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112-1
ATOPIC DERMATITIS
The Itch that Erupts when Scratched . . . . . . . . . . . . Level I
Rebecca M.T. Law, PharmD
CASE SUMMARY
A 3½-year-old girl who has had atopic dermatitis since age
6 months has had a worsening over the past 2–3 weeks. The child
also has behavioral issues likely related to stressors such as recent
placement in day care; and there are other aggravating factors.
The child requires both nonpharmacologic and pharmacologic
management of the atopic dermatitis flare. Nonpharmacologic
management includes avoidance of triggers and social aspects such
as behavior modification for the child, counseling for the parents,
appropriate skin care, and environmental changes. Pharmacologic
agents include a medium-strength corticosteroid topical cream,
copious use of scent-free moisturizers, pimecrolimus or tacrolimus
if not controlled, and control of itching.
QUESTIONS
Problem Identification
1.a. Create a drug therapy problem list for this patient.
• Julia has signs and symptoms of atopic dermatitis insufficiently
managed with hydrocortisone cream and moisturizers.
• Recent stressors (eg, placement in day care) and related behavioral issues are likely exacerbating Julia’s atopic dermatitis.
• Julia’s caregivers (her parents) are under stress. They require
social support and psychological assistance to prevent inadequate or inappropriate care of Julia.
1b. What signs and symptoms of atopic dermatitis does this
patient demonstrate?
• Generally dry skin (xerosis).1,2 In atopic dermatitis, transepidermal water loss is increased.3
• There are likely pruritic papules in flexure areas and excoriations from scratching. There is some bleeding but areas do not
appear to be infected. Some cracking skin lesions are seen
behind the ears and knees. There are no lesions on the extensor parts of the body. Sparing of the skin on top of the nose is
a characteristic feature (known as the “headlight sign”).1,2 The
groin and axillary region are also usually spared.3,4
• There is itch-induced scratching and subsequent excoriations.
Pruritus is a quintessential feature of atopic dermatitis, and a
diagnosis cannot be made if there is no history of itching.1–4
Scratching or rubbing itchy, atopic skin characterizes this
eczema.4 This can further irritate the skin, increase inflammation, and exacerbate itchiness.1 Itching is especially problematic
during sleep when conscious control of scratching is lost.1 Julia’s
mother has sewn mittens on her pajamas to prevent her from
scratching. Also, once there is pruritus, the likelihood that surrounding skin (whether inflamed or noninflamed) will react to
light stimuli with itching is increased; this is called allokinesis
and is typical of atopic dermatitis. Allokinesis describes a state
• Serum IgE is usually elevated in patients with atopic dermatitis1,4 and the level may correlate somewhat with AD disease
severity.4 However, elevated allergen-specific IgE levels can
be found in 55% of the general US population.4 There is a
genetic predisposition in patients with atopy to demonstrate
Th2 predominance—hence increased Th2 cell activity.3,4 Several candidate genes that encode cytokines involved in the
regulation of IgE synthesis have been identified, notably on
chromosome 5q31-33.5 Increased Th2 activity leads to release
of IL-3, IL-4, IL-5, IL-10, and IL-13, which causes eosinophilia,
increases IgE, and increases the growth and development
of mast cells.3 These cytokines also affect B cell maturation,
causing a genomic rearrangement that favors isotype class
switching from IgM to IgE.5 In addition, increased serum
IgE antibodies to a particular food is consistent with a food
allergy,1,2 which is common in patients with atopic dermatitis—
and Julia has multiple food allergies.
• Eosinophilia in peripheral blood.
• Positive RAST (radioallergosorbent) test. This is an allergenspecific IgE antibody test used to screen for allergy to a specific
substance or substances; in some cases it may be used to monitor immunotherapy or to see if a child has outgrown a specific
allergy. Positive (elevated) results usually indicate an allergy to
a suspected or known allergen. However, the level of IgE may
not correlate with the severity of an allergic reaction, and the
IgE level may remain elevated for years after an allergy has
been outgrown.
• In addition, Julia demonstrates behavioral problems, which are
likely related to the stress of beginning day care. She has lots of
temper tantrums, appears unhappy, has lost her toilet training
and is using diapers again.
• A clinically useful set of criteria for the diagnosis of atopic
dermatitis is as follows: Essential features (must be present) are
pruritus and eczema (acute, subacute, and chronic); important
features (usually present and supports the diagnosis) are early
age of onset, atopy, and xerosis.4 Atopy can be demonstrated by
a personal and/or family history, and by IgE reactivity.4 Julia’s
signs and symptoms are all consistent with a diagnosis of atopic
dermatitis, perhaps exacerbated by stress.
1c. What risk factors or aggravating factors may have contributed to the patient’s atopic dermatitis flare?
• Strong family history of atopic diseases and food allergies:
severe shellfish allergy in Julia’s father, hay fever in her mother,
multiple food allergies in her paternal aunt, asthma in her
maternal grandmother, infantile eczema in her paternal first
cousin, and severe peanut allergy in her maternal first cousin.
The strongest risk factor for atopic dermatitis is a parental history of atopy or eczema, with maternal atopy possibly more
predictive than paternal atopy.2,4
• Genome-wide scans have identified atopic dermatitis-related
loci on 1q21, 3q21, 16q, 17q25, 20p, and 3p26.3 The filaggrin gene (FLG) on chromosome 1q21.3 has been found to
encode a key protein in epidermal differentiation.5 Mutations of FLG were identified in 30% of European patients
Copyright © 2017 by McGraw-Hill Education. All rights reserved.
Atopic Dermatitis
Poh Gin Kwa, MD, FRCPC
CHAPTER 112
112
wherein a normally nonpruritic stimulus induces pruritus
in the skin surrounding the active lesion; this is experienced
by patients with atopic dermatitis as “pruritic attacks” when
their skin is touched accidentally by mechanical factors such
as clothing. Interleukin-31 (IL-31), a strongly pruritogenic
cytokine, has been implicated as a major factor in the genesis
of pruritus in atopic dermatitis, along with other cytokines and
chemokines.5 However, IL-31 and others are not sensitive or
specific enough to be biomarkers for atopic dermatitis.4
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Dermatologic Disorders
with atopic dermatitis, and distinctive FLG mutations have
also been reported in Japanese patients.5 Mutations of FLG
confer a risk for early-onset atopic dermatitis4,5 and for more
severe, persistent disease.4 Other genetic variants coding for
other epidermal structures may also be involved. As discussed
earlier, genes encoding major elements of the immune system are also involved. Thus, atopic dermatitis appears to be
a complex genetic disease with gene–gene interactions and
gene–environment interactions. The two major groups of genes
involved are genes encoding epidermal or other epithelial
structural proteins, and genes encoding major elements of the
immune system.3–5
• Environmental influences including lifestyle changes over the
past few decades have led to altered prevalences of allergic diseases including atopic dermatitis.3 Environmental factors may
include climate, urban versus rural living, diet, breastfeeding
and time of weaning, obesity, and pollution/tobacco smoke.4,6
The largest international study of the prevalence of atopic dermatitis (ISAAC—International Study of Asthma and Allergies
in Childhood) has shown that prevalence differs from country
to country, with large increases in prevalence occurring in
developing countries and a decrease in prevalence in developed countries.7 The hygiene hypothesis attributes increasing
atopic dermatitis to reduced exposure to various childhood
infections and bacterial endotoxins.3,4,6 Support for the hygiene
hypothesis includes the following observations: urban living
increases risk; exposures to endotoxin, farm animals (even the
pregnant mother), and dogs are protective; attending day care
within the first year of life is protective; and the consumption
of unpasteurized milk and acquired helminth infections may
be protective but are not recommended due to health risks.4
Julia just started day care about a month ago (at age 3½). The
ISAAC study also suggested that a maximum prevalence plateau of about 20% has emerged.7 Refer to the corresponding
Pharmacotherapy textbook chapter on atopic dermatitis for
additional details.
• Strawberries, raspberries, tomatoes, and eggs appear to be
aggravating factors for Julia. This is consistent with the age of
onset and the extent of atopic dermatitis in this child. Patients
with atopic dermatitis have a higher prevalence of food allergy
than those in the general population,1 particularly those of
younger age and with more severe disease.6 However, the role
of food antigens in the pathogenesis of atopic dermatitis is controversial.3 A current belief is that food allergy may be caused
by atopic dermatitis because, in most patients with both conditions, atopic dermatitis precedes the food allergy. In general,
the worse the atopic dermatitis and the younger the child, the
more likely it is that some type of food allergy is present.1,6 The
most common allergenic foods are eggs, milk, peanuts, wheat,
soy, and fish.1 Julia is reported to be sharing other children’s
foods at the day care; this increases the likelihood that she has
recently been exposed to an allergenic food.
• Starting day care appears to be an aggravating factor for Julia,
and she is still exhibiting clinging behavior after a month.
Other stressors for Julia may include being taken care of by
various babysitters rather than her parents (the parents’ stressful
lifestyle). Emotional factors may play a role in atopic dermatitis.1
• Being bottle-fed from 2 months of age may be a risk factor.
Studies on allergies and breastfeeding indicate that breastfeeding an infant for at least 4 months may protect the child from
developing allergic conditions.1
• Being exposed to cigarette smoke (the mother has restarted
smoking) may be a risk factor.
Copyright © 2017 by McGraw-Hill Education. All rights reserved.
• Environmental aeroallergens (the child had been left by the
babysitter on the floor/carpet) may have been contributing
factors. Dust mites, pollens, molds, and dander from animal
hair or skin may worsen the symptoms of atopic dermatitis.1,6
Reactivity to aeroallergens seems to increase with age, and
skin contact with an aeroallergen may trigger eczematous skin
lesions in some patients.6
1d. Could the patient’s signs and symptoms be caused by a
drug?
• No. The child is currently receiving topical medications for
atopic dermatitis, which should not cause her current signs
and symptoms.
• Oral diphenhydramine used to relieve the itch should also not
cause atopic dermatitis, and the drowsiness it causes may be
relaxing and may promote more restful sleep.
Desired Outcome
2.What are the treatment goals for this patient?
• Control the itching. Itching is one of the most bothersome features of atopic dermatitis, and in this child it has led to excoriations. Furthermore, because of the child’s atopic skin, she might
experience parental touching differently; and an altered tactile
experience in early infancy could affect the development of
stable physical and emotional boundaries; some patients may use
scratching to define their physical boundaries and needs.8 Body
image and self-esteem can be affected as the child grows. Selfesteem is often diminished in patients with atopic dermatitis.
• Control the atopic dermatitis.
• Eliminate any food triggers and environmental aeroallergens.
• Prevent future flare ups of atopic dermatitis.
• Minimize drug toxicity.
• Provide cost-effective therapies.
• Provide adequate relief of the stressors affecting the child
(to help control her behavior).
• Provide social support and psychological assistance/counseling
for the parents to ensure continuing appropriate care of the
child.
• Improve the quality of life (for Julia and her parents).
Therapeutic Alternatives
3.What feasible nonpharmacologic and pharmacologic alternatives are available managing this patient’s pruritus and atopic
dermatitis?
Pruritus
• Cool compresses and tepid baths, followed by liberal use of moisturizers (see below) are important nonpharmacologic measures
to relieve itching.9,10
• Oatmeal baths, lotions containing menthol or phenol, EMLA
cream (rarely used), and 5% doxepin cream (rarely used)
are potential topical pharmacologic treatments for reducing
pruritus.8 Short-term adjunctive use of topical doxepin may
reduce pruritus but is limited by side effects.
• Topical corticosteroids decrease pruritus9 and also control the
underlying atopic dermatitis.
• Tacrolimus and pimecrolimus are topical immunomodulating
agents that appear to be the most promising antipruritic agents
for atopic dermatitis.2,3
• Oral antihistamines, antidepressants (doxepin, SSRIs), and anxiolytics are systemic pharmacologic therapies sometimes used
112-3
Atopic dermatitis
• Both nonpharmacologic and pharmacologic management
strategies are important in controlling the disease. These
include minimizing preventable risk factors such as stress, avoiding triggers and known allergens, environmental control, proper
bathing and moisturizing techniques, use of scent-free moisturizers, medium-strength topical corticosteroids, topical immunomodulators, and phototherapy.1–4,9–11
• Nonpharmacologic management strategies are important in
controlling flare-ups of atopic dermatitis and reducing its primary symptom (itching). Minimizing preventable risk factors
and eliminating or avoiding what provokes the flare ups should
be the objective.6 Regardless of disease severity, basic management strategies should be implemented for every patient
with atopic dermatitis. These strategies include: proper skin
care (discussed below), antiseptic measures (ie, dilute bleach
baths—discussed below), and patient-specific trigger/irritant
avoidance (discussed below).10 Acute treatment is added to
these baseline maintenance strategies for flares.
• Hydration is crucial, and adequate skin hydration is a fundamental part of managing atopic dermatitis.1,9,10 Transepidermal water loss is greater in atopic skin than in normal skin.
Thus, any measures to improve skin moisturization (discussed
below) would be beneficial. It is recommended that the humidity in the home be kept at or above 50% and the room temperature be kept on the cool side.
• Identifying food or environmental allergens/triggers specific to
the patient may be important. If triggers can be identified,
avoidance may lead to longer intervals between flares and even
complete disease clearance in some cases.10 Nonspecific triggers may include harsh soaps, detergents, wool and other abrasive fabrics, tight-fitting clothing, certain chemicals, airborne
irritants (tobacco smoke and air pollution), and extremes or
transitions in temperature and humidity.10 Relevant allergens
differ by age, with young children more likely to have food
allergies and older children and adults more likely to be sensitive to aeroallergens.10 The National Institute of Allergy and
Infectious Diseases (NIAID) Food Allergy Expert Panel suggests limited food allergy testing (ie, cow’s milk, eggs, wheat,
soy, and peanut) if a child <5 years old has moderate-to-severe
atopic dermatitis and (1) persistent disease despite optimized
therapies; (2) reliable history of an immediate allergic reaction
after ingesting a specific food; or (3) both.6 Tests include skin
prick testing (SPT) and serum-specific IgE levels using in vitro
assays such as radioallergosorbent (RAST) testing or immunoCAP testing.6,10
• Managing identified food allergies is important. The role of food
as a trigger or clinical association should be considered in all
• Reducing dust mites or molds in the house may help reduce
allergen exposure (eg, encasing mattresses and pillows in dustmite protective covers, washing bedding regularly with hot
water, removing carpets if possible, and frequent vacuuming of
bare floors and any carpeting—especially if the child sits/plays
on the floor). However, evidence to support the routine use of
house dust mite covers is limited.6
• Avoiding woolen or other rough/irritating fabrics may be helpful
for both child and parents.1–3,6,10 Smooth clothing may minimize
skin irritation, and soft cotton or silk are preferred. There are a
few controlled studies showing that specialty silk garments may
improve atopic dermatitis severity scores. However, it is unclear
whether silk and specialty silks impregnated with antibacterial
agents provide significantly more improvement than soft cotton.6
• Tobacco smoke may be an irritant and should be avoided.1,10 Air
pollution may also be an irritant.10 However, study results are
inconsistent, and personal or secondhand/household smoking
status do not appear to significantly affect the development of
atopic dermatitis, even though smoking is detrimental to those
with asthma and has many other negative health risks.4 Because
the mother has restarted smoking, she should be encouraged to
use other methods to handle her stress and enroll in a smoking cessation program if needed. The mother should also avoid
using perfumes or any fragranced products (eg, fabric softener
sheets, deodorant sprays, hair sprays, and room deodorants).
• Minimizing stress is also important. Psychotherapeutic
approaches with a combination of educational and psychological interventions may be beneficial.
• Educating patients and caregivers is an important intervention.6
A written action plan (regarding when to apply moisturizers
and topical medications, when to step-up or step-down treatment, when to seek medical advice, what triggers to avoid) may
reinforce teachings6 and is critical to ensuring good long-term
Copyright © 2017 by McGraw-Hill Education. All rights reserved.
Atopic Dermatitis
• Topical antihistamines should be avoided due to their potentially irritant or sensitizing effects.2
infants with moderately severe to severe atopic dermatitis.
However, the role of food antigens in the pathogenesis of
atopic dermatitis remains controversial, as discussed earlier.3
Food allergies may coexist and do represent important triggers in a small subset of individuals with atopic dermatitis,6,10
but the true frequency of food allergies causing an isolated
flare of disease is probably low.6 Thus restricted elimination
diets (eg, exclusion of eggs, cow’s milk, peanuts, nuts, and fish
especially in children under age 2) which was once thought to
be helpful is currently a controversial practice, and most physicians currently do not withdraw food from the diet.3 Multiple
dietary restrictions and long-term dietary avoidance should
only be done with documented, clinically relevant food allergies.6 Food elimination diets based solely on the findings of
food allergy test results are not recommended for managing
of atopic dermatitis.6 Excessively restrictive diets, especially in
atopic children, have resulted in weight loss, poor growth, calcium deficiency, hypovitaminosis, and kwashiorkor.6 Current
research attempts to desensitize patients by inducing tolerance:
results using desensitization protocols from limited studies have
shown benefit in a few patients with food allergies. Avoidance of
known offending foods in the particular patient (ie, tomatoes,
strawberries, raspberries, and eggs for Julia) may improve skin
symptoms in a subset of patients with moderately severe to
severe atopic dermatitis.6 Sometimes, elimination of a particular food may be difficult, and recurring flare-ups may be caused
by missed hidden offending food ingredients (eg, a utensil used
to serve cookies with or without peanut butter can contaminate
the peanut-free cookie with enough peanut protein to cause a
reaction; egg may be hidden in pasta, sweets, or cake).
4,6
CHAPTER 112
for itching. There is little evidence that sedating or nonsedating antihistamines are effective when used alone for the
itch in atopic dermatitis.8 Several trials with fexofenadine and
cetirizine used in conjunction with topical corticosteroids
showed some benefit (fexofenadine further reduced the pruritus symptom score when added to a topical corticosteroid,
and cetirizine reduced the duration of corticosteroid use).2
Other recent trials with loratadine and chlorpheniramine did
not show benefit.2 However, sedating antihistamines such as
diphenhydramine may reduce nighttime scratching and promote more restful sleep when taken at bedtime.1,11 These may
be useful for patients with significant sleep disruption due to
itch, allergic dermatographism, or allergic rhinoconjunctivitis.8
1–3
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SECTION 14
Dermatologic Disorders
treatment adherence.10 A formal, 6-week educational program
of patients and their families, led by an interprofessional team
having dermatologic, nutritional, and psychological components, resulted in decreased severity of disease in a randomized, controlled trial with 825 children and adolescents with
moderate-to-severe atopic dermatitis.6
• Appropriate skin care is crucial in preventing flare-ups.1,3,9,10 A
daily skin care routine should include the following:
✓Using scent-free moisturizers ad lib throughout the day.
Large quantities can be used. There are presently no recommendations regarding the appropriate amount or dosing
frequency of moisturizers.9
✓ Bathing in lukewarm water (never hot) for 5–10 minutes one
or more times daily.9 Soaking daily for 20 minutes followed
immediately by application of topical agents (eg, corticosteroids) without towel drying is known as the “soak and
smear” technique and is useful when the topical agent alone
is inadequate.9 Twice-daily bathing during disease flares
may also be a useful method for enhancing skin penetration of topical therapies and for debridement of crusting
and staphylococcal colonization. Dilute bleach baths with
intranasal topical mupirocin may be helpful in moderate-tosevere atopic dermatitis patients with frequent bacterial skin
infections and may be particularly useful as maintenance
therapy.9 There is insufficient evidence to recommend other
routine bath additives (such as bath oils) or topical antimicrobial preparations (such as antiseptics, antibacterial bath
soaps) other than dilute bleach baths.9
✓The skin should be lightly towel dried except when the “soak
and smear” technique is used (pat to dry, avoid rubbing, or
brisk drying).9
✓Moisturizer (scent-free) should then be applied while the
skin is still moist or slightly damp (within 3 minutes of towel
drying).2 Some fragrance-free moisturizers include Aveeno
Moisture Cream, Cetaphil, Neutrogena Hand Cream, and
Vanicream. Lotions may be used on the scalp and other
hairy areas and for mild dryness on the face, trunk, and
limbs; creams are more occlusive than lotions; ointments
are the most occlusive and can be used for drier, thicker or
more scaly areas.2 Occlusive moisturizers are the best since
they slow transepidermal water loss by providing a layer of
oil on the skin surface, increasing the moisture content of the
stratum corneum.
✓ Limited use of nonsoap skin cleansers that are neutral to low
pH, hypoallergenic, and fragrance free is recommended.9
Lipid-free and fragrance-free skin cleansers may be particularly advantageous (eg, Cetaphil Gentle Skin Cleanser, Free
and Clear Liquid Cleanser, Spectro Jel for sensitive problem
prone skin). Aquanil, Dove, Neutrogena, and pHisoderm
sensitive skin products have also been recommended as low
irritant products, and some are lipid-free.
✓Avoiding alcohol-containing topical products including
lotions, swabs and wipes (they may be drying).
✓The use of specific laundering techniques, such as double
rinsing, detergents, or other laundry products cannot be
recommended for atopic dermatitis treatment because of the
lack of clinical studies.6
• Pharmacologic management strategies:
✓Topical corticosteroids (TCS) are the standard of care to
which other treatments are compared.9,10 However, despite
their extensive use, there is limited data regarding optimal
TCS concentrations, duration and frequency of therapy, and
quantity of application.1,2,9 The use of long-term intermittent
Copyright © 2017 by McGraw-Hill Education. All rights reserved.
TCS appeared to be beneficial and safe in two randomized
controlled studies. To maximize the anti-inflammatory benefit and minimize adverse effects, the choice of TCS should
ideally be matched with the severity and site of disease.3
Low-potency TCS, such as hydrocortisone 1% cream, are
suitable for the face, and medium-potency TCS such as
betamethasone valerate 0.1% may be used for the body. For
longer-duration maintenance therapy, low-potency TCS are
recommended.9 There is no established optimum regimen
for controlling flare-ups—starting with a short burst of
high-potency TCS to rapidly control active disease followed
by a rapid taper in potency is equally acceptable as using the
lowest-potency agent thought to be needed and then adjusting upward if treatment fails.9 Although twice-daily application is the usual clinical practice, there is some evidence of
efficacy with once-daily use of some potent TCS.9
Refer to the psoriasis chapter of the Pharmacotherapy
textbook for a corticosteroid potency comparison chart.
Ointment bases are preferred due to their occlusive properties. There is still limited data regarding optimal duration
and frequency of application. There should be a beneficial
response in 10–14 days.2 If no improvement is seen, a dermatologist should be consulted for further assessment. Daily
TCS applications should continue until the inflammatory
lesions are significantly improved, which may take up to
several weeks at a time.9 Once disease activity is controlled,
TCS should be tapered to a less potent preparation and used
intermittently (eg, once or twice weekly) or withdrawn (with
moisturizers used alone). Applying a TCS once or twice
weekly to areas of the patient’s body where frequent/repeated
flare-ups occur has reduced rates of relapse for patients who
experience frequent flare-ups at the same body sites.9
Corticosteroids should not be used continuously for
more than several weeks because they can cause cutaneous side effects such as skin atrophy, stretch marks (striae),
purpura, telangiectasias, focal hypertrichosis, and acneiform
or rosacea-like eruptions, as well as less common systemic
side effects including adrenal suppression, infections, and
growth retardation in children.9,10 Growth retardation may
be related to the chronicity of the illness rather than to corticosteroid use or dietary factors. Although tachyphylaxis
is a clinical concern, there is no experimental documentation.9 Although cataracts and glaucoma are possible with
systemic corticosteroid use, a definite association with TCS
is unclear.9 Nevertheless, minimizing use at periocular sites
is prudent.9
✓Wet wrap therapy (WWT) involves covering TCS application with a wetted first layer of tubular bandages, gauze, or
a cotton suit, followed by a dry second/outside layer. WWT
has been shown to quickly reduce disease severity and can be
used in patients with significant flare-ups and/or recalcitrant
disease in either hospital or ambulatory settings.9 WWT
provides occlusion, decreases water loss, and acts as a physical barrier against scratching. The wrap can be worn from
several hours to 24 hours at a time, depending on patient
tolerance.9
✓Topical immunomodulators such as the calcineurin inhibitors tacrolimus ointment (Protopic) and pimecrolimus cream
(Elidel) are approved for atopic dermatitis in adults and
children older than age 2.1–4,9,10 Although clinical trials
conducted in younger infants (eg, 2–23 months old) also
showed significant efficacy without appreciable adverse
effects, use in children younger than age 2 is not FDA
approved. Calcineurin inhibitors have been shown to reduce
112-5
✓Tar preparations are another topical alternative that may
be beneficial.9 However, there are few clinical trials and
use is limited by poor adherence. Tar preparations can be
malodorous, and adverse effects include tar folliculitis, acneiform eruptions, irritant dermatitis, photosensitivity, and a
burning sensation.
✓Topical phosphodiesterase inhibitors are a new class of antiinflammatory treatments that are presently available only in
clinical trials.9
✓Phototherapy (ie, ultraviolet light therapy) is effective and
may also be corticosteroid-sparing, allowing for the use
✓Systemic therapies are not routinely used in managing atopic
dermatitis. Cyclosporine is effective for severe or recalcitrant
atopic dermatitis but has limiting side effects including
nephrotoxicity and hypertension. Systemic corticosteroids
may be effective for rapid disease suppression, but little
evidence exists to support their use. Rebound flaring occurs
with short courses of oral corticosteroids,11 and long-term
side effects are limiting and of particular concern in the
growing child. Thus they are generally not recommended
due to an unfavorable risk-benefit profile.11 Recombinant
interferon gamma or oral methotrexate may be effective in
a subset of patients with severe disease. With respect to the
efficacy of azathioprine, mycophenolate mofetil, and intravenous immunoglobulin (IVIG), the limited data are primarily
in small case series or open-label studies in adults with recalcitrant atopic dermatitis.11 Biologic agents are not currently
approved for atopic dermatitis, and theoretically, using
protein-based therapies may be inherently risky in a patient
population more prone to developing IgE-sensitization
to protein antigens. There are a few case reports and
small case series, but additional research is needed.11 Oral
antihistamines have mixed evidence of efficacy for disease
control, except for sedating antihistamines used at night for
patients with poor sleep due to pruritus.11
✓Probiotics may prove to be beneficial for treatment of atopic
dermatitis. Probiotics are live microorganisms that confer a
health benefit on the host when administered in adequate
amounts. However, a 2010 review of 18 prevention or treatment studies concluded that results are mixed.12 One prevention study showed a 50% reduction in the incidence of atopic
dermatitis, whereas another study showed no reduction.
The results sometimes appeared to depend on the specific
strain of probiotics used. Treatment studies also demonstrated conflicting results.12 Presently, issues including which
organisms are effective, optimal dosing, duration of therapy,
efficacy and safety issues all require further investigation,
although adverse effects have been uncommon. Thus, at the
moment there is insufficient evidence to support a recommendation for using probiotics for prevention or treatment
of atopic dermatitis.6
Optimal Plan
4.What treatment regimen is best suited for this patient?
• Institute all of the nonpharmacologic management strategies
described previously that are applicable in this situation, such
as avoiding woolen or other rough fabrics, appropriate skin
care and proper bathing techniques, minimizing food triggers
and allergens. The teachers at day care should be instructed
to monitor that Julia is not sharing other children’s food. In
addition, the following psychotherapeutic approaches, combining educational and psychological interventions, should be
provided:
✓Counseling for the parents regarding handling of stress and
behavior modification for Julia (who has lost her toilettraining and has behavioral issues such as frequent tantrums).
Encourage the parents to seek additional social support.
Copyright © 2017 by McGraw-Hill Education. All rights reserved.
Atopic Dermatitis
✓Prescription emollient devices (PEDs) are barrier creams that
act to repair the damaged skin barrier and may provide
some anti-inflammatory activities.9 The FDA has approved
their use as “medical devices,” (which is a less rigorous
process), based on the assertion that they serve a structural
role in skin barrier function and do not exert their effects
by any chemical actions.9 There is limited efficacy and safety
data.9 Products include Atopiclair, which contains hyaluronic and glycyrrhetinic acids, MimyX, which contains
N-palmitoylethanolamine, and EpiCeram, which contains
ceramides, cholesterol and free fatty acids. These are generally recommended for use two to three times daily.9
of lower potency TCS. Phototherapy is a recommended
second-line intervention for treatment of atopic dermatitis
and may be used for acute or maintenance therapy in children and adults.11 Patients require eye protection during UV
treatments. Adverse effects include erythema, skin burning
(“sunburn”), pruritus, pigmentation, photoaging, and risk of
skin cancer.
CHAPTER 112
the extent, severity, and symptoms of atopic dermatitis in
children and adults.9 Due to continuing concerns regarding
a possible risk of cancer, both drugs are recommended for
use as second-line treatments for short-term and noncontinuous chronic use in atopic dermatitis when the use of TCS
is ineffective or inadvisable.9 They may be appropriate in
patients with corticosteroid-related side effects, patients with
large body-surface areas of disease, patients unresponsive
to corticosteroids, or where treatment with corticosteroids
is otherwise inadvisable. Unlike topical corticosteroids,
calcineurin inhibitors can be used on all body locations for
prolonged periods.2 They may be used as two to three times
weekly chronic therapy for long-term maintenance10 and
may also be used as steroid-sparing agents (sequentially or
concomitantly with TCS), although clinical data are limited.9
Pimecrolimus cream provides a rapid and sustained
effect in controlling pruritus, with benefit often seen within
48 hours. The relief of pruritus is seen across a diverse
patient population in terms of age (>3 months) and severity
of disease. It provides rapid and sustained relief of exacerbations and minimizes recurrence better than conventional
treatment (ie, intermittent topical corticosteroids for disease
flare-ups). The cream should be applied at the first signs of
a flare (eg, local redness and pruritus) and continued for
5–7 days after clearance of lesions.2
Tacrolimus ointment also provides a rapid and sustained
benefit in controlling signs and symptoms of atopic dermatitis in children and adults with moderate-to-severe disease.
The 0.03% ointment is approved for moderate-to-severe
disease for ages 2 and older, whereas the 0.1% ointment is
limited to ages 16 and older.
The most common adverse effect of both agents is transient discomfort (burning sensation) at the application site.
This usually disappears within 2–3 days. There does not
appear to be an increased risk of bacterial or viral infections,
although there is a possible risk of cutaneous malignancy;
sun protection is recommended.2 A high sun protection factor (SPF) broad-spectrum sunblock (eg, SPF 30 or higher)
should be applied daily to all exposed skin, especially for
those with the highest risk of developing skin cancers
(eg, patients receiving phototherapy).
112-6
SECTION 14
✓Parental education regarding environmental changes such
as reducing dust mites and removing carpets, stopping
smoking, and education about atopic dermatitis. Encourage
the mother to seek a smoking cessation program if needed.
Provide a written action plan with specific management
strategies tailored for Julia’s atopic dermatitis (see Ref. #10
for details).10
Dermatologic Disorders
• Give diphenhydramine 6.25 mg PO at bedtime nightly, and
consider giving it every 4–6 hours as needed (maximum
37.5 mg/day) for not more than 14 days.
• Apply a medium-strength corticosteroid (eg, betamethasone
dipropionate 0.1% cream) twice daily to lesions for 10–14 days
and reassess. Use hydrocortisone 1% ointment on face and
skinfolds. Once the disease activity is controlled, either withdraw the corticosteroid cream or use it intermittently if longterm therapy is needed to control flare-ups. The least potent
preparation that maintains adequate control of the disease
should be selected. If no improvement is seen in 14 days, start
pimecrolimus 1% cream and continue for 5–7 days after the
lesions have cleared, or continue intermittently as maintenance.
parents should be taught how to apply the topical corticosteroid cream, some side effect information for the medications,
the appropriate daily skin care routine for Julia, the triggers
to avoid, and appropriate environmental control measures,
as discussed previously. The written action plan should be
patient-specific for Julia with detailed courses of action about
treatment of acute flares, maintenance/control therapies, and
other management strategies (see Ref. #10).
• The parents should be provided with personal psychologic
assistance and social support to ensure compliance with the
child’s care—both overall care and specific care for the atopic
dermatitis condition. Ensuring that Julia has a restful night’s
sleep (and hence the mother’s sleep) will help ease her stress.
As mentioned earlier, the parents would benefit from stress
management instruction.
• In addition, Julia’s mother should be encouraged to enroll in
a smoking cessation program. This is important for both her
and Julia. Cigarette smoke may be a trigger for Julia’s atopic
dermatitis and may potentially increase her risk of developing
asthma.
• Apply petroleum jelly to the affected areas ad lib.
Outcome Evaluation
5.What efficacy and adverse effects monitoring is needed for the
management strategies you recommended?
Efficacy Monitoring
• Itching should improve in 3–4 days.
• The appearance of the atopic skin should improve within
3–7 days, definitely by 10–14 days.
• The skin should appear less dry over time with continued use
of moisturizers and appropriate skin care.
• It is important to involve the parents in monitoring their child’s
progress and ensuring that excoriated/bleeding lesions do not
become secondarily infected.
• It is important to also monitor for behavioral improvements in
Julia. If allowed to continue, stress and lack of social interaction
may lead to further psychological issues.
Adverse Effect Monitoring
• Diphenhydramine may cause dry mouth and daytime
sleepiness.
• Topical corticosteroids may cause local side effects including
skin atrophy, fungal or bacterial skin infections, striae, skin
pigmentation, and acne, especially if use is prolonged. Systemic
side effects including HPA-axis suppression, growth suppression, osteoporotic changes, and Cushing’s syndrome are also
possible especially with high-potency topical corticosteroids or
weaker ones used under occlusion.9
• If pimecrolimus is required, there may be some transient burning at the application sites.
Patient Education
6.How would you inform the patient’s caregiver about the treatment regimen to enhance compliance and ensure successful
therapy?
• The importance of adequate and appropriate education of the
patient’s caregivers about atopic dermatitis and its management
cannot be overemphasized. Julia’s parents should be informed
about the prognosis including time to healing and possible
effects on emotional health, body image and self-esteem. The
Copyright © 2017 by McGraw-Hill Education. All rights reserved.
REFERENCES
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