bubble baths. Importantly, moisturizers should be liberally applied within 3 minutes
after the bath to minimize water evaporation from the
epidermis and maximize moisture retention.37
Ceramide-rich barrier repair mixtures and other
moisturizers, emollients, and hydrophilic ointments
may improve symptoms associated with AD by
enhancing moisture retention within the skin and
providing a mechanical barrier to irritants.30,37 These
and other moisturizers should be applied 2 to 3 times
daily for best effect. Ointments are more effective
than creams, though lack of compliance, particularly
among school-aged children, can limit their usefulness. In these cases, ointments may be most successfully applied while children are sleeping. In addition,
hydrogels may provide relief from pruritus, burning,
and pain associated with AD and other types of dermatitis. These devices are described in further detail
in the context of CD treatment.
Disease flares, which can be triggered by seasonal
variation, vaccinations, respiratory illness, bacterial
infections, and allergies, among other factors, are
often unavoidable despite conscientious trigger avoidance and proper skin care.22 It is, therefore, important
that children and their families understand and recognize flares as short-term setbacks that may require
pharmacologic intervention.
Pharmacologic Management
Mild or moderate (minor) AD flares involve itching
and moderate erythema with few or no excoriations,
papules, or lichenification, but can quickly progress to
severe (major) AD flares involving persistent, intense
itching, erythema with extensive excoriations, oozing
and crusting, and pronounced lichenification. In treating children with severe flares, it can be challenging
to balance caution and effective treatment. Topical
agents that inhibit the inflammatory response are
mainstays of therapy, with appropriate management
tailored to the site and severity of the flare and the
age of the patient. Although families of children
experiencing severe flares can be understandably
anxious, some of their concerns can be alleviated by
clear, detailed explanations of treatment agents and
their use. An open dialogue on these subjects
encourages children to take an active role in their
own treatments and may improve patient and family
compliance.
Topical corticosteroids. Topical corticosteroids (TCSs)
have been used for the treatment of AD flares for
several decades. The anti-inflammatory effects of
TCSs include diminishment of dermal edema and
capillary dilation, attenuation of the humoral
inflammation process, and reduced movement of
inflammatory cells within the skin.38 In a classic
clinical trial, hydrocortisone acetate effectively
resolved long-standing symptoms of AD in 66% of
children and adults evaluated, although beneficial
results diminished 4 to 5 days after hydrocortisone
was discontinued.39 Despite widespread use of
TCSs, the results of a large meta-analysis indicate
that existing clinical trials do not adequately compare their efficacy and do not provide a clear consensus on appropriate dosing regimens.40
Topical corticosteroids are grouped according to
their potency and are selected based on disease
severity, area of the body affected, and age of the
patient. A stepwise approach to treatment is appropriate, beginning with the lowest-potency steroid
likely to be effective and avoiding underdosing to
minimize the risk of flare rebound.40 Table 3 lists
some commonly available corticosteroid agents
according to potency.41 Application frequency can be
decreased from twice daily to several times weekly
after flare symptoms are controlled and a less potent
TCS can be used. Available data do not support the
efficacy of short-term bursts of more potent corticosteroids versus long-term use of mild agents for
children with mild to moderate AD.42
Although TCSs offer effective treatment for AD,
adverse events (AEs) associated with long-term use
limit their clinical use.40 Three weeks of continuous
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Managing Pediatric Dermatitis / Fleischer
Table 3.
Relative Potency of Select Topical Corticosteroidsa
Potency
Class 1 (superpotent)
Class 2 (potent)
Class 3 (upper midstrength)
Class 4 (midstrength)
Class 5 (lower midstrength)
Class 6 (mild strength)
Class 7 (least potent)
337
Topical Corticosteroid
Betamethasone dipropionate 0.05% ointment/gel
Clobetasol propionate 0.05% ointment/cream
Diflorasone diacetate 0.05% ointment
Halobetasol propionate 0.05% ointment/cream
Amcinonide 0.1% ointment
Betamethasone dipropionate 0.05% ointment
Desoximetasone 0.25% ointment/cream; 0.05% gel
Fluocinonide 0.05% ointment/cream
Halcinonide 0.1% cream
Betamethasone dipropionate 0.05% cream
Betamethasone valerate 0.1% ointment
Fluticasone propionate 0.005% ointment
Mometasone furoate 0.1% ointment
Triamcinolone acetonide 0.5% cream
Betamethasone valerate 0.12% foam
Clocortolone pivalate 0.1% cream
Desoximetasone 0.05% cream
Fluocinolone acetonide 0.025% ointment; 0.2% cream
Flurandrenolide 0.05% ointment
Triamcinolone acetonide 0.1% ointment/cream
Betamethasone dipropionate 0.05% lotion
Betamethasone valerate 0.1% cream/lotion
Fluocinolone acetonide 0.025% cream
Flurandrenolide 0.05% cream
Fluticasone propionate 0.05% cream
Hydrocortisone butyrate 0.1% cream
Hydrocortisone valerate 0.2% cream
Prednicarbate 0.1% cream
Triamcinolone acetonide 0.1% cream/lotion
Alclometasone dipropionate 0.05% ointment/cream
Desonide 0.05% cream
Fluocinolone acetonide 0.01% cream/solution/oil
Topicals with hydrocortisone, dexamethasone, flumethasone, methylprednisolone, and prednisolone
a . Adapted with permission from Del Rosso and Friedlander.41
or intermittent TCS treatment has been shown to
substantially decrease collagen synthesis in the
skin,43 causing local AEs such as skin atrophy, striae,
telangiectasias, hypopigmentation, rosacea, perioral
dermatitis, and acne.40,44 Topical corticosteroids therapy
should, therefore, be used conservatively and should
be limited to 3 to 7 days in patients with acute AD, and
to 2 to 3 weeks in those with chronic symptoms.45
Topical corticosteroids also may be absorbed systemically when used on thin, highly absorptive skin
areas, such as the face and groin, and they are associated with greater potential for AEs.46,47 Rare but
significant AEs can include suppression of the
hypothalamic-pituitary-adrenal axis, growth retardation,
and reduced bone density, all of which are of particular
concern in the pediatric population.40,46 Cushing’s
syndrome, cataract formation, and glaucoma also may
occur.46 Prolonged use of TCSs, particularly on highly
absorptive skin areas, is therefore contraindicated.46
Step-down to nonsteroid pharmacotherapy. Because
of the potential for AEs related to TCS treatment,
parents and physicians should routinely monitor
their children’s treated skin for potential AEs and to
gauge therapeutic response. As an alternative to
long-term steroid therapy, patients can be stepped
down to nonsteroid pharmacotherapies, such as topical calcineurin inhibitors (TCIs), after initial treatment with appropriate TCSs (Figure 2). Alternatives
to TCS therapy are valuable for a variety of situations, including symptom relapse after TCS therapy,
steroid insensitivity, steroid allergy, and the so-called
steroid phobia, in which parents refuse TCS therapy
out of concern about potential AEs.48 In such cases,
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338
Clinical Pediatrics / Vol. 47, No. 4, May 2008
Figure 2. The management of atopic dermatitis. Long-term management requires daily preventive care and pharmacologic
treatment with topical corticosteroids, topical calcineurin inhibitors, and adjunctive therapies (when appropriate). TCI = topical
calcineurin inhibitor; TCS = topical corticosteroid.
parents’ fears about AEs have implications for treatment compliance. In a recent investigation, 72.5%
of the respondents worried about TCS use on their
own or their children’s skin, and 24% of the respondents reported noncompliance with therapy as a
result.48 Additionally, the results of the International
Study of Life with Atopic Eczema (ISOLATE)
underscore the need not only for accurate family
education about safety, potency, and appropriate use
of TCSs,48 but also for steroid-sparing treatment
alternatives.
Topical calcineurin inhibitors. Recent findings indicate that 62% of patients (aged >13 years) and 74% of
caregivers would prefer to prevent an AD flare from
occurring or getting worse through use of a nonsteroidal treatment.7 The TCIs tacrolimus and pimecrolimus offer an alternative to steroid treatment and
have become part of an effective long-term treatment
strategy for many patients. These agents inhibit the
action of calcineurin and block T-cell activation and
the production of inflammatory cytokines,49,50 a more
selective mechanism of action than that of the TCSs.
Tacrolimus and pimecrolimus have been effective
and well tolerated as short-term and intermittent longterm treatment in clinical trials of adults and children.
The most common AE noted during clinical trials of
TCIs was a transient burning sensation at the application site that diminished during further treatment.51
In one clinical comparison, the efficacy of 0.1%
tacrolimus ointment was comparable to that of 0.1%
hydrocortisone butyrate ointment in the treatment
of 570 adults with moderate to severe AD.52 Skin
burning and pruritus were the only AEs with a significantly higher incidence in the tacrolimus group
than in the hydrocortisone group.52 Additional clinical trial data have shown that tacrolimus enhances
quality of life, reduces flare incidence, and provides
safe, effective treatment of cutaneous symptoms and
pruritus in patients aged ≥2 years with moderate to
severe AD.51,53 A retrospective chart review has also
suggested that tacrolimus is effective in children
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Managing Pediatric Dermatitis / Fleischer
aged <2 years; AEs such as burning, pain, stinging,
and itching at the application site are uncommon.54
Pimecrolimus, indicated for the short-term,
noncontinuous chronic treatment of AD in adults
and children aged ≥2 years, is effective for preventing the progression to flares, reducing the severity of
flares, and prolonging the time between major
flares.55-57 Treatment with pimecrolimus has been
shown to reduce pruritus and other cutaneous
symptoms associated with AD.55,56,58 Thus, pimecrolimus can help break the itch-scratch cycle that can
exacerbate AD. Clinical trial data have also indicated that pimecrolimus significantly improves
patients’ quality of life after 6 weeks of treatment.59
Although pimecrolimus is not indicated for use in
infants aged <2 years, it has been found to be effective in this population, with most AEs related to disorders commonly encountered in early childhood or
commonly observed in AD.59-61 Furthermore, early
application of pimecrolimus at the first signs or
symptoms of a flare has been shown to prevent flare
progression.55,57,60 Additional trials evaluating the
safety and efficacy of pimecrolimus in infants and
children aged <2 years are currently under way.62
Pharmacokinetic studies indicate that tacrolimus
and pimecrolimus exhibit minimal systemic absorption, perhaps explaining the low incidence of AEs,63-65
and do not cause systemic immunosuppression.65-71
If symptoms persist for more than 6 weeks, the
physician should confirm the diagnosis of AD, and if
it is confirmed, treatment with TCIs may be continued beyond 6 weeks with frequent reevaluation.
Since their introduction TCIs have been used to
treat several million people worldwide72-74; however,
postmarketing case reports of skin cancer and lymphomas prompted the US Food and Drug Administration to recommend the addition of a boxed
warning to TCI labeling, indicating that long-term
safety of TCIs has not yet been established and that
their use carries a theoretical risk of malignancy.
Importantly, case reports of malignancies associated
with TCI therapy do not distinguish between preexisting and posttreatment conditions. Furthermore,
lymphomas reported in postmarketing surveillance
are not of the posttransplantation lymphoproliferative disorder type, which is characteristic of systemic
immunosuppression. In light of these data, several
professional organizations have subsequently issued
statements indicating that the data do not support a
causal link between TCIs and malignancy.72,75-77
339
Adjunctive therapy. Although no objective evidence
currently exists to support the use of antihistamines
in treating AD,78 these agents often are used for
their soporific effect and to help break the itchscratch cycle at nighttime. The resulting improvement in children’s sleep quality may benefit children
by improving their daytime alertness and school performance and, owing to less nighttime disruption,
enhance the families’ overall quality of life.
Both children and adults with AD are at increased
risk for secondary bacterial, viral, and fungal infections, and in such cases, anti-infective agents become
necessary.32,44,79 Topical or systemic antibiotics may be
used, but treatment duration should be optimized to
reduce the associated risk of tachyphylaxis. Infection
with herpes simplex virus is of particular concern in
children with widespread AD, and antiviral therapy is
warranted in such cases. Although cyclosporine,
mycophenolate mofetil, azathioprine, and interferon-γ
have been used to treat AD,79 systemic immunomodulatory therapy should be avoided in children except
in extremely severe cases.80
Seborrheic Dermatitis
Overview and Epidemiology
Seborrheic dermatitis is a chronic, recurrent, inflammatory skin condition that typically affects areas of
the skin that are well supplied with sebaceous
glands (eg, nasolabial folds, ears, eyebrows, scalp,
chest, etc).81,82 As with AD, the etiology of SD is not
completely understood although its presence has
been associated with overgrowth of yeast species
such as Malassezia (previously Pityrosporum) that
normally inhabit sebaceous skin.83 Hormone levels,
nutritional deficiencies, fungal infections, altered
essential fatty acid patterns, and neurogenic factors
can also be associated with SD.84 Diagnosis of SD is,
therefore, based on location, appearance of the dermatitis, and patient age.
In children, SD has a bimodal peak of occurrence, commonly appearing in both infancy (cradle
cap) and after puberty (dandruff). Cradle cap
appears in infants within the first 3 months of life,
is self-limiting, and commonly resolves by the age of
1 year.3 Because of this onset and resolution, it has
been suggested that transplacental hormones (the
levels of which are elevated in infancy and decrease
by the first year of life) may be a causative factor.3,85-87
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Clinical Pediatrics / Vol. 47, No. 4, May 2008
Cradle cap is characterized by nonpruritic, thick,
greasy scales (white, off-white, or yellow) on the vertex of the scalp. Although the center of the face,
ears, and forehead may have fine scaling, generalized SD (ie, SD appearing on the flexural folds) is
uncommon in healthy children and is usually associated with immunodeficiencies. Therefore, infants
with generalized SD should be evaluated for more
serious disease.84 Dandruff typically appears during
puberty when sebaceous glands have matured.
Pubescent scaling in the nasolabial creases, pinnae,
eyebrows, retroauricular areas, glabella, eyelids, and
aural canals may also occur.1
In a survey of 1116 Australian children, the overall prevalence of SD was 10% in boys and 9.5% in
girls.88 In most children (72%), SD was minimal or
mild, and the highest prevalence occurred in the first
3 months of life and decreased rapidly by the age of 1
year. Cradle cap (mostly minimal to mild) was evident
in 42% of children.88 Although SD is reported to be
rare between infancy (ie, resolution of cradle cap) and
adolescence (ie, appearance of dandruff) due to the
immaturity of sebaceous glands,89 a recent, crosssectional study of 300 children found that SD was
present in 6% of children between the ages of 2 and
10 years (roughly 3 times less prevalent in children
less than the age of 2 years).90 The SD in the 2-yearold to 10-year-old children appeared as both the
greasy-scale SD characteristic of cradle cap as well as
the fine, nongreasy scale seen in dandruff.90 Although
more study is needed to confirm the prevalence of SD
between infancy and puberty, physicians should note
that SD in this age group may occur.
Diagnosis
Diagnosis of SD in children involves an evaluation
of patient history (onset of SD, attempts by family of
treatment) and physical examination of the type,
location, configuration, and pattern of scales.3 As
mentioned, cradle cap (greasy, nonpruritic white, offwhite, or yellow scales) appears predominantly on the
vertex of the scalp. Differential diagnosis includes
AD, tinea capitis (rare in infancy), and psoriasis.3 In
adolescents, the appearance and the distribution of
scales render diagnosis straightforward. Differential
diagnosis includes the same conditions listed for differential diagnosis of cradle cap, with the addition of
histiocytic disorders and dermatomyositis. The
appearance of SD in adolescents is rarely confused
with other dermatoses, with the exception of psoriasis.
In psoriasis, however, lesions may extend onto the
forehead, whereas SD is confined to the scalp.1
Disease Management
The treatment of childhood SD involves parent and
patient education, as well as nonpharmacologic
(hygienic) and pharmacologic strategies.
Education
Parents who seek medical attention for their child’s
cradle cap should be informed that the cause is
unknown and should receive brief explanations of
the existing theories. The main message to parents is
that cradle cap can be easily and effectively treated
and that it usually resolves within the first year of
life. Possible regimens for treatment and care should
be discussed and should be accompanied by printed
instructions that parents can take home. Similarly,
parents and adolescent patients should be educated
regarding treatment regimens for adolescent SD.
Treatment of Cradle Cap
The treatment of cradle cap is very straightforward
and consists of a combination of scale loosening and
shampooing. In mild cases, daily shampooing with a
nonmedicated shampoo for 1 week may be effective
in loosening and removing scales, and emollients
can be applied to loosen scales should simple shampooing prove ineffective. Emollients can be left on
the scalp overnight and white petrolatum or slightly
warmed mineral or olive oil can be applied to the
scalp for a minimum of 20 minutes. Subsequent to
the emollients, the scales can be gently removed
with an infant hairbrush or fingertips, followed by a
nonmedicated shampoo.3,91
Treatment of Adolescent SD
The management of adolescent SD involves a combination of nonpharmacologic and pharmacologic
approaches. Emollients help relieve xerosis23 and
frequent cleansing of the affected area removes
excess oil from the skin and is part of a preventive
strategy.91 Antifungal creams, such as ketoconazole,
and antifungal or antidandruff shampoos are part of
first-line pharmacologic therapy81,92 and are used to
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Managing Pediatric Dermatitis / Fleischer
decrease colonization by yeasts.93 The recently approved
2% ketoconazole gel, Xolegel, has been shown to
improve erythema and scaling scores, as well as the
Investigator’s Global Assessment score in children
aged 12 years and older.94 The product is applied once
daily to the affected area for 2 weeks.94 The most common adverse reactions are application-site burning
and headache.94 Short courses of low-potency TCSs
aid in resolution of erythema and itching and are a
common treatment. The TCIs have been proposed as
a steroid-sparing therapy for SD,84 and several smallscale studies and case reports have suggested that
tacrolimus and pimecrolimus may be useful in adults
with this condition.93,95-100 The most common side
effects are mild local burning and irritation.93,95,98
Further study is needed in adolescent patients with
SD to evaluate the utility of this treatment option.
Contact Dermatitis
341
buckles) is the most common form of pediatric ACD,
but is still relatively rare.102
Lip-Licking or Drooling
Lip-licking is localized to the area around the
mouth; saliva and air mix to cause a dryness that can
become inflamed.102 The drool of teething infants
may cause ICD of the perioral area, neck, and
chest.22 First-line treatment of these straightforward
ICDs involves minimizing trigger exposure by use of
protective barriers as complete trigger avoidance in
children and infants in these cases is difficult. For
example, in the case of teething infants who develop
ICD of the perioral area, neck, and chest because of
chronic skin exposure to saliva, food, and saturated
bibs, a thick emollient may act as an effective barrier
when applied before and after meals.22 Similarly,
emollients for the perioral area of children who lick
their lips (especially in the winter months) can provide an effective barrier.
Overview
The CD is caused by direct skin exposure to an allergen
or irritant101 and is categorized into 2 common subtypes: irritant CD (ICD) and allergic CD (ACD).101
Environmental factors are primarily responsible for
these dermatoses, especially in the case of ICD. The
ICD is a result of cellular injury caused by direct
chemical contact with common triggers, such as
soaps, detergents, solvents, acids, and alkali. The
ICD may occur minutes to hours after exposure to a
strong irritant (acute reactions), or after repeated
exposure to milder agents (cumulative insult reactions). The ACD occurs in individuals previously
exposed and immunologically sensitized to a particular chemical, such as nickel sulfate (commonly
found in everyday items such as keys, buttons, and
clothing), or pentadecylcatechols (the active agent
in poison ivy, poison oak, and poison sumac).101 The
ACD is similar to AD in that the disease is manifested
through immune-mediated mechanisms, specifically
a type IV (delayed-type) hypersensitivity reaction.101
Contact Dermatoses in Children
In infants and children, the most common forms of ICD
are lip-licking or drooling and diaper dermatitis.102,103
Other forms of ICD in children are uncommon.102
Nickel allergy (from snaps on clothing or on belt
Diaper Dermatitis
Diaper dermatitis, the most common dermatologic
problem in infancy,103 results directly from the irritation caused by diapers.3 Prevalence is estimated to
be between 7% and 35% but is almost certainly
underreported.3,104 Diaper dermatitis most commonly occurs in infants 9 to 12 months of age, and
almost half of all diaper-wearing infants and children seen by pediatricians will experience diaper
dermatitis.2 The warmth and wetness of the diaper
area create an impairment of the barrier function of
the skin.103 Moisture renders the skin more fragile
and thereby makes the skin more vulnerable to damage caused by friction, which occurs in the areas
covered by diapers (abdomen, buttocks, genitals).2
Exposure of the skin to urine and feces also compromises the skin and increases the permeability of
irritants. Although the pathogenic significance of
Candida albicans in the induction of diaper dermatitis remains unclear, extensive colonization increases
severity of the dermatitis.2,103
Diaper dermatitis, which is self-limiting with a
mean duration of 2 to 3 days per episode,2 most commonly presents as erythema and mild scaling of the
buttocks, thighs, lower abdomen, and gluteal crease
but may also present as shiny plaques or erosions
with a macular, papular, or vesicular composition.3,103
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342
Clinical Pediatrics / Vol. 47, No. 4, May 2008
Differential diagnosis includes AD, psoriasis, and SD.
The child’s hygienic routine should be discussed with
parents, and potential irritating agents used for the
child’s cleansing routine should be identified. Firstline treatment includes hygienic measures, such as
increasing the frequency of diaper changes, ensuring
adequate airflow into diapers (ie, fastening diapers
loosely), or, when possible, allowing the infant or
child to remain diaper-free. The use of disposable diapers designed to be superabsorbant that provide a barrier between wetness and the skin should be used
instead of cloth diapers. Water-repellant barrier
creams (eg, zinc oxide) should be applied to areas
prone to wetness and friction, and frequent bathing
(once or twice daily) is also recommended. The use of
baby wipes that contain fragrances or alcohol should
be avoided, as they may further irritate the skin.2,103
If diaper dermatitis persists after these conservative measures, a short course of 1% hydrocortisone
cream (twice daily for a maximum of 2 weeks) can
be applied to decrease inflammation, alone or, if
C albicans colonization is extensive, in combination
with an antifungal cream. Until recently, no topical
antifungal was indicated for the treatment of diaper
dermatitis in infants. In 2006, however, an ointment
containing 0.25% miconazole nitrate in a base of
zinc oxide and white petrolatum was approved by the
US Food and Drug Administration for the adjunctive
treatment of diaper dermatitis specifically complicated by C albicans.105 Although not indicated for
the treatment of diaper dermatitis in the United
States, short courses of low-potency, nonhalogenated TCSs are often prescribed. Higher-potency
TCSs (both alone and when used in combination
products) should be avoided for the treatment of
diaper dermatitis due to the AEs covered in the section on AD.2 When a secondary bacterial infection is
suspected due to the decreased integrity of the skin,
a topical antibiotic is appropriate.2
Nickel ACD
Nickel ACD, the most common ACD in infants, produces a pruritic dermatitis that is difficult to distinguish
from AD. The location and pattern of exposure is helpful in differentiating nickel ACD from AD; the area
where the child has exposure to nickel snaps or buttons
is the most frequent area of presentation. The only cure
is to remove the allergen; inflammation can be controlled with a short course of a nonhalogenated TCS.1
Contact Dermatoses in Adolescents
Adolescents also suffer ICD and ACD. Due to the
adolescent’s mobility and independence, the range of
irritating substances and potential allergens is
increased. As with ICD or ACD in infancy and childhood, trigger recognition and avoidance are paramount, and conservative measures should be used as
a first-line treatment. During an outbreak of ICD or
ACD, skin should be cleansed with minimal use of
soap, relying instead on plain water to remove dry particulates from the skin, and a slurry of fine cornmeal
and water to remove soil or grease. Mild soaps with
neutral pH can be used as needed to fight microbial
contamination. Skin hydration and emollients may be
useful in treating ICD. Wet compresses with Burow’s
solution help reduce the discomfort of ACD lesions
and have a mild antimicrobial effect.101 Other treatments, such as TCSs, antihistamines, phototherapy,
and systemic agents, may be useful, depending on the
severity of the disease and the age of the patient. The
TCIs may offer a steroid-sparing treatment for some
forms of CD.106-111 Evaluation of tacrolimus ointment
has shown a treatment benefit in nickel allergy,107,109
protein contact dermatitis,106 and eyeglass frame dermatitis.107 Similarly, pimecrolimus has exhibited efficacy in the treatment of nickel110 and chronic hand
dermatitis.111 Further study in pediatric populations is
warranted to fully evaluate these treatments.
Hydrogels, which can consist of a water-soluble
network of polymer chains, a colloidal gel in an
aqueous dispersion medium, or superabsorbent natural or synthetic polymers, are recently introduced
medical devices that may speed lesion healing in
some patients with CD. In a clinical trial of 20 men
and women aged 18 to 65 years, the efficacy of a
nonsteroid hydrogel compound was demonstrated in
treatment of ICD induced by exposure to sodium
laurel sulfate.112 Further data are needed to determine whether hydrogels will prove superior to highquality moisturizers in the treatment of CD and to
test these treatments in children.
Conclusion
The AD, SD, and CD comprise a group of chronic
diseases that can significantly affect quality of life for
children and their families. Comprehensive treatment of these conditions requires the integration of
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Managing Pediatric Dermatitis / Fleischer
appropriate nonpharmacologic and pharmacologic
therapies.
With respect to AD, 75% of patients and caregivers
indicate that effectively controlling their disease would
be the “single most important improvement to their
quality of life.”7 Proper skin care and trigger avoidance
are key components in preventing exacerbations, but
most patients will experience periodic disease flares
and recalcitrant dermatoses that require pharmacologic treatment. The TCSs are a mainstay of therapy,
but their clinical utility is limited by AEs associated
with long-term use. The TCIs provide a means of
stepping down to nonsteroidal pharmacotherapy after
initial treatment with TCSs.
The occurrence of SD typically exhibits a
bimodal pattern, with peaks during infancy and after
puberty. Although SD is considered rare between
infancy and adolescence, clinicians should remain
alert to the possibility of the disease among children
in this age group. Antifungals and low-potency TCSs
are commonly used to treat this condition and its
symptoms, and emerging data suggest that TCIs may
be useful as steroid-sparing therapy.
The optimal management of irritant and allergic
forms of CD requires collaboration between clinicians and parents or patients to identify triggers and
implement strategies for minimizing or avoiding
exposure to these factors. A variety of barrier treatments and topical therapies may be beneficial.
As therapies for common dermatoses continue to
evolve, clinicians are being presented with broader
options that may enhance prospects for tailoring
treatment to the individual patient. Pediatric studies
of newer therapies such as the TCIs will help clinicians determine how to integrate assorted treatments
into comprehensive strategies to help children and
parents effectively and safely manage these diseases.
References
1. Lee DJ, Eichenfield LF. Atopic, contact, and seborrheic
dermatitis in adolescents. Adolesc Med. 2001;12:269-283.
2. Shin HT. Diaper dermatitis that does not quit. Dermatol
Ther. 2005;18:124-135.
3. Singleton JK. Pediatric dermatoses: three common skin
disruptions in infancy. Nurse Pract. 1997;22:32-33,37,
43-44,49-50.
4. Lapidus CS, Kerr PE. Social impact of atopic dermatitis. Med Health R I. 2001;84:294-295.
343
5. Carroll CL, Balkrishnan R, Feldman SR, Fleischer AB
Jr, Manuel JC. The burden of atopic dermatitis: impact
on the patient, family, and society. Pediatr Dermatol.
2005;22:192-199.
6. Fivenson D, Arnold RJG, Kaniecki DJ, Cohen JL, Frech F,
Finlay AY. The effect of atopic dermatitis on total burden
of illness and quality of life on adults and children in a
large managed care organization. J Manag Care Pharm.
2002;8:333-342.
7. Zuberbier T, Orlow SJ, Paller AS, et al. Patient
perspectives on the management of atopic dermatitis.
J Allergy Clin Immunol. 2006;118:226-232.
8. Rudikoff D, Lebwohl M. Atopic dermatitis. Lancet.
1998;351:1715-1721.
9. Dahl RE, Bernhisel-Broadbent J, Scanlon-Holdford S,
Sampson HA, Lupo M. Sleep disturbances in children
with atopic dermatitis. Arch Pediatr Adolesc Med. 1995;
149:856-860.
10. Paller AS, McAlister RO, Doyle JJ, Jackson A.
Perceptions of physicians and pediatric patients about
atopic dermatitis, its impact, and its treatment. Clin
Pediatr (Phila). 2002;41:323-332.
11. Su JC, Kemp AS, Varigos GA, Nolan TM. Atopic eczema:
its impact on the family and financial cost. Arch Dis
Child. 1997;76:159-162.
12. Ellis CN, Drake LA, Prendergast MM, et al. Cost of
atopic dermatitis and eczema in the United States. J Am
Acad Dermatol. 2002;46:361-370.
13. Larsen FS, Hanifin JM. Epidemiology of atopic dermatitis. Immunol Allergy Clin North Am. 2002;22:1-24.
14. Laughter D, Istvan JA, Tofte SJ, Hanifin JM. The prevalence of atopic dermatitis in Oregon schoolchildren.
J Am Acad Dermatol. 2000;43:649-655.
15. Wuthrich B. Epidemiology and natural history of atopic
dermatitis. Allergy Clin Immunol Int. 1996;8:77-82.
16. Rajka G, ed. Essential Aspects of Atopic Dermatitis.
Berlin, Germany: Springer-Verlag; 1989: 4-55.
17. Worldwide variation in prevalence of symptoms of
asthma, allergic rhinoconjunctivitis, and atopic eczema:
ISAAC. The International Study of Asthma and Allergies
in Childhood (ISAAC) Steering Committee. Lancet.
1998;351:1225-1232.
18. Bergmann RL, Edenharter G, Bergmann KE, et al.
Atopic dermatitis in early infancy predicts allergic airway
disease at 5 years. Clin Exp Allergy. 1998;28:965-970.
19. Eichenfield LF, Hanifin JM, Beck LA, et al. Atopic dermatitis and asthma: parallels in the evolution of treatment. Pediatrics. 2003;111:608-616.
20. Hanifin JM, Rajka G. Diagnostic features of atopic dermatitis. Acta Derm Venereol Suppl (Stockh). 1980;92: 44-47.
21. Eichenfield LF, Hanifin JM, Luger TA, Stevens SR,
Pride HB. Consensus conference on pediatric atopic
dermatitis. J Am Acad Dermatol. 2003;49:1088-1095.
Downloaded from http://cpj.sagepub.com by Roberto Hernandez Sampieri on October 12, 2008
344
Clinical Pediatrics / Vol. 47, No. 4, May 2008
22. Sidbury R, Poorsattar S. Pediatric atopic dermatitis: should
we treat it differently? Dermatol Ther. 2006;19: 83-90.
23. Correale CE, Walker C, Murphy L, Craig TJ. Atopic dermatitis: a review of diagnosis and treatment. Am Fam
Physician. 1999;60:1191-1198.
24. Sanfilippo AM, Barrio V, Kulp-Shorten C, Callen JP.
Common pediatric and adolescent skin conditions. J
Pediatr Adolesc Gynecol. 2003;16:269-283.
25. Clarke P. Why am I so itchy? Aust Fam Physician.
2004;33:489-494.
26. Sweeney SM, Wiss K, Mallory SB. Inflammatory tinea
pedis/manuum masquerading as bacterial cellulitis.
Arch Pediatr Adolesc Med. 2002;156:1149-1152.
27. Leung DYM, Boguniewicz M, Howell MD, Nomura I,
Hamid QA. New insights into atopic dermatitis. J Clin
Invest. 2004;113:651-657.
28. Ring J. Diseases due to environmental factors. Available
from www.science .ngfn.de/dateien/NUWS31T05_Ring.
pdf#search=%22 EDC%20atopic%20dermatitis%22. Accessed
September 28, 2006.
29. Weidinger S, Illig T, Baurecht H, et al. Loss-of-function
variations within the filaggrin gene predispose for atopic
dermatitis with allergic sensitizations. J Allergy Clin
Immunol. 2006;118:214-219.
30. Coderch L, Lopez O, de la Maza A, Parra JL. Ceramides
and skin function. Am J Clin Dermatol. 2003;4:107-129.
31. Imokawa G, Abe A, Jin K, Higaki Y, Kawashima M,
Hidano A. Decreased level of ceramides in stratum
corneum of atopic dermatitis: an etiologic factor in
atopic dry skin? J Invest Dermatol. 1991;96:523-526.
32. Ellis C, Luger T, Abeck D, et al. International Consensus
Conference on Atopic Dermatitis II (ICCAD II): clinical
update and current treatment strategies. Br J Dermatol.
2003;148(suppl 63):3-10.
33. Lever R, MacDonald C, Waugh P, Aitchison T. Randomised
controlled trial of advice on an egg exclusion diet in
young children with atopic eczema and sensitivity to
eggs. Pediatr Allergy Immunol. 1998;9:13-19.
34. Leung DYM, Bieber T. Atopic dermatitis. Lancet. 2003;
361:151-160.
35. Dohil MA, Eichenfield LF. A treatment approach for
atopic dermatitis. Pediatr Ann. 2005;34:201-210.
36. Darsow U, Lübbe J, Taïeb A, et al. Position paper on
diagnosis and treatment of atopic dermatitis. J Eur Acad
Dermatol Venereol. 2005;19:286-295.
37. Simpson EL, Hanifin JM. Atopic dermatitis. Med Clin
North Am. 2006;90:149-167.
38. Hughes J, Rustin M. Corticosteroids. Clin Dermatol.
1997;15:715-721.
39. Sulzberger MB, Witten VH, Smith CC. Hydrocortisone
(compound F) acetate ointment in dermatological therapy. JAMA. 1953;151:468-472.
40. Hoare C, Li Wan Po AL, Williams H. Systematic review
of treatments for atopic eczema. Health Technol Assess.
2000;4:1-191.
41. Del Rosso J, Friedlander SF. Corticosteroids: options in
the era of steroid-sparing therapy. J Am Acad Dermatol.
2005;53:S50-S58.
42. Thomas KS, Armstrong S, Avery A, et al. Randomised
controlled trial of short bursts of a potent topical corticosteroid versus prolonged use of a mild preparation for
children with mild or moderate atopic eczema. BMJ.
2002;324:1-7.
43. Nuutinen P, Riekki R, Parikka M, et al. Modulation of
collagen synthesis and mRNA by continuous and intermittent use of topical hydrocortisone in human skin. Br
J Dermatol. 2003;148:39-45.
44. Hanifin JM, Cooper KD, Ho VC, et al. Guidelines of
care for atopic dermatitis. J Am Acad Dermatol.
2004;50:391-404.
45. National Prescribing Centre. Atopic eczema in primary
care. MeReC Bull. 2003;14:1-4.
46. Turpeinen M, Salo OP, Leisti S. Effect of percutaneous
absorption of hydrocortisone on adrenocortical responsiveness in infants with severe skin disease. Br J Dermatol.
1986;115:475-484.
47. Aalto-Korte K, Turpeinen M. Pharmacokinetics of topical hydrocortisone at plasma level after applications
once or twice daily in patients with widespread dermatitis. Br J Dermatol. 1995;133:259-263.
48. Charman CR, Morris AD, Williams HC. Topical
corticosteroid phobia in patients with atopic eczema. Br
J Dermatol. 2000;142:931-936.
49. Grassberger M, Baumruker T, Enz A, et al. A novel antiinflammatory drug, SDZ ASM 981, for the treatment of
skin diseases: in vitro pharmacology. Br J Dermatol.
1999;141:264-273.
50. Bornhövd EC, Burgdorf WHC, Wollenberg A.
Immunomodulatory macrolactams for topical treatment
of inflammatory skin diseases. Curr Opin Investig Drugs.
2002;3:708-712.
51. Ruzicka T, Bieber T, Schöpf E, et al. A short-term trial
of tacrolimus ointment for atopic dermatitis. N Engl J
Med. 1997;337:816-821.
52. Reitamo S, Rustin M, Ruzicka T, et al. Efficacy and safety
of tacrolimus ointment compared with that of hydrocortisone butyrate ointment in adult patients with atopic dermatitis. J Allergy Clin Immunol. 2002;109: 547-555.
53. Boguniewicz M, Fiedler VC, Raimer S, Lawrence ID,
Leung DYM, Hanifin JM. A randomized, vehiclecontrolled trial of tacrolimus ointment for treatment of
atopic dermatitis in children. J Allergy Clin Immunol. 1998;
102:637-644.
54. Housman TS, Norton AB, Feldman SR, et al.
Tacrolimus ointment: utilization patterns in children
under age 2 years. Dermatol Online J. 2004;10:2.
55. Meurer M, Fartasch M, Albrecht G, et al. Long-term
efficacy and safety of pimecrolimus cream 1% in adults
with moderate atopic dermatitis. Dermatology. 2004;208:
365-372.
Downloaded from http://cpj.sagepub.com by Roberto Hernandez Sampieri on October 12, 2008
Managing Pediatric Dermatitis / Fleischer
56. Eichenfield LF, Lucky AW, Boguniewicz M, et al. Safety
and efficacy of pimecrolimus (ASM 981) cream 1% in
the treatment of mild and moderate atopic dermatitis in
children and adolescents. J Am Acad Dermatol. 2002;46:
495-504.
57. Wahn U, Bos JD, Goodfield M, et al. Efficacy and safety
of pimecrolimus cream in the long-term management of
atopic dermatitis in children. Pediatrics. 2002;110:e2.
58. Meurer M, Fölster-Holst R, Wozel G, Weidinger G,
Jünger M, Bräutigam M. Pimecrolimus cream in the
long-term management of atopic dermatitis in adults: a
six-month study. Dermatology. 2002;205:271-277.
59. McKenna SP, Whalley D, de Prost Y, et al. Treatment of
paediatric atopic dermatitis with pimecrolimus (Elidel®,
SDZ ASM 981): impact on quality of life and healthrelated quality of life. J Eur Acad Dermatol Venereol.
2006;20:248-254.
60. Papp KA, Werfel T, Fölster-Holst R, et al. Long-term
control of atopic dermatitis with pimecrolimus cream
1% in infants and young children: a two-year study. J Am
Acad Dermatol. 2005;52:240-246.
61. Lübbe J, Friedlander SF, Cribier B, et al. Safety, efficacy,
and dosage of 1% pimecrolimus cream for the treatment
of atopic dermatitis in daily practice. Am J Clin
Dermatol. 2006;7:121-131.
62. Ho VC, Gupta A, Kaufmann R, et al. Safety and efficacy
of nonsteroid pimecrolimus cream 1% in the treatment of
atopic dermatitis in infants. J Pediatr. 2003;142:155-162.
63. Staab D, Pariser D, Gottlieb AB, et al. Low systemic
absorption and good tolerability of pimecrolimus,
administered as 1% cream (Elidel®) in infants with
atopic dermatitis—a multicenter, 3-week, open-label
study. Pediatr Dermatol. 2005;22:465-471.
64. Hultsch T. Elidel (Pimecrolimus) cream 1% safety. Available
from http://www.fda.gov/ohrms/dockets/ac/05/slides/20054089s2_02_02_Novartis%20Core%20Safety%20(CS).pdf.
Accessed July 31, 2007.
65. Harper J, Smith C, Rubins A, et al. A multicenter study
of the pharmacokinetics of tacrolimus ointment after
first and repeated application to children with atopic
dermatitis. J Invest Dermatol. 2005;124:695-699.
66. Allen BR, Lakhanpaul M, Morris A, et al. Systemic exposure,
tolerability, and efficacy of pimecrolimus cream 1% in atopic
dermatitis patients. Arch Dis Child. 2003;88:969-973.
67. Thaçi D, Steinmeyer K, Ebelin M-E, Scott G,
Kaufmann R. Occlusive treatment of chronic hand dermatitis with pimecrolimus cream 1% results in low systemic exposure, is well tolerated, safe, and effective: an
open study. Dermatology. 2003;207:37-42.
68. Van Leent EJM, Ebelin M-E, Burtin P, Dorobek B, Spuls PI,
Bos JD. Low systemic exposure after repeated topical application of pimecrolimus (Elidel®, SDZ ASM 981) in patients
with atopic dermatitis. Dermatology. 2002;204:63-68.
69. Billich A, Aschauer H, Aszódi A, Stuetz A. Percutaneous
absorption of drugs used in atopic eczema: pimecrolimus
70.
71.
72.
73.
74.
75.
76.
77.
78.
79.
80.
81.
82.
83.
84.
85.
86.
87.
345
permeates less through skin than corticosteroids and
tacrolimus. Int J Pharm. 2004;269:29-35.
Protopic [prescribing information]. Deerfield, IL:
Astellas Pharma Inc; 2006.
Reitamo S, Wollenberg A, Schöpf E, et al. Safety and
efficacy of 1 year of tacrolimus ointment monotherapy
in adults with atopic dermatitis. Arch Dermatol. 2000;
136:999-1006.
Fonacier L, Spergel J, Charlesworth EN, et al. Report of
the Topical Calcineurin Inhibitor Task Force of the American
College of Allergy, Asthma and Immunology and the
American Academy of Allergy, Asthma and Immunology.
J Allergy Clin Immunol. 2005;115:1249-1253.
Hultsch T, Kapp A, Spergel J. Immunomodulation and
safety of topical calcineurin inhibitors for the treatment of atopic dermatitis. Dermatology. 2005;211:
174-187.
Lebwohl M, Gower T. A safety assessment of topical
calcineurin inhibitors in the treatment of atopic dermatitis.
Medscape Gen Med. 2006;8:8.
Ring J, Barker J, Behrendt H, et al. Review of the
potential photo-cocarcinogenicity of topical calcineurin
inhibitors: position statement of the European Dermatology Forum. J Eur Acad Dermatol Venereol. 2005;
19:663-671.
Bieber T, Cork M, Ellis C, et al. Consensus statement
on the safety profile of topical calcineurin inhibitors.
Dermatology. 2005;211:77-78.
Berger TG, Duvic M, Van Voorhees AS, Frieden IJ. The use
of topical calcineurin inhibitors in dermatology: safety concerns. Report of the American Academy of Dermatology
Association Task Force. J Am Acad Dermatol. 2006;54:
818-823.
Klein PA, Clark RAF. An evidence-based review of the
efficacy of antihistamines in relieving pruritus in atopic
dermatitis. Arch Dermatol. 1999;135:1522-1525.
Abramovits W. A clinician’s paradigm in the treatment of
atopic dermatitis. J Am Acad Dermatol. 2005;53:S70-S77.
Sidbury R, Hanifin JM. Systemic therapy of atopic dermatitis. Clin Exp Dermatol. 2000;25:559-566.
Gee BC. Seborrhoeic dermatitis. Clin Evid. 2004;
2344-2352.
Gupta AK, Bluhm R, Cooper EA, Summerbell RC, Batra R.
Seborrheic dermatitis. Dermatol Clin. 2003;21:401-412.
Gupta AK, Madzia SE, Batra R. Etiology and management
of seborrheic dermatitis. Dermatology. 2004;208:89-93.
Schwartz RA, Janusz CA, Janniger CK. Seborrheic dermatitis: an overview. Am Fam Physician. 2006;74:125-130.
Hurwitz S. An overview of dermatologic diagnosis. In: Clin
Pediatr Dermatol. Philadelphia, PA: WB Saunders; 1981:1-5.
Janniger CK. Infantile seborrheic dermatitis: an
approach to cradle cap. Cutis. 1993;51:233-235.
Mimouni K, Mukamel M, Zeharia A, Mimouni M.
Prognosis of infantile seborrheic dermatitis. J Pediatr.
1995;127:744-746.
Downloaded from http://cpj.sagepub.com by Roberto Hernandez Sampieri on October 12, 2008
346
Clinical Pediatrics / Vol. 47, No. 4, May 2008
88. Foley P, Zuo Y, Plunkett A, Merlin K, Marks R. The frequency of common skin conditions in preschool-aged
children in Australia: seborrheic dermatitis and pityriasis
capitis (cradle cap). Arch Dermatol. 2003;139:318-322.
89. Elewski BE. Clinical diagnosis of common scalp disorders. J Investig Dermatol Symp Proc. 2005;10:190-193.
90. Williams JV, Eichenfield LF, Burke BL, Barnes-Eley
M, Friedlander SF. Prevalence of scalp scaling in prepubertal children. Pediatrics. 2005;115:e1-e6.
91. Johnson BA, Nunley JR. Treatment of seborrheic dermatitis. Am Fam Physician. 2000;61:2703-2710.
92. Gupta AK, Nicol K, Batra R. Role of antifungal agents
in the treatment of seborrheic dermatitis. Am J Clin
Dermatol. 2004;5:417-422.
93. Braza TJ, DiCarlo JB, Soon SL, Mccall CO. Tacrolimus
0.1% ointment for seborrhoeic dermatitis: an openlabel pilot study. Br J Dermatol. 2003;148:1242-1244.
94. Xolegel Gel [package insert]. Princeton, NJ: Barrier
Therapeutics Inc; 2006.
95. Meshkinpour A, Sun J, Weinstein G. An open pilot
study using tacrolimus ointment in the treatment of
seborrheic dermatitis. J Am Acad Dermatol. 2003;49:
145-147.
96. Crutchfield CE III. Pimecrolimus: a new treatment for
seborrheic dermatitis. Cutis. 2002;70:207-208.
97. Brownell I, Quan LT, Hsu S. Topical pimecrolimus in the
treatment of seborrheic dermatitis. Dermatol Online J.
2003;9:13.
98. Rallis E, Nasiopoulou A, Kouskoukis C, Koumantaki E.
Pimecrolimus cream 1% can be an effective treatment
for seborrheic dermatitis of the face and trunk. Drugs
Exp Clin Res. 2004;30:191-195.
99. Warshaw E, Wohlhuter J, Drake D, et al. Randomized,
double-blind, vehicle-controlled efficacy trial of pimecrolimus cream 1% for the treatment of moderate to
severe facial seborrheic dermatitis [abstract 920]. J
Invest Dermatol. 2005;125:A3.
100. Cunha PR. Pimecrolimus cream 1% is effective in seborrhoeic dermatitis refractory to treatment with topical
corticosteroids. Acta Derm Venereol. 2006;86:69-70.
101. Akhavan A, Cohen SR. The relationship between atopic
dermatitis and contact dermatitis. Clin Dermatol. 2003;
21:158-162.
102. Krol A, Krafchik B. The differential diagnosis of atopic
dermatitis in childhood. Dermatol Ther. 2006;19:73-82.
103. Scheinfeld N. Diaper dermatitis: a review and brief
survey of eruptions of the diaper area. Am J Clin
Dermatol. 2005;6:273-281.
104. Ward DB, Fleischer AB Jr, Feldman SR, Krowchuk DP.
Characterization of diaper dermatitis in the United
States. Arch Pediatr Adolesc Med. 2000;154:943-946.
105. Vusion [package insert]. Princeton, NJ: Barrier
Therapeutics, Inc; 2006.
106. Mercader P, Cuadra-Oyanguren J, Rodríguez-Serna M,
Pitarch-Bort G, Fortea-Baixauli JM. Treatment of protein contact dermatitis with topical tacrolimus. Acta
Derm Venereol. 2005;85:555-556.
107. Nakada T, Iijima M, Maibach HI. Eyeglass frame allergic contact dermatitis: does tacrolimus prevent recurrences? Contact Derm. 2005;53:219-221.
108. Anderson BE, Marks JG Jr, Mauger DT. Efficacy of
tacrolimus ointment in the prevention and treatment
of contact dermatitis. Dermatitis. 2004;15:158-159.
109. Alomar A, Puig L, Gallardo CM, Valenzuela N. Topical
tacrolimus 0.1% ointment (Protopic®) reverses nickel
contact dermatitis elicited by allergen challenge to a similar
degree to mometasone furoate 0.1% with greater suppression
of late erythema. Contact Derm. 2003;49:185-188.
110. Queille-Roussel C, Graeber M, Thurston M, et al.
SDZ ASM 981 is the first non-steroid that suppresses
established nickel contact dermatitis elicited by allergen challenge. Contact Derm. 2000;42:349-350.
111. Belsito DV, Fowler JF Jr, Marks JG Jr, et al.
Pimecrolimus cream 1%: a potential new treatment for
chronic hand dermatitis. Cutis. 2004;73:31-38.
112. Zhai H, Villarama CD, Hasan Hafeez Z, Maibach HI.
Efficacy of a topical agent, MAS063D (‘Atopiclair’),
in the treatment of sodium lauryl sulphate-induced
irritant contact dermatitis. Exog Dermatol. 2003;2:
301-305.
Downloaded from http://cpj.sagepub.com by Roberto Hernandez Sampieri on October 12, 2008