Atopic Dermatitis

The n e w e ng l a n d j o u r na l of m e dic i n e
Review Article
Allan H. Ropper, M.D., Editor
Atopic Dermatitis
Sonja Ständer, M.D.
A
From the Department of Dermatology topic dermatitis is one of the most prevalent inflammatory
and Center for Chronic Pruritus (KCP), skin diseases. It usually develops in childhood and may persist into adult-
University Hospital Münster, Münster,
Germany. Address reprint requests to Dr. hood; less frequently, it starts in midlife or late life. The disorder is char-
Ständer at the Department of Dermatol- acterized by recurrent, pruritic, localized eczema, often with seasonal fluctua-
ogy and Center for Chronic Pruritus tions. Many patients also have allergic asthma, allergic rhinoconjunctivitis, food
(KCP), University Hospital Münster, Von-
Esmarch-Str. 58, Münster, Germany 48149, allergies, and other immediate hypersensitivity (type 1) allergies. The disease was
or at sonja.staender@ukmuenster.de. described and termed atopic dermatitis in the 1930s, with “atopic” reflecting the
N Engl J Med 2021;384:1136-43. Greek word atopos (“without place”) to indicate the frequent, concomitant occur-
DOI: 10.1056/NEJMra2023911 rence of IgE-mediated hypersensitivity reactions such as asthma.1 Atopic dermati-
Copyright © 2021 Massachusetts Medical Society. tis remains the preferred term for the disorder, but several other labels have been
used, including atopic eczema, neurodermatitis, atopiform dermatitis, and most
commonly, eczema.
Epidemiol o gic Fe at ur e s
The prevalence and incidence of atopic dermatitis have increased over the past
several decades.2,3 The Global Burden of Disease study showed a prevalence of 15
to 20% among children and up to 10% among adults, making atopic dermatitis
the 15th most common nonfatal disease and the skin disorder with the highest
disease burden, in terms of disability-adjusted life-years.4 In a retrospective study,
health care utilization and annual treatment costs were higher for patients with
atopic dermatitis than for matched controls without atopic dermatitis and were
associated with the severity of the disease.5 Both sexes are affected, and the
prevalence varies among races and ethnic groups.6,7 For example, in the United
States, the prevalence is higher among Black children (19.3%) than among White
children (16.1%).8 The increasing prevalence in high-income and industrialized
countries has been tentatively attributed to environmental factors such as exposure
to air pollution and household hygiene products.
Cl inic a l Fe at ur e s
The clinical characteristics of atopic dermatitis vary depending on age, disease
stage, race or ethnic group, and geographic location. Typical acute lesions in White
patients and Black patients are circumscribed patches of eczema (Fig. 1A through
1D); erythema is more frequently violaceous or even invisible in Black patients. The
lesions are characterized by papules, papulovesicles, edema, crusting, and scaling
(Fig. 1E), with hyperpigmentation or hypopigmentation of lesions after healing. In
severe atopic dermatitis, areas of eczema coalesce into larger regions of general-
ized redness of the skin (erythroderma) (Fig. 1F).
In children, eczema may be widespread on the body, involving the head, face,
cheeks (Fig. 1A and 1B), and arms and legs, with frequent involvement of the
1136 n engl j med 384;12 nejm.org March 25, 2021
The New England Journal of Medicine

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Atopic Dermatitis
A B C D
E F G H
Figure 1. Clinical Presentations of Atopic Dermatitis.

Shown are acute eczema in a 14-month-old girl (Panel A), rarefaction of the lateral eyebrows (Hertoghe’s sign) in a 12-year-old boy (Panel B),
leg eczema with violaceous erythema in a child (Panel C), leg eczema in a 4-year-old patient (Panel D), dry skin (xerosis) (Panel E), erythro-
derma in an 85-year-old patient (Panel F), circumscribed and hyperpigmented lichenification overlying eczema in a 7-year-old patient
(Panel G), and eczema herpeticum in a 17-year-old boy with atopic dermatitis (Panel H). Panels C and G are used with permission from
VisualDx.
ventral wrists and trunk.9 In contrast to previous is aggravated by stress, sweating from physical
assumptions, the area of skin covered by a child’s activity or environmental heat, and humidity, as
diaper is also frequently involved.9 With increas- well as from contact with woolen clothes.12
ing age of the patient, lesions tend to be more Pruritus-related scratching induces excoriations,
circumscribed and confined to the arms and bleeding, or the formation of hemorrhagic
legs, mainly the popliteal flexures and the crusts. Persistent scratching leads to lichenifica-
hands, lower legs and feet, neck, and periocular tion (Fig. 1G), as well as prurigo nodularis,
region. The rates of hand and foot dermatitis are which is characterized by generalized, severely
higher among adults than among children.9 itchy nodules.
The appearance of lesions also varies in rela- Patients with atopic dermatitis have a range
tion to race or ethnic group and geographic of associated clinical signs, such as a rarefaction
region.9 Phenotypes that are more common in of the lateral eyebrows (Hertoghe’s sign) (Fig. 1B)
White, Black, or Asian patients have been pro- or increased density and depth of palmar creases
posed,9-11 but these findings need to be con- (hyperlinear palms).9 In most patients (75%),
firmed. For example, lesions on the trunk are areas of dry skin (xerosis) (Fig. 1E) occur, even
found in all races and ethnic groups but are during remission of eczema.9 The presence of
most clearly demarcated and most common in these signs helps establish the diagnosis of
Asians.9-11 atopic dermatitis, but their absence does not rule
Pruritus is a hallmark of atopic dermatitis,9 it out. Atopic dermatitis has a chronic, fluctuat-
and the intensity of the itching broadly corre- ing course. However, the aforementioned clini-
sponds to the severity of the disease.12 Pruritus cal signs and chronic scratching-related lesions,
n engl j med 384;12 nejm.org March 25, 2021 1137

Table 1. Diagnostic Criteria for Atopic Dermatitis According to the American Academy of Dermatology.*
Clinical Features Description

Essential features
Eczema Chronic or relapsing eczema with characteristic morphologic features and age-
specific patterns
Stage Acute, subacute, or chronic
Severity Mild, moderate, or severe
Immunoendotype Th2 cells in Whites and in Blacks, Th2 and Th17 cells in Asians
Pruritus
Important features
Early age at onset Typically between 2 mo and 6 mo of age
Atopy Personal or family history or both, IgE reactivity (elevated total or allergen-specific
serum IgE or both, seen in up to 80% of patients)†
Xerosis
Associated features
Atypical vascular responses Facial pallor or white dermographism, for example
Perifollicular lesions Keratosis pilaris, perifollicular accentuation
Ocular or periorbital changes Hertoghe’s sign
Other regional findings Perioral changes, periauricular lesions, pityriasis alba, hyperlinear palms, ichthyosis
Scratching-related chronic lesions Lichenification, prurigo lesions
Related conditions Bacterial skin infections (impetigo, skin abscesses), viral skin infections (eczema
herpeticum, molluscum contagiosum infection), fungal skin infections (derma-
tophytosis, candidiasis), allergic disorders (asthma, rhinitis, rhinoconjunctivitis,
food allergy), inflammatory bowel disease, rheumatoid arthritis, cardiovascular
disease (debated), quality-of-life impairment (sleep disturbance), anxiety,
depression, suicidality
* The information presented is modified from Eichenfield et al.15 Essential features are those required for the diagnosis
of atopic dermatitis. Important features are those observed in most cases, adding support to the diagnosis. Associated
features suggest the diagnosis but are too nonspecific to be used in defining or detecting atopic dermatitis for clinical
and epidemiologic studies. Th2 denotes type 2 helper T cell, and Th17 type 17 helper T cell.
† Monitoring of IgE levels is not recommended for the routine assessment of disease severity.
such as lichenifications, persist during periodstion of skin lesions, the presence of associated
when eczema is quiescent. clinical signs, and a characteristic medical his-
Chronic and relapsing eczema, severe pruri- tory.15 A list of 23 clinical signs and symptoms
tus, clinical signs, coexisting medical conditions,
of atopic dermatitis was published by Hanifin
and dermatologic complications of atopic der- and Rajka in 1980 and is still used as a bench-
matitis lead to a decreased quality of life for mark in clinical research. The American Acade-
patients and their families. These symptoms re- my of Dermatology has established core features
sult in sleep disruption and decreased productiv-
used to diagnose the disease (Table 1).15 The
ity at work or school, with detrimental effects on
severity of atopic dermatitis can be quantitated
emotional and social life.13 Depression, anxiety,
with the use of multi-item scoring tools such as
and suicidality have been associated with long- the Eczema Area and Severity Index (EASI) and
standing atopic dermatitis.14 the Scoring Atopic Dermatitis (SCORAD) scale;
both are used in practice and in clinical trials.16
The EASI assesses the severity of redness, thick-
Di agnosis
ness, excoriation, and lichenification and the
The clinical diagnosis of atopic dermatitis is percentage of skin involvement in four body ar-
based on the morphologic features and distribu- eas (the head, trunk, arms, and legs). The scores

Atopic Dermatitis
are summed, for an overall score ranging from tis. A risk of cardiovascular diseases has been
0 to 72. An EASI score of 7 or lower is consid- suggested, but estimates of this risk have varied.14,23
ered to indicate mild disease, 8 to 21 moderate
disease, 22 to 50 severe disease, and 51 to 72 very Patho gene sis
severe disease. The SCORAD score takes into
account more lesion types and body areas than Interactions among genetic and environmental
the EASI score and is calculated on the basis of factors, skin barrier dysfunction, microbial im-
the area of skin involved and the severity of red- balance, immune dysregulation, and environmen-
ness, swelling, oozing, crusting, lichenification, tal triggers of skin inflammation play a role in
and dryness, assessed separately for the head and the pathogenesis of atopic dermatitis (Fig. 2).24-26
neck, arms and legs, anterior trunk, back, and Inflammation is thought to be initiated by dis-
genitals. The score includes patient-reported ruption of the epidermal barrier and activation
symptom severity on the basis of two 100-point of epidermal inflammatory dendritic and innate
visual analogue scales, one for sleep loss and lymphoid cells, which attract and interact with
one for pruritus. The total score ranges from invading Th2 cells. The proximate mechanism
0 to 103, with a score of 25 or lower indicating for eczematous lesions is inflammation related
mild disease, 26 to 50 moderate disease, and 51 to dysregulation of Th2 cells.26 Activated T cells
to 103 severe disease.16 release cytokines into the skin, mainly interleu-
kin-4, interleukin-13, and interleukin-31, which
activate downstream Janus kinase (JAK) pathways.
C oe x is t ing C ondi t ions
The cytokines promote inflammation, pruritus,
Patients with atopic dermatitis are at risk for an and the production of antigen-specific IgE by
“atopic march,” the sequential development of activating B cells and plasma cells.
allergic disorders, including food allergies (espe- Studies have identified other immunoendo-
cially in children), allergic rhinitis, rhinoconjunc- types, such as those associated with activation of
tivitis, and asthma.17 This apparent induction of other helper T-cell pathways (i.e., Th1, Th17, and
allergies has been considered to be related to skin Th22), in part associated with race or ethnic
barrier leakage, with penetration of allergens group.11 For example, activation of the Th2 and
and a predisposition of the immune system to Th17 pathways has been reported in Asian pa-
react to the allergens with a response in CD4+ tients, whereas in patients of European ancestry,
type 2 helper T (Th2) cells and subsequent B-cell there is mostly activation of the Th2 pathway.
antibody production. Patients of any age with Activation of the Th1 and Th17 pathways is also
atopic dermatitis are at risk for the development absent in Black patients with atopic dermatitis.8
of bacterial, viral, or fungal skin infections due to These differences may explain the various mani-
skin barrier defects, bacterial skin colonization festations of eczematous lesions according to
(especially by Staphylococcus aureus), and an altered race or ethnic group. However, targeting media-
skin microbiome.18,19 Common skin infections tors and cytokines in the Th2 pathway seems to
in patients with atopic dermatitis are S. aureus– be the most promising individualized approach
induced infections (impetigo and abscesses), to treatment.27-29
herpes simplex virus 1–related eczema herpeticum Among the genetic factors that promote skin
(Fig. 1H), and molluscum contagiosum infec- barrier dysfunction, mutations in the filaggrin
tion.18,20,21 Fungal infections such as candidiasis gene (FLG) have emerged as the most prominent,
of the skin or nails can also occur.19 Because of affecting 30 to 50% of White patients.25 Filag-
skin infections, patients with atopic dermatitis grin, which is produced by upper-layer epider-
have a higher risk of life-threatening systemic in- mal keratinocytes, promotes the production of
fections (e.g., osteomyelitis, septic arthritis, and natural moisturizing factors and the lipid matrix,
endocarditis) than patients who do not have which acts like mortar, keeping keratinocytes in
atopic dermatitis, although such complications are the horny layer together. A loss-of-function mu-
rare.18,22 Other disorders that have been associated tation in FLG leads to disturbed skin barrier
to varying extents with atopic dermatitis are information and increased transepidermal water
flammatory bowel disease and rheumatoid arthri- loss, resulting in dry skin. The lack of skin lipids

Predisposing Factors Triggering Factors Disease State
Persistent Stigmata
Genetic Susceptibility Dry skin (xerosis) Lichenification

Filaggrin mutation
Stress Recurrent Eczema Psychosocial Consequences

Skin barrier disturbance Quality-of-life impairment
Sweating
Immune dysregulation Eczema and Scratching-induced Sleep disturbance
Woolen clothes
Microbial dysbiosis pruritus excoriations Anxiety
Skin allergens
Depression
Environmental Factors
Transient Complications
Temperature
Ultraviolet radiation
Atopic march:
Air pollution
allergic asthma,
Water hardness Bacterial infections
rhinitis, rhino-
Household hygiene Viral infections
conjunctivitis,
food allergy
Figure 2. Predisposing and Triggering Factors for Eczema and Psychosocial Consequences.
The pathogenesis of atopic dermatitis is based on a complex interaction of predisposing factors (genetic and environmental factors,
skin barrier dysfunction, microbial dysbiosis, and immune dysregulation) and triggering factors. All these single factors influence one
another and ultimately lead to a disease state that is composed of acute atopic dermatitis lesions, persistent stigmata, and transient
complications.
also reduces production of epidermal antimicro- Pruritus in atopic dermatitis is based on signal-
bial peptides, leading to increased microbial ing between pruritogens released by keratino-
dysbiosis.25,26 This disturbance in the skin barrier cytes, mast cells, and immune cells (T cells and
makes it possible for allergens to penetrate the eosinophils) and the small sensory-nerve fibers
skin and induces allergic sensitization. in the skin. The pruritogens comprise Th2 cyto-
Environmental factors play a role in a predis- kines (especially interleukin-4, -13, and -31),
position to, and worsening of, atopic dermatitis. thymic stromal lymphopoietin (an epithelium-
Established factors include extreme tempera- derived proinflammatory cytokine), histamine,
tures, ultraviolet radiation exposure, air pollu- proteases, and neuropeptides. These pruritogens
tion exposure (through activation of the epider- bind to receptors on sensory C-nerve fibers and
mal aryl hydrocarbon receptor), increased water Aδ-nerve fibers in the epidermis and dermis,
hardness, and increased frequency of household which sense pruritus and pain. Patients with
product use.24 The last of these factors refers to atopic dermatitis frequently report painful sen-
the “hygiene hypothesis,” which proposes that sations, including burning and stinging, in addi-
increasing cleanliness leads to the decreasing tion to pruritus, in eczematous skin regions.30
incidence of infections in Western countries, The majority of pruritogens bind to nonhista-
which is associated with the increasing inci- minergic nerve fibers. A small subgroup (<5%)
dence of allergic and autoimmune diseases, of skin C-nerve fibers are histamine-sensitive;
including atopic dermatitis.24 A study of the skin however, blocking histamine 1 receptors with
microbiome in patients with atopic dermatitis antihistamines has not led to control of pruri-
has shown that it is predominantly colonized by tus. Accordingly, guidelines do not recommend
pathogenic S. aureus.24 This shift in the microbi- histamine 1 receptor antihistamines for pruritus
ome, together with the reduced production of control.31
epidermal antimicrobial peptides, may have clini- Pruritogens are released not only by inflam-
cal implications for the development of impetigo mation but also by scratching. This might result
and skin abscesses in areas of eczema. in hypersensitization of nerve fibers due to the

Atopic Dermatitis
Table 2. Therapeutic Strategies for Atopic Dermatitis in Children and Adults.*
Stage of Atopic Dermatitis

Strategy Measures or Agent (Age Limitation)
General
Decolonization Education about personal daily skin care and hygiene All stages
practices, frequent hand washing with soap and
water, daily bathing or showering, avoiding reuse or
sharing of personal hygiene items that contact the
skin, avoiding contamination of topical medications
and moisturizers, environmental hygiene measures
(cleaning of surfaces, equipment, devices), wearing
silver-coated clothing (for its antibacterial properties)
Therapy for skin infection, if necessary Depends on the infection (e.g., topical disinfectants, All stages
systemic antibiotics, systemic acyclovir, removal of
molluscum contagiosum)
Basic wound care Covering open or weeping wounds All stages
Avoidance of triggers Reducing allergen exposure, for example All stages
Education Using behavioral therapy techniques, relaxation tech- All stages
niques, educational measures for affected adults and
parents of affected children
Topical therapies
Emollients Moisturizers with a hydrophilic base, emollients with All stages (emollients with
urea, bath oils, shower gels, wet-wrap therapy urea not used in children
(increases penetration of topical agents, decreases ≤5 yr)
water loss)
Antipruritic agents containing emollients Menthol and menthol derivates, polidocanol, or lidocaine All stages
Immunosuppressants Glucocorticoids, calcineurin inhibitors (pimecrolimus, All stages; choice of gluco-
tacrolimus), phosphodiesterase-4 inhibitor corticoid class depends
(crisaborole) on patient’s age and se-
verity of atopic dermatitis
Topical therapies, not yet approved
JAK inhibitors Cerdulatinib (pan-JAK, SYK), delgocitinib (pan-JAK), rux-
olitinib (JAK1 and JAK2), tofacitinib (JAK1 and JAK3)†
Aryl hydrocarbon receptor inhibitor Tapinarof
Systemic therapies
Ultraviolet phototherapy Narrow-band UVB (311–313 nm), UVA1 (340–400 nm) Moderate (rarely used in pre-
pubertal children)
Immunosuppressants (oral or subcutaneous) Azathioprine, glucocorticoids (only short courses), cyclo- Severe; should be main-
sporine, methotrexate tained during coronavi-
rus pandemic39
Biologic therapy (subcutaneous) Interleukin-4Rα antagonist (dupilumab) Severe (≥6 yr)
JAK inhibitor (oral) Baricitinib (JAK1 and JAK2)† Moderate to severe (adults)
Potential systemic therapies (not yet approved)
JAK inhibitors (oral) Abrocitinib (JAK1), gusacitinib (pan-JAK, SYK), tofacitinib
(JAK1 and JAK3), upadacitinib (JAK1)†
Interleukin-13 receptor antibodies (subcutaneous) Lebrikizumab, tralokinumab
Interleukin-22 receptor antibody (intravenous) Fezakinumab
Interleukin-31 receptor A antibody (subcutaneous) Nemolizumab
Interleukin-33 receptor A antibody (intravenous) Etokimab
Phosphodiesterase-4 inhibitor (oral) Roflumilast
* Information about therapeutic strategies is from Sidbury et al.,35 Wollenberg et al.,36 Wollenberg et al.,37 and Eichenfield et al.38 JAK denotes
Janus kinase, SYK spleen tyrosine kinase, UVA1 ultraviolet A1, and UVB ultraviolet B.
† Targets of JAK inhibitors are shown in parentheses.

itch–scratch cycle, a hypothesis that is consistent tive test, systemic immunosuppressive therapy
with reports by patients of increased pruritus can be reinitiated after recovery from Covid-19.40
after scratching to relieve itch.32,33 The interleukin- There has been progress in the development
4α receptor subunit is expressed on pruritus- of Th2-targeted therapies. Promising agents are
sensing nerve fibers and may hypersensitize monoclonal interleukin-4, -13, -22, and -31 re-
them to pruritus on continuous stimulation with ceptor antibodies, phosphodiesterase-4 inhibi-
interleukin-4.34 This might partly explain the tors, and JAK inhibitors (topical and systemic),
itch–scratch cycle and the rapid benefit from most of which have been tested in phase 2–3
inhibition of downstream JAK1 and JAK2 and trials. In a comparative study, the interleukin-4
the interleukin-4α receptor pathways. antibody dupilumab and the JAK inhibitor
abrocitinib both were associated with reductions
in signs and symptoms of atopic dermatitis as
T r e atmen t
compared with placebo; abrocitinib was superior
Therapy for atopic dermatitis is selected accord- to dupilumab in reduction of itch at 2 weeks, but
ing to the clinical stage of disease (mild, moder- otherwise the two drugs had similar outcomes.41
ate, or severe), the extent of body-surface area Adverse effects such as skin infections or wors-
involved, age, coexisting conditions and medica- ening of asthma necessitate careful evaluation of
tions being taken by the patient, the severity of the future use of these new therapies in sensitive
pruritus, the degree to which quality of life is populations (children) and in patients with typi-
impaired, and the goals of the patient.35,36 For all cal complications of atopic dermatitis. For ex-
disease stages, including eczema-free intervals, ample, many patients have long-term, function-
general measures such as the use of emollients ally impairing conjunctivitis with dupilumab
(with or without antipruritic agents) and avoid- therapy, especially when it is combined with
ance of infections and trigger factors are advised seasonal allergic conjunctivitis. JAK inhibitors
(Table 2). When eczema occurs, the use of topi- carry a risk of thromboembolism and cancer42
cal immunosuppressive therapies is recommend- and may be associated with respiratory tract in-
ed as a first approach. Crisaborole, a phosphodi- fections, herpes zoster infection, headache, nau-
esterase-4 inhibitor, has recently been approved sea, diarrhea, and a decrease in the white-cell
for treatment of atopic dermatitis in the United count.43
States, but it is not available in all countries. For
moderate eczema, ultraviolet phototherapy can C onclusions
be applied, but it is not used in children and
young adults because of the potential for the Atopic dermatitis is a burdensome skin disease,
development of skin cancer with long-term use. particularly in children. Geographic and race or
For severe atopic dermatitis, several conventional ethnic group variations, as well as a complex
systemic immunosuppressants such as glucocor- pathogenesis, have impeded the development of
ticoids, cyclosporine, or methotrexate have been targeted therapies. Pruritus associated with the
used. However, these agents do not target spe- disorder affects quality of life and is a focus of
cific points of immune dysregulation in atopic treatment and a determinant of treatment effi-
dermatitis and may result in severe adverse cacy, as well as a primary concern in the devel-
events, including liver and kidney dysfunction. opment of new medications to treat atopic der-
Regarding the coronavirus disease 2019 matitis.
(Covid-19) pandemic, most dermatologic soci- Dr. Ständer reports receiving lecture fees from Beiersdorf
eties, including the American Academy of Der- and Eli Lilly, lecture fees and consulting fees from Galderma
and Sanofi R&D, and consulting fees from Kiniksa and Pfizer.
matology, recommend that patients with atopic No other potential conflict of interest relevant to this article
dermatitis continue to receive systemic immuno- was reported.
suppressive therapy unless they have a positive Disclosure forms provided by the author are available with the
full text of this article at NEJM.org.
test for severe acute respiratory syndrome coro- I thank the American Journal Experts for assistance in editing
navirus 2 (SARS-CoV-2). For patients with a posi- an earlier version of the manuscript.

Atopic Dermatitis
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The n e w e ng l a n d j o u r na l of m e dic i n e

Allan H. Ropper, M.D., Editor

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The New England Journal of Medicine

Figure 1. Clinical Presentations of Atopic Dermatitis.

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Clinical Features Description

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The New England Journal of Medicine

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Predisposing Factors Triggering Factors Disease State

Genetic Susceptibility Dry skin (xerosis) Lichenification

Stress Recurrent Eczema Psychosocial Consequences

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The New England Journal of Medicine

Table 2. Therapeutic Strategies for Atopic Dermatitis in Children and Adults.*

Stage of Atopic Dermatitis

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