Atopic Dermatitis

Karl T. Clebak, MD, MHAa,*, Leesha Helm, MD, MPHa,

Prabhdeep Uppal, DO, MSb,c,1, Christopher R. Davis, a
MD, MPH ,
Matthew F. Helm, MDd

KEYWORDS
 Atopic dermatitis  Emollients and skin care  Topical therapy  Systemic therapy
 Phototherapy

KEY POINTS
 Atopic dermatitis (AD) is a common, chronic relapsing, and remitting inflammatory skin
disease that is characterized by erythematous, scaly, and pruritic lesions often located
over the flexural surfaces.
 Good skin hygiene and the use of emollients are recommended for chronic treatment in all
patients with AD.
 Topical corticosteroids are first-line treatments during AD exacerbations.
 Systemic therapies including monoclonal antibody treatments and phototherapy are
effective in patients with moderate-to-severe AD not responsive to topical therapies.

INTRODUCTION

Atopic dermatitis (AD), also known as atopic eczema, is a chronic relapsing inflamma-
tory skin disease that is characterized by erythematous, scaly, and pruritic lesions
often located over the flexural surfaces in adults (Fig. 1).1 In infants, the lesions pre-
dominantly affect the face, scalp, trunk, and extensor surfaces. Acutely, the lesions
are vesicular with open weeping and crusting eruption. In the subacute phase, the le-
sions present as scaly and dry fissures, which over time are lichenified from repeated
scratching. Another feature of chronic AD is decreased erythema compared with the

This article originally appeared in Primary Care: Clinics in Office Practice, Volume 50 Issue 2,
June 2023.
a
Department of Family and Community Medicine, Penn State Health Milton. S Hershey
Medical Center, 500 University Drive, H154/C1613 Hershey, PA 17033, USA; b Department of
Family and Community Medicine, ChristianaCare, 1401 Foulk Road, Suite 100B, Wilmington, DE
19803, USA; c Department of Emergency Medicine, ChristianaCare, 1401 Foulk Road, Suite
100B, Wilmington, DE 19803, USA; d Department of Dermatology, Penn State Health Milton. S
Hershey Medical Center, 500 University Drive, Suite 4300, MC HU14, Hershey, PA 17033, USA
1
Present address: 4755 Ogletown-Stanton Road, Newark, DE 19718, USA
* Corresponding author. 500 University Drive, H154/C1613, Hershey, PA 17033.
E-mail address: Kclebak@pennstatehealth.psu.edu

Med Clin N Am 108 (2024) 641–653

https://doi.org/10.1016/j.mcna.2023.08.012 medical.theclinics.com
0025-7125/24/ª 2023 Elsevier Inc. All rights reserved.

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642 Clebak et al

Fig. 1. Atopic dermatitis: pink scaly papules and plaques in the antecubital fossa.

acute state.1 AD is often associated with atopic conditions, such as allergies and
asthma. In addition to the association with closely related atopic conditions, AD is
related to other diseases such as obesity, cardiovascular disease, and psychological
diseases such as anxiety and depression.2,3
Multiple theories exist regarding the pathophysiology of AD and include a complex
interplay of factors including genetics, the immune system, the environment, and the
skin surface microbiome. Two major theories exist to explain the pathophysiology of
AD: the inside-out and outside-in hypotheses. The inside-out hypothesis suggests
inflammation or dysregulation of the immune system creates skin barrier defects
that further allow penetration of allergens and irritants.2,3 The outside-in hypothesis
suggests that epidermal skin barrier impairments lead to immune dysregulation and
allergic sensitization.4
Both innate and acquired immune responses have a role in the pathogenesis of AD.
The Th2 response is further exacerbated by Langerhans cells in the epidermis, which
are specialized immune cells that have a heightened response to allergen and irritant
antigens. Implicated cytokines in this causal pathway include IL-4, IL-13, IL-31, and IL-
22 many of which are targeted by new biologic medications.5,6 IL-31 has specifically
been shown to be important in the pathogenesis of pruritus. This itch–scratch cycle
ultimately worsens the inflammation of AD by decreasing filaggrin (FLG), ceramides,
and antimicrobial peptides while increasing bacterial colonization and infections of
the skin, which become difficult to control.
The pathogenesis of AD involves skin barrier dysfunction, often times triggered by
FLG mutations. Emerging evidence shows that disorder in FLG expression plays a
critical role in developing AD. FLG are proteins that bind keratin in epidermal cells.
Loss of FLG leads to flattening of skin surface cells, a decrease in natural moisturizing
factors of the skin, and an increase in skin pH, which leads to increased activity of pro-
teases and enzymes that break down proteins that hold skin epidermal cells together
and ultimately cytokines that promote skin inflammation.6–8
Other factors to consider that contribute to the process of inflammation include the
skin microbiome, viral, bacterial, and fungal infections, stress, climate, food, and envi-
ronmental allergens.6

OBSERVATION/ASSESSMENT/EVALUATION

The 3 phases of AD are infantile, childhood, and adult.

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 Atopic Dermatitis 643

Infantile Atopic Dermatitis

Clinical presentation and differential diagnosis
Infantile AD typically manifests from birth to 2 years and is part of a multitude of allergic
conditions that develop during infancy known as “atopic march.” This progressive
atopy begins with the development of AD and subsequently allergic rhinitis and
asthma in later childhood. Infants typically present with erythematous papules and
vesicles seen on the cheeks, forehead, or scalp. In infants, atopic lesions often involve
the face, scalp, and extensor surfaces (as opposed to adult AD), and the affected
areas can have serous oozing and crusting (Fig. 2). The diaper area is often spared
due to moisture retention of the diaper.9

Diagnosis and classification

The “Hanifin and Rajka” criteria and the UK Working Party’s Diagnostic Criteria for
Atopic Dermatitis are the most widely cited criteria used.10–13
Five major clinical features based on these criteria are (4 required for diagnosis) as
follows:
1. pruritus
2. a chronic, relapsing course
3. typical distribution
4. family or personal history of atopy
5. onset before 2 years of age.
Minor criteria are also frequently observed and include the following:
 Early age of onset
 Xerosis
 Palmar hyperlinearity, ichthyosis, keratosis pilaris
 Immediate skin test reactivity, elevated serum IgE
 Cutaneous infection, including Staphylococcus aureus and Herpes simplex virus
 Nipple eczema
 Cheilitis
 Pityriasis alba
 White dermatographism, delayed blanching
 Perifollicular accentuation
 Anterior subcapsular cataracts

Fig. 2. Infantile atopic dermatitis: pink oozing vesicles on the cheeks.

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644 Clebak et al

 Itch when sweating

 Nonspecific hand or foot dermatitis
 Recurrent conjunctivitis
 Dennie-Morgan folds
 Keratoconus
 Facial erythema or pallor
Scoring tools to measure disease severity such as the Severity Scoring of Atopic
Dermatitis index and the Eczema Area and Severity index can be used for research
and clinical practice. It is also important to note that infantile AD affects quality of
life not just for the patient but also for the parent and caretaker. Infants often have
intense pruritus and sleep disturbances, and parents or caretakers are often affected
by the cost of medication, poor sleep, time off of work, and emotional stress because
of their care for their child with AD.9

Management
Treatment of infantile AD includes topical emollients and corticosteroids. Emollients
improve skin hydration and have been shown to decrease the number of flares. There
is little evidence to show whether certain emollients are superior to others but ideally
should be free of sensitizing agents. First-line medication option in the management of
AD is topical corticosteroids (TCS), which are classified into 7 groups based on po-
tency. Low-potency TCS should be used for long-term management because children
are more prone to develop side effects. Because infants have thinner skin and a larger
surface-area-to-weight ratio, they are likely to absorb increased amounts of the medi-
cation compared with adults. Commonly used TCS approved for infants aged
3 months and older include low-to-medium potency TCS such as desonide, fluocino-
lone acetonide oil, hydrocortisone butyrate, or triamcinolone. Ointment is based in
petrolatum and is more effective at healing the skin than lotions or creams that are wa-
ter based. Current treatment guidelines do not recommend more than twice-daily
application of TCS. Side effects include skin atrophy, striae, acne, and telangiectasia.
For this reason, they should be used for the shortest duration needed to control the
flare-up and on an as-needed basis after that.
Topical calcineurin inhibitors such as tacrolimus and pimecrolimus are second-line
treatment options. These nonsteroidal medications inhibit calcineurin in the skin,
blocking T-cell activation, and the release of cytokines. They are approved in the
United States by the Food and Drug Administration for children aged 2 years and older
and are usually used in conjunction with TCS. Adverse effects include skin burning and
irritation, so patients should be counseled on using sun protection.9
Wet wrap therapy is a useful technique to treat persistent and refractory AD. They
are best done in the evening before bed where a topical steroid is placed on
eczematous lesions, a moist dressing is placed over the lesion and then a dry
one on top of that. Then the patient puts on their clothing and leaves them on for
several hours over night. Results are quite remarkable even after a few days using
this method.
Importantly, peanut introduction should not be delayed in children simply due to
the presence of AD. The Learning Early about Peanut Allergy trial examined the
introduction of peanuts in infants with severe AD or egg allergy, and concluded
that early and sustained peanut consumption in this group resulted in notably
lower rates of peanut allergy at 60 months of age.14 In 2017, the National Institute
of Allergy and Infectious Diseases developed an addendum of guidelines specif-
ically to address the prevention of peanut allergy for infants at various risk levels15
(Table 1).

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 Atopic Dermatitis 645

Table 1
Summary of addendum guidelines for the prevention of peanut allergy

Earliest Age of Peanut

Infant Criteria Recommendations Introduction
Severe eczema, egg Strongly consider evaluation 4–6 mo
allergy, or both with peanut-specific
IgE and/or skin prick test
and, if necessary, an
oral food challenge. Based
on test results, introduce
peanut-containing foods
Mild-to-moderate eczema Introduce peanut-containing Around 6 mo
foods
No eczema or any food Introduce peanut-containing Age-appropriate and in
allergy foods accordance
with family preferences
and
cultural practices

From Togias A, Cooper SF, Acebal ML, Assa’ad A, Baker JR Jr, Beck LA, Block J, Byrd-Bredbenner C,
Chan ES, Eichenfield LF, Fleischer DM, Fuchs GJ 3rd, Furuta GT, Greenhawt MJ, Gupta RS, Habich M,
Jones SM, Keaton K, Muraro A, Plaut M, Rosenwasser LJ, Rotrosen D, Sampson HA, Schneider LC,
Sicherer SH, Sidbury R, Spergel J, Stukus DR, Venter C, Boyce JA. Addendum guidelines for the pre-
vention of peanut allergy in the United States: Report of the National Institute of Allergy and In-
fectious Diseases-sponsored expert panel. J Allergy Clin Immunol. 2017 Jan;139(1):29-44.

Toddler and School Age Atopic Dermatitis

The distribution of dermatitis changes as children age. From age 2 to 12 years, with
walking, flexural surface involvement (antecubital fossae, popliteal fossae, neck,
wrists, and ankles) is often seen. With eating and drooling, dermatitis can spread to
the mouth and chin. Lichenification due to chronicity of symptoms and scratching
also occurs. Although during the school years, AD will improve, the function of the
skin barrier will never be normal. The differential for manifestations of AD in this age
group includes discoid eczema, pityriasis alba, and lip licker’s dermatitis.16

Clinical presentation and differential diagnosis

Similar diagnosis strategies to that used for infantile AD can be used. See guidelines
and therapeutics table for specific age-based options for treatment.

Adult Atopic Dermatitis

There is a variety of presentations of the adult phase. The flexural pattern can persist
and is common or become more diffuse. Some adults who had complete resolution of
AD as a child, may develop hand dermatitis due to occupational exposures. The upper
eyelids and lips are other frequent affected areas in adults. Denni-Morgan folds, or a
fold of skin under the lower eyelids, can be seen when chronic eyelid dermatitis de-
velops. Dry skin, white dermographism, hyperlinear palms, ichthyosis vulgaris, and
keratosis pilaris are common associated manifestations of AD in adults. Lichenifica-
tion and fissuring can commonly occur with chronicity (Figs. 3 and 4) Adult-onset
dermatitis also can occur but is unusual.17
Scoring tools used now to assess disease severity in patients with skin of color can
underestimate the severity of disease due to erythema in adult AD in skin of color be-
ing violaceous. Postinflammatory hypopigmentation and hyperpigmentation occur

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646 Clebak et al

Fig. 3. Chronic atopic dermatitis: lichenified plaques on the ankle.

more commonly in skin of color and is often a source of distress (Fig. 5). With scratch-
ing and rubbing, patients with skin of color can also more commonly develop lichen
simplex or nodular prurigo.18
Similar diagnosis strategies to that used for infantile AD can be used. See the guide-
lines and therapeutics table below for specific age-based options for treatment.

PREVALENCE/INCIDENCE

AD affects 10% to 20% of the population in developed countries.19 It is ranked as the

third most prevalent dermatologic condition but was the greatest contributor to
disability-adjusted life years, which measure years of life lost due to premature mor-
tality plus years lost due to disability or its consequences. All races are affected and
people with “atopic tendency” often display a higher prevalence of hay fever, asthma,
and food allergies.20 Among populations, genetic studies show that AD affects diverse
populations.18
Although AD most commonly affects children, all ages can be affected. In approx-
imately 60% of cases, AD presents in the first year of life.19,21,22 About 57% of children
develop AD before age 6.22

Fig. 4. Atopic dermatitis: thickened lichenified plaques on the ankles.

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 Atopic Dermatitis 647

Fig. 5. Atopic dermatitis: lichenified plaques and hyperpigmentation of eczematous patch.

WORLDWIDE/REGIONAL INCIDENCE AND MORTALITY RATES

There seems to be an association between higher socioeconomic status and AD prev-

alence and morbidity. Lifetime prevalence worldwide of AD is greater than 15%, espe-
cially in wealthy developed countries.18,23
The prevalence of AD globally varies around the world. According to the latest avail-
able data, AD continues to increase in prevalence in young children, aged 6 to 7 years
and 13 to 14 years, in low-income countries. Some of the countries in which this trend
is noted are Latin America or in Southeast Asia.24
Studies show that AD is a prevalent problem all around the world, among infants,
children, young adults, and adults. The global prevalence of AD is highest in younger
children compared with older children, adolescents, and adults. The significant pre-
dictors of AD were age, weather, food, race, ethnicity, place of birth, sex, current
working status, and family history of atopy and maternal age.25

DISCUSSION
Goals of Treatment
The primary goals of treatment of AD are to reduce skin inflammation and pruritus,
restore skin barrier function, and improve quality of life.26 As previously discussed,
treatments can be classified into the categories of moisturizing and basic skin care,
topical therapies, phototherapy, and systemic therapies.26–28 Reduction of itching
and burning, as well as complete clearing of all skin changes, are the most important
treatment goals for patients.29
Approach
The optimal management of AD requires a multipronged approach that involves the
elimination of exacerbating factors, restoration of the skin barrier function and hydra-
tion of the skin, patient education, and pharmacologic treatment of skin inflammation.
AD is a chronic disease that can first present in childhood and persist across a life-
time with exacerbations. The general approach toward the treatment of AD is to
reduce symptoms of inflammation and pruritis, prevent exacerbations, and limit the
side effects of therapies to improve the overall quality of life.26,29 The primary
approach includes the avoidance of potential triggers and skin care with emollients
to limit water loss, restore the epidermal barrier, and spare the use of steroids in ex-
acerbations. Topical therapies include the use of TCS and calcineurin inhibitors.28

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648 Clebak et al

Table 2
Frequently used topical corticosteroids for atopic dermatitis treatment

Classification Topical Corticosteroid

Class 1 Very High Potency  Augmented betamethasone dipropionate 0.05% (ointment,
gel)
 Augmented diflorasone diacetate 0.05% (ointment)
 Clobetasol propionate 0.05% (ointment, gel, cream, lotion,
foam, solution, spray, shampoo)
 Desoximetasone 0.25% (spray)
 Fluocinonide 0.1% (cream)
 Flurandrenolide 4 mg/cm2 (tape)
 Halobetasol propionate 0.05% (ointment, cream)
Class 2  Amcinonide 0.1% (ointment)
 Augmented diflorasone diacetate 0.05% (cream)
 Augmented betamethasone dipropionate 0.5% (cream, lotion)
 Betamethasone dipropionate 0.05% (ointment)
 Desoximetasone 0.05% (gel)
 Desoximetasone 0.25% (ointment, cream)
 Diflorasone diacetate 0.05% (ointment)
 Fluocinonide 0.05% (ointment, gel, cream, lotion, solution)
 Halcinonide 0.1% (ointment cream)
 Mometasone fluroate 0.1% (ointment)
 Triamcinolone acetonide 0.5% (ointment)
Class 3  Amcinonide 0.1% (cream, lotion)
 Betamethasone dipropionate 0.05% (cream, lotion)
 Betamethasone valerate 0.1% (ointment)
 Betamethasone valerate 0.12% (foam)
 Diflorasone diacetate 0.05% (cream)
 Fluticasone propionate 0.005% (ointment)
 Triamcinolone acetonide 0.1% (ointment)
 Triamcinolone acetonide 0.5% (cream)
Class 4  Betamethasone valerate 0.12% (foam)
 Desoximetasone 0.05% (cream)
 Fluocinolone acetonide 0.025% (ointment)
 Flurandrenolide 0.05% (ointment)
 Hydrocortisone valerate 0.2% (ointment)
 Mometasone furoate 0.1% (cream, lotion)
 Triamcinolone acetonide 0.1% (ointment, cream)
 Triamcinolone acetonide 0.2% (spray)
Class 5  Betamethasone dipropionate 0.05% (lotion)
 Betamethasone valerate 0.1% (cream, lotion)
 Clocortolone pivalate 0.1% (cream)
 Fluocinolone acetonide 0.025% (cream)
 Fluocinolone acetonide 0.01% (oil, shampoo)
 Fluticasone propionate 0.05% (cream, lotion)
 Flurandrenolide 0.05% (cream)
 Hydrocortisone butyrate 0.1% (ointment, cream, lotion,
solution)
 Hydrocortisone probutate 0.1% (cream)
 Hydrocortisone valerate 0.2% (cream)
 Prednicarbate 0.1% (ointment, cream)
 Triamcinolone acetonide 0.025% (ointment)
 Triamcinolone acetonide 0.01% (lotion)

(continued on next page)

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 Atopic Dermatitis 649

Table 2
(continued )
Classification Topical Corticosteroid
Class 6  Alclometasone dipropionate 0.05% (ointment, cream)
 Betamethasone valerate 0.05% (lotion)
 Desonide 0.05% (ointment, gel, cream, lotion, foam)
 Fluocinolone acetonide 0.01% (cream, solution)
 Triamcinolone acetonide 0.025% (cream, lotion)
Class 7 Lowest Potency  Dexamethasone sodium phosphate 0.1% (cream)
 Hydrocortisone 0.5%–2.5% (ointment, gel, cream, lotion, foam)
 Methylprednisolone acetate 0.25% (cream)

Adapted from Eichenfield LF, Tom WL, Berger TG, Krol A, Paller AS, Schwarzenberger K, Bergman
JN, Chamlin SL, Cohen DE, Cooper KD, Cordoro KM, Davis DM, Feldman SR, Hanifin JM, Margolis
DJ, Silverman RA, Simpson EL, Williams HC, Elmets CA, Block J, Harrod CG, Smith Begolka W,
Sidbury R. Guidelines of care for the management of atopic dermatitis: section 2. Management
and treatment of atopic dermatitis with topical therapies. J Am Acad Dermatol. 2014
Jul;71(1):116 to 32.

Topic calcineurin inhibitors are second-line and are useful in patients who have not
responded to TCS, in sensitive areas (eg, face, anogenital, skin folds), sites with
steroid-associated atrophy, and long-term uninterrupted TCS use.28 Phototherapy
is recommended in children and adults for both acute and chronic AD not responding
to topical therapies.30 Systemic immunomodulatory agents are indicated in adult and
pediatric patients in whom optimized topical regimens using emollients, topical anti-
inflammatory therapies, adjunctive methods, and/or phototherapy do not provide
adequate disease control.30
Evaluation
Dermoscopy of AD often shows focal white scales, yellow serous crust, and dotted
vessels distributed in clusters or randomly with associated dilated capillaries in irreg-
ularly elongated dermal papillae. In cases where intense itching occurs, hemorrhages
are also seen.31 The diagnosis is primarily made through history and physical exami-
nation findings; however, skin biopsy may be useful in cases where there is
uncertainty.
Current Clinical Guidelines
Guidelines from the American Academy of Dermatology note that topical agents form
the foundation of therapy for AD.27,28,30 These include frequent use of topical moistur-
izers and effective bathing practices (duration and frequency are nonstandardized but
it is recommended to apply moisturizers soon after bathing and limit the use of non-
soap cleansers). TCS are the mainstay of topical anti-inflammatory treatment. It is
generally recommended to apply twice daily, applying every day during flares, and
once or twice weekly afterward to prevent recurrence. Topical calcineurin inhibitors
include tacrolimus and pimecrolimus, second-line agents that have been approved
for moderate-to-severe and mild-to-moderate AD, respectively. These do not carry
the risk of skin atrophy that topical steroids do, making them potentially advantageous
options in sensitive areas but commonly cause localized stinging/burning. Topical an-
timicrobials/antiseptics have generally not been shown to be effective, with the excep-
tion that diluted bleach baths seem to improve clinical outcomes in those with
moderate-to-severe AD who have frequent bacterial skin infections.28
Phototherapy is a second-line treatment that has also been shown to be effective for
AD. Many types of light and protocols for therapy can be used, with limited

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650 Clebak et al

comparison trials available. It can be used on either an intermittent or continuous ba-

sis, as monotherapy or in combination with emollients and topical steroids (it is recom-
mended to avoid combining it with topical calcineurin inhibitors). Side effects are low
but it can cause erythema, burning, itching, and actinic damage.30

Further Treatment Options

Exciting new medications are now approved for moderate-to-severe AD. Dupilumab
(Dupixent) is now FDA approved for patients with AD aged 6 months and older. It is
an injection given 2 weeks apart and has a good safety profile with conjunctivitis being
the most common side effect. In two phase 3 trials, the human monoclonal antibody
against interleukin-4 receptor alpha dupilumab was shown to improve pruritus and in-
crease the likelihood of achieving decreased scores on the Investigator’s Global
Assessment. In patients 18 years of age and older, dupilumab is administered
300 mg every other week via subcutaneous injection (after a 600 mg loading
dose).32 Dosing for the pediatric population is weight-based. Although crisaborole
and dupilumab are FDA approved, their cost (ranging from US$700–3000 per month)
make them impractical for many patients.1
JAK inhibitors such as upadacitinib and abrocitinib have been used with great suc-
cess in moderate-to-severe AD.33,34 Abrocitinib is an oral medication taken at doses
of 100 or 200 mg once per day.33 Side effect includes immunosuppression and poten-
tially increased risk of upper respiratory tract infection, blood clots, and elevated liver
enzymes. There are many other targeted treatments such as IL-13 and IL-31 inhibitors
that are undergoing clinical trials.
An ointment of crisaborole (a phosphodiesterase 4 inhibitor) was found to be effec-
tive at reducing itching faster than vehicle alone; however, it is expensive and burning
is a common complaint.35

Therapeutic Options
(Tables 2 and 3)

Table 3
Therapeutic approaches

Mild AD Moderate AD Severe AD

Intermittent, short-term Intermittent, short-term Class 2 topical steroids for
use of class 6 or 7 topical use of class 3–4 topical flares (see Table); class 3–
steroids (see steroids (see 5 topical
Table)  topical Table)  topical steroids  tacrolimus
calcineurin inhibitors calcineurin inhibitors ointment for
Bathing and barrier repair Oral antihistamines maintenance
with emollients Bathing and barrier repair Oral antihistamines
Avoidance of irritant and Avoidance of irritant and Bathing and barrier repair
allergic triggers allergic triggers Avoidance of irritant and
Treat superinfection Treat superinfection allergic triggers
Treat superinfection
Consider systemic anti-
inflammatory agents,
ultraviolet light therapy,
biologics

Adapted from Paller A, Mancini AJ. Chapter 3 – Eczematous Eruptions in Childhood. Hurwitz Clin-
ical Pediatric Dermatology: A Textbook of Skin Disorders of Childhood and Adolescence. 5th edi-
tion. Elsevier; 2015: 38-72e7.

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 Atopic Dermatitis 651

SUMMARY

AD is an extremely common skin condition that significantly decreases quality of life

for both the patient and their caregivers. It is important for the primary care provider
to be knowledgeable on the condition and its diagnosis and management/treatment
options that are available.
Emollients such as creams and ointments are extremely important for the mainte-
nance of patients with AD. For AD flares, TCS are considered first-line treatment. In
moderate and severe AD, topical calcineurin inhibitors can be used in combination
with topical steroids as a steroid-sparing therapy or for areas with thin skin such as
the face and intertriginous areas. Second-line treatment of moderate and severe AD
that can be used is Ultraviolet light B (UVB) phototherapy. For severe AD, dupilumab
is an established and effective treatment option, and Janus kinase (JAK) inhibitors are
also approved and effective for severe AD. Immunosuppressants such as metho-
trexate, azathioprine, mycophenolate mofetil, and cyclosporine can be used for AD
but they all have their own side effect profile.
Routine evaluation of AD should not include blood tests or skin prick tests. Although
secondary infection is the most common complication of AD, without evidence for
clinical infection in patients with AD, oral antibiotics should not be used. Lichenifica-
tion and postinflammatory scarring can be seen in chronic AD. Long-term treatment
of AD should not include systemic corticosteroids.
Noncompliance to treatment regimens effect treatment outcomes and patients.
Every effort should be made to assess the multifactorial issues that contribute to
noncompliance for a patient including cost, patient bias, complex regimens, infre-
quent follow-up, and lack of knowledge. Frequent follow-ups, patient education,
and AD action plans can help improve patient outcomes through adherence.1
Because this is a common and chronic condition, primary care physicians should
be aware of its diagnosis and treatment and be able to set realistic expectations for
these patients.

CLINICS CARE POINTS

 The diagnosis of AD is primarily based on history and physical examination findings. SORT C
 Skincare, emollients, and avoidance of triggers are recommended in all patients for chronic
treatment. SORT A
 TCS are first-line treatments during AD exacerbations. SORT A
 Topic calcineurin inhibitors are useful in patients who have not responded to TCS, and for
maintenance therapy in sensitive areas (eg, face, anogenital, skin folds), sites with steroid-
associated atrophy, and long-term uninterrupted TCS use. SORT A
 Monoclonal antibody treatments are effective in patients with moderate-to-severe AD not
responsive to topical therapies. SORT A

DISCLOSURE

The authors have nothing to disclose.

ACKNOWLEDGMENTS

The authors would like to thank the Penn State Health Milton S. Hershey Medical Cen-
ter Department of Dermatology for the contribution of the photographs for this article.

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652 Clebak et al

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