Atopic Dermatitis 

Updated: Mar 13, 2019
Author: Brian S Kim, MD, MTR, FAAD; Chief Editor: William D James, MD 

Overview

Practice Essentials

Atopic dermatitis (AD) is a chronic, pruritic inflammatory skin disease (see image below) of unknown origin that usually starts in early infancy, but also affects a substantial number of adults. AD is commonly associated with elevated levels of immunoglobulin E (IgE). That it is the first disease to present in a series of allergic diseases—including food allergy, asthma, and allergic rhinitis, in order—has given rise to the “atopic march” theory, which suggests that AD is part of a progression that may lead to subsequent allergic disease at other epithelial barrier surfaces.[1, 2]

Flexural involvement in childhood atopic dermatiti Flexural involvement in childhood atopic dermatitis.

See All About Allergies: Be Ready for Spring, a Critical Images slideshow, to help identify a variety of allergens and symptoms.

Signs and symptoms

Incessant pruritus is the only symptom of AD. The disease typically has an intermittent course with flares and remissions occurring, often for unexplained reasons.

Primary physical findings include the following:

  • Xerosis

  • Lichenification

  • Eczematous lesions

The eczematous changes and its morphology are seen in different locations, depending on the age of the patient (ie, infant, child, or adult).

The following is a constellation of symptoms and features commonly seen in AD:

  • Pruritus

  • Early age of onset

  • Chronic and relapsing course

  • IgE reactivity

  • Peripheral eosinophilia

  • Staphylococcus aureus superinfection

  • Personal history of asthma or hay fever or a history of atopic diseases in a first-degree relative

See Clinical Presentation for more detail.

Diagnosis

The following features should be considered in the diagnosis of AD in accordance with the American Academy of Dermatology (AAD) 2014 Guidelines[3] :

Essential features (must be present) are as follows:

  • Pruritus
  • Eczema (acute, subacute, chronic): (1) Typical morphology and age-specific patterns (facial/neck/extensor involvement in children, flexural involvement in any age group, sparing the groin and axillary regions); (2) chronic or relapsing history

Important features (supports the diagnosis) are as follows:

  • Early age of onset

  • Atopy: (1) Personal and/or family history; (2) IgE reactivity

  • Xerosis

Associated features (nonspecific but suggest the diagnosis of AD) are as follows:

  • Atypical vascular responses (eg, facial pallor, delayed blanch response)

  • Keratosis pilaris/pityriasis alba/hyperlinear palms/ichthyosis

  • Ocular/periorbital changes

  • Other regional findings (eg, perioral changes/periauricular lesions)

  • Perifollicular accentuation/lichenification/prurigo

Exclusionary conditions (conditions that should be excluded) are as follows:

  • Scabies
  • Seborrheic dermatitis
  • Contact dermatitis
  • Ichthyoses
  • Cutaneous T-cell lymphoma
  • Psoriasis
  • Photosensitivity dermatoses
  • Immune deficiency diseases
  • Erythroderma of other causes

Additional considerations in the diagnosis of AD are as follows:

  • No reliable biomarker exists for the diagnosis of AD

  • Laboratory testing is seldom necessary but a complete blood cell count can be useful to exclude immune deficiency; an IgE level can be helpful to confirm an atopic pattern; a swab of skin can be helpful to identify S aureus superinfection

  • Allergy and radioallergosorbent testing is of little value

  • Biopsy shows an acute, subacute, or chronic spongiotic dermatitis pattern that is nonspecific but can be helpful to rule out other conditions (eg, cutaneous T-cell lymphoma)

See Workup for more detail.

Management

Agents typically used to treat AD include the following:

  • Moisturizers: Petrolatum, Aquaphor, or newer agents such as Atopiclair and Mimyx

  • Topical steroids (current mainstay of treatment; commonly used in conjunction with moisturizers): Hydrocortisone, triamcinolone, or betamethasone; ointment bases are generally preferred, particularly in dry environments

  • Broad immunomodulators: Tacrolimus and pimecrolimus (calcineurin inhibitors; generally considered second-line therapy)

  • Targeted biologic therapies: Dupilumab (anti-IL-4Ra monoclonal antibody)

Other treatments that have been tried include the following:

  • Ultraviolet (UV)-A, UV-B, a combination of both, psoralen plus UV-A (PUVA), or UV-B1 (narrow-band UV-B) therapy

  • In severe disease, methotrexate, azathioprine, cyclosporine, and mycophenolate mofetil[4]

  • Everolimus[5, 6]

  • Probiotics

  • Antibiotics for clinical infection caused by S aureus or flares of disease[7]

  • Intranasal mupirocin ointment and diluted bleach (sodium hypochlorite) baths

Nonmedical measures that may be helpful include the following:

  • Using soft clothing (eg, cotton) next to the skin; wool products should be avoided

  • Maintaining mild temperatures, particularly at night

  • Using a humidifier (cool mist) in both winter and summer

  • Washing clothes in a mild detergent, with no bleach or fabric softener

  • Avoiding specific foods as appropriate if there is concomitant food allergy

See Treatment and Medication for more detail.

Background

Atopic dermatitis (AD) is a pruritic disease of unknown origin that usually starts in early infancy (an adult-onset variant is recognized); it is characterized by pruritus, eczematous lesions, xerosis (dry skin), and lichenification (thickening of the skin and an increase in skin markings).

AD may be associated with other atopic (immunoglobulin E [IgE]–associated) diseases (eg, acute allergic reaction to foods, asthma, urticaria, and allergic rhinitis).[8] AD has enormous morbidity, and the incidence and prevalence appear to be increasing. Further, AD is the first disease to present in a series of allergic diseases such as food allergy, asthma, and allergic rhinitis (in order), provoking the “atopic march” theory, which suggests that early or severe AD and cutaneous sensitization to environmental allergens may lead to subsequent allergic disease at other epithelial barrier surfaces (eg, gastrointestinal or respiratory tract). This hypothesis is supported by cross-sectional and longitudinal studies.[1]

Pathophysiology

Despite recent advances in the understanding of the genetics of atopic dermatitis (AD), the pathophysiology remains poorly defined. Two main hypotheses have been proposed regarding the development of inflammation that leads to AD. The first suggests a primary immune dysfunction resulting in IgE sensitization, allergic inflammation, and a secondary epithelial barrier disturbance. The second proposes a primary defect in the epithelial barrier leading to secondary immunologic dysregulation and resulting in inflammation.

In healthy individuals, balance exists between important subsets of T cells (eg, Th1, Th2, Th17, Th22). The primary immune dysfunction hypothesis invokes an imbalance in the T cell subsets, with Th2 cells predominating; this results in the production of type 2 cytokines such as interleukin (IL)–4, IL-5, and IL-13, causing an increase in IgE from plasma cells. Later, in persons with chronic AD, the Th1 cells have been shown to predominate. More recently, Th17 cells have been found to be elevated in patients with AD.[9] Although primarily considered a Th2 cell‒associated cytokine-mediated disease, the precise contributions of Th1 and Th17 cell responses remain to be fully defined.

In addition to the role of T and B cells in AD, other innate immune cells have also been implicated in the pathogenesis of AD, including eosinophils and mast cells.[10, 11] More recently, basophils and newly identified innate immune cells called group 2 innate lymphoid cells (ILC2s) have been shown to underlie the pathogenesis of AD.[12, 13, 14, 15, 16] Together, basophils and ILC2s are critical sources of the type 2 cytokines IL-4, IL-5, and IL-13.[12, 13] Further, these cells appear to be potently regulated by a family of epithelial cell‒derived cytokines directly released from damaged keratinocytes, including thymic stromal lymphopoietin (TSLP), IL-25, and IL-33.[17] Taken together, these studies highlight a new paradigm in which, in addition to classical adaptive Th2 cells, innate type 2 immune cells play critical roles in the etiology of AD through interactions with epidermal-derived cytokines.

In terms of AD-associated itch, Th2 cells are known to be significant sources of the itch-inducing cytokine or pruritogen IL-31.[18] Emerging clinical trials data indicate that blocking this pathway may be a key mechanism by which atopic itch can be treated clinically. Additionally, a 2017 study identified that neuronal, rather than immune, signaling of the type 2 cytokines IL-4 and IL-13 critically regulate AD-associated itch.[19] Indeed, the dual IL-4 and IL-13 blocker, dupilumab, has emerged as a highly effective treatment for AD, which received FDA approval in March of 2017. Thus, blocking cytokine-nerve interactions with targeted biologic therapies has emerged as a novel therapeutic strategy in AD.

The epidermal barrier dysfunction hypothesis suggests that AD patients develop AD as a result of skin barrier defects that allow for the entry of antigens, resulting in the production of inflammatory cytokines. Some authors question whether such antigens can also be absorbed from the gut (eg, from food) and/or the lungs (eg, from house dust mites). Xerosis and ichthyosis are known to be associated signs in many AD patients. Clinically, 37-50% of people with ichthyosis vulgaris have atopic disease and up to 37% of people with AD have clinical evidence of ichthyosis vulgaris. Mutations in the gene encoding filaggrin, a key epidermal barrier protein, cause ichthyosis vulgaris and are the strongest known genetic risk factors for the development of AD.[20, 21]  

Further, filaggrin mutations are associated with early-onset AD and with airway disease in the setting of AD.[22] One mechanism by which filaggrin defects may influence inflammation is by the release of epithelial cell‒derived cytokines, including TSLP, IL-25, and IL-33, which are all known to be up-regulated in the context of AD.[23, 24, 25, 26] TSLP has been shown to be a potent promoter of basophil and ILC2 responses in the skin, while IL-25 and IL-33 preferentially elicit ILC2s.[12, 13, 16] Although filaggrin is strongly linked to AD, mutations are only found in 30% of European patients, begging the question of whether other genetic variants may also be responsible for some of the findings in the pathogenesis of AD. Indeed, genetic variants of TSLP have been shown to interact with mutations in filaggrin to influence AD disease persistence in patients.[27]

In AD, transepidermal water loss is increased. Whether the primary immune dysregulation causes secondary epithelial barrier breakdown or primary epithelial barrier breakdown causes secondary immune dysregulation that results in disease remains unknown. However, given the fact that filaggrin is critical for epithelial integrity, it is now thought that loss of filaggrin function leads to increased transepidermal penetration of environmental allergens, increasing inflammation and sensitivity and potentially leading to the atopic march.[28]

Etiology

Genetics[29, 30]

A family history of atopic dermatitis (AD) is common. The strongest known genetic risk factor for developing AD is the presence of a loss-of-function mutation in filaggrin. More recently, genome-wide association studies (GWAS) have identified susceptibility loci at 11q13.5 in European populations, at 5q22.1 and 1q21.3 in a Chinese Han population, and at 20q13.33 in both Chinese Han and German populations. A recent meta-analysis of GWAS studies in European populations identified SNPs rs479844 near OVOL1, rs2164983 near ACTL9, and rs2897442 in intron 8 of KIF3A. Many of these loci contain genes that encode proteins involved in epidermal proliferation and differentiation or inflammatory cytokines.

Infection

The skin of patients with AD is colonized by S aureus. Clinical infection with S aureus often causes a flare of AD, and S aureus has been proposed as a cause of AD by acting as a superantigen. Similarly, superinfection with herpes simplex virus can also lead to a flare of disease and a condition referred to as eczema herpeticum.

Hygiene

The hygiene hypothesis is touted as a cause for the increase in AD. This attributes the rise in AD to reduced exposure to various childhood infections and bacterial endotoxins.[31, 32]

Climate

AD flares occur in extremes of climate. Heat is poorly tolerated, as is extreme cold. A dry atmosphere increases xerosis. Sun exposure improves lesions, but sweating increases pruritus. These external factors act as irritants or allergens, ultimately setting up an inflammatory cascade.

Food antigens

The role of food antigens in the pathogenesis of AD is controversial, both in the prevention of AD and by the withdrawal of foods in persons with established disease. Because of the controversy regarding the role of food in AD, most physicians do not withdraw food from the diet. Nevertheless, acute food reactions (urticaria and anaphylaxis) are commonly encountered in children with AD.

Probiotics[33]

The role of probiotics in the diet of patients with AD remains controversial.

Aeroallergens

A role for aeroallergens and house dust mites has been proposed, but this awaits further corroboration.

Tobacco

A study by Lee et al suggested a correlation between early and/or current exposure to cigarette smoking and adult onset of AD.[34] The study also determined that exposure to tobacco smoke in childhood is linked to adult onset of AD.

Epidemiology

Frequency

United States

The prevalence rate for atopic dermatitis (AD) is 10-12% in children and 0.9% in adults. More recent information examining physician visits for AD in the United States from 1997-2004 estimates a large increase in office visits for AD occurred. In addition, blacks and Asians visit more frequently for AD than whites. Note that this increase involves all disease under the umbrella of AD and it has not been possible to allocate which type has increased so rapidly.[35]

International

The prevalence rate of AD is rising, and AD affects 15-30% of children and 2-10% of adults. This figure estimates the prevalence in developed countries. In China and Iran, the prevalence rate is approximately 2-3%. The frequency is increased in patients who immigrate to developed countries from underdeveloped countries.[36]

Race

AD affects persons of all races. Immigrants from developing countries living in developed countries have a higher incidence of AD than the indigenous population, and the incidence is rapidly rising in developed countries.

Sex

The male-to-female ratio for AD is 1:1.4.

Age

In 85% of cases, AD occurs in the first year of life; in 95% of cases, it occurs before age 5 years. The incidence of AD is highest in early infancy and childhood. The disease may have periods of complete remission, particularly in adolescence, and may then recur in early adult life.

In the adult population, the rate of AD frequency is 3% or higher, but onset may be delayed until adulthood.

Prognosis

Most patients improve; this can occur at any age. While the frequency of atopic dermatitis (AD) is as high as 20% in childhood,[37] it is 0.9% in adults. One third of patients develop allergic rhinitis. One third of patients develop asthma.

In a longitudinal study of 7157 children and adolescents with AD from the Pediatric Eczema Elective Registry, researchers found that symptoms of mild to moderate AD are likely to persist into the teen years or beyond.[38, 39, 40]

Approximately two-thirds of the patients were followed for at least 2 years and the rest were followed for at least 5 years. From ages 2 to 26 years, more than 80% of patients reported having continued symptoms and/or use of topical medications to control symptoms. By age 20, approximately half of the patients had experienced at least one 6-month symptom- and medication-free period. Living in southern states, having a relative with an atopic illness, and exposure to pollen, wool, pets, cigarettes, fumes, some foods or drinks, and soaps/detergents were linked to persistent symptoms.[38, 39, 40]

Mortality/morbidity

Incessant itch and work loss in adult life is a great financial burden. A number of studies have reported that the financial burden to families and government is similar to that of asthma, arthritis, and diabetes mellitus. In children, the disease causes enormous psychological burden to families and loss of school days. Mortality due to AD is unusual.

Kaposi varicelliform eruption (eczema herpeticum) is a well-recognized complication of AD. It usually occurs with a primary herpes simplex infection, but it may also be seen with recurrent infection. Vesicular lesions usually begin in areas of eczema and spread rapidly to involve all eczematous areas and healthy skin. Lesions may become secondarily infected. Timely treatment with acyclovir ensures a relative lack of severe morbidity or mortality.

Another cause of Kaposi varicelliform eruption is vaccination with vaccinia for the prevention of small pox, but because this is no longer mandatory, patients with AD do not develop the sequelae of eczema vaccinatum that has been seen in the past. It was usually contracted by the patient from the vaccination of themselves or their close relatives. This condition had a high mortality rate (up to 25%). In the current climate of threats of bioterrorism, vaccination may once again become necessary, and physicians should be aware of eczema vaccinatum in this setting.

Note that chickenpox vaccine does not carry the same risk as herpes simplex and vaccinia.

Bacterial infection with S aureus or Streptococcus pyogenes is not infrequent in the setting of AD. The skin of patients with AD is colonized by S aureus. Colonization does not imply clinical infection, and physicians should only treat patients with clinical infection. The emergence of methicillin-resistant S aureus (MRSA) may prove to be a problem in the future in these patients. Eczematous and bullous lesions on the palms and soles are often infected with beta-hemolytic group A Streptococcus.

Urticaria and acute anaphylactic reactions to food occur with increased frequency in patients with AD. The food groups most commonly implicated include peanuts, eggs, milk, soy, fish, and seafood. In studies in peanut-allergic children, the vast majority were atopic.

Latex and nickel allergy is more common in patients with AD than in the general population.

Of AD patients, 30% develop asthma and 35% have nasal allergies.

Patient Education

Frequently reinforce treatment and maintenance regimens with patients. Advise patients to contact the National Eczema Association for Science and Education at 4460 Redwood Hwy, Suite 16-D, San Rafael, CA 94903-1953.

Inform patients that treatment does not produce cure but good control can be achieved

Show videos to patients that show how to apply medication and that discuss the role of moisturization. A randomized controlled trial by Armstrong et al demonstrated improved patient education and clinical outcome in patients who watched a video on atopic dermatitis (AD) compared with those who received a pamphlet.[41] The study emphasized the importance of lifestyle changes and daily care in the successful treatment of AD.

For patient education resources, see Eczema.

 

Presentation

History

Incessant pruritus is the central and most debilitating symptom of atopic dermatitis (AD); children often scratch themselves uncontrollably. Although pruritus may be present in the first few weeks of life, parents become more aware of the itch as the itch-scratch cycle matures when the patient is aged approximately 3 months. The disease typically has an intermittent course with flares and remissions occurring, often for unexplained reasons.

Data from a study by Garmhausen et al indicate that the natural course of the disease can be divided into subgroups with different clinical features.[42] The most frequent course type (31.1% of the sample) was characterized by an early disease onset (before age 2 years) and a chronic persisting course through adulthood.

Of the 607 patients in the study, 85.7% were categorized into 5 main different course types.[42] The greatest differences in the number of sensitizations, total immunoglobulin E serum levels, and predilection of skin lesions were seen between subjects with early-onset disease and a chronic persisting course until adulthood and those with late-onset AD developing after age 20 years.

AD patients often present with a personal or family history of type I hypersensitivity, allergic rhinitis, and asthma.

Essential historical features (must be present) are as follows:

  • Pruritus
  • Chronic or relapsing history of disease

Important historical features (supports the diagnosis) are as follows:

  • Early age of onset

  • Atopy: Personal and/or family history

Physical Examination

Perform a routine skin examination to look for features associated with atopic dermatitis (AD). In younger patients, examine for dermatographism as many patient may have acute urticaria in the setting of AD.

Primary findings of AD include xerosis, lichenification, and eczematous lesions. Excoriations and crusting are common and some patients exhibit prurigo nodularis‒like lesions. The eczematous changes and its morphology are seen in different locations depending on the age of the patient.

Essential features (must be present) are as follows:

  • Pruritus
  • Eczema (acute, subacute, chronic): (1) Typical morphology and age-specific patterns (facial/neck/extensor involvement in children, flexural involvement in any age group, sparing the groin and axillary regions); (2) chronic or relapsing history

Important features (supports the diagnosis) are as follows:

  • Early age of onset

  • Atopy: (1) Personal and/or family history; (2) IgE reactivity

  • Xerosis

Associated features (nonspecific but suggest the diagnosis of AD) are as follows:

  • Atypical vascular responses (eg, facial pallor, delayed blanch response)
  • Keratosis pilaris/pityriasis alba/hyperlinear palms/ichthyosis

  • Ocular/periorbital changes

  • Other regional findings (eg, perioral changes/periauricular lesions)

  • Perifollicular accentuation/lichenification/prurigo

Infancy

AD is usually noticed soon after birth. Xerosis occurs early and often involves the whole body; the diaper area is usually spared.

The earliest lesions affect the creases (antecubital and popliteal fossae), with erythema and exudation. Over the following few weeks, lesions usually localize to the cheeks, the forehead and scalp, and the extensors of the lower legs; however, they may occur in any location on the body, usually sparing the diaper area and the nose. Lesions are ill-defined, erythematous, scaly, and crusted (eczematous) patches and plaques.

Lichenification is seldom seen in infancy. A typical presentation is shown in the image below.

Typical atopic dermatitis on the face of an infant Typical atopic dermatitis on the face of an infant.

Childhood

Xerosis is often generalized. The skin is flaky and rough.

Lichenification is characteristic of childhood AD. It signifies repeated rubbing of the skin and is seen mostly over the folds, bony protuberances, and forehead.

Lesions are eczematous and exudative. Pallor of the face is common; erythema and scaling occur around the eyes. Dennie-Morgan folds (ie, increased folds below the eye) are often seen. Flexural creases, particularly the antecubital and popliteal fossae, and buttock-thigh creases are often affected. See the image below.

Flexural involvement in childhood atopic dermatiti Flexural involvement in childhood atopic dermatitis.

Excoriations and crusting are common. The crusting with AD should not be confused with infection because both may manifest oozing and crusting.

Children with AD are likely to experience symptoms into their teens and beyond.[38, 39, 40]

Adulthood

Lesions become more diffuse with an underlying background of erythema. The face is commonly involved and is dry and scaly. Xerosis is prominent. Lichenification may be present. A brown macular ring around the neck is typical but not always present. It represents localized deposition of amyloid. See the image below.

Dirty neck sign in chronic atopic dermatitis. Dirty neck sign in chronic atopic dermatitis.

Diagnostic criteria

Until Hanifin and Rajka[43] developed diagnostic criteria for the diagnosis of AD in 1980, no standardized methods were available to make the diagnosis. Since then, numerous other experts have developed different criteria suitable for their own environment, and varying with age. The original criteria of Hanifin and Rajka have been modified many times. Efforts to develop practical clinical criteria have not been successful, and those available are not suitable for all geographic areas and age groups. The lack of a good biomarker for diagnosing the disease is an enormous obstacle to the study of AD.

Exclusionary conditions (conditions that should be excluded) are as follows:

  • Scabies
  • Seborrheic dermatitis
  • Contact dermatitis
  • Ichthyoses
  • Cutaneous T-cell lymphoma
  • Psoriasis
  • Photosensitivity dermatoses
  • Immune deficiency diseases
  • Erythroderma of other causes
 

DDx

Diagnostic Considerations

Atopic dermatitis (AD) is indistinguishable from other causes of dermatitis. In infancy, the most common difficulty is distinguishing it from seborrheic dermatitis (SD). This entity is not seen with the same frequency as a decade ago. Both AD and SD are associated with cradle cap (a retention hyperkeratosis) found on the vertex of the scalp, which is greasy and yellow in individuals with SD and dry and crusted in individuals with AD. Other areas of involvement in SD are the intertriginous areas and diaper area; erythema and a greasy scale can be seen over the eyebrows and the sides of the nose. In AD, xerosis of the skin and pruritus occur, which are not usually features of SD. Both conditions should be distinguished from psoriasis.

Scabies manifests in infancy or childhood as a pruritic eruption. Other members of the family are usually itchy, and the primary sites of involvement are moist, warm areas. The eruption is polymorphic with a dermatitis, nodules, urticaria, and 6-10 burrows. Pustules on the hands and feet are almost diagnostic of scabies in infancy. Facial involvement is rare, and xerosis does not occur.

Allergic contact dermatitis from nickel in infants and children is sometimes difficult to distinguish from AD. A central area of dermatitis on the chest from nickel snaps in undershirts or around the umbilicus from snaps in jeans is helpful for making the diagnosis, although a dermatitic eruption may occur as an id reaction in other areas, particularly the antecubital fossae. Xerosis and facial involvement are absent. AD usually starts earlier than contact dermatitis.

Infants with a severe itch and generalized dermatitis in the setting of recurrent infections should be investigated for evidence of an immunodeficiency. Failure to thrive and repeated infections help distinguish the eruption from AD. In Wiskott-Aldrich syndrome, bleeding may be prominent with the dermatitis, because of the associated thrombocytopenia. A population-based cohort study by Schmitt J et al. suggested a possible link to the development of mental health issues in patients who experienced infant eczema and concurrent sleeping problems.[44]

In older children, mycosis fungoides (a form of T-cell lymphoma) often presents with hypopigmented patches associated with a dermatitis. This entity is being recognized with increased frequency as physicians become more aware of the disease, and it is sometimes difficult to distinguish between the 2 entities.

Tinea corporis usually manifests as a single lesion, but inappropriate treatment with steroids may cause a widespread dermatitis. Facial involvement, the presence of xerosis, the age of appearance, and an early onset (in AD) help distinguish between the two conditions.

One report describes localized varicella lesions developing in preexisting infectious or inflammatory dermatitis; no clear evidence of full-blown chickenpox was seen. The authors suggest viral testing may be needed if vesicular or ulcerative lesions develop within a preexisting dermatitis.[45]

Differential Diagnoses

 

Workup

Laboratory Studies

No biomarker for the diagnosis of atopic dermatitis (AD) is known. Laboratory testing is seldom necessary.

A swab of infected skin may help with the isolation of a specific organism (eg, Staphylococcus or Streptococcus) and antibiotic sensitivity. Allergy and radioallergosorbent testing is of little value.

A swab for viral polymerase chain reaction (PCR) may help identify superinfection with herpes simplex virus and identify a diagnosis of eczema herpeticum.

A complete blood cell count for thrombocytopenia helps exclude Wiskott-Aldrich syndrome, and testing to rule out other immunodeficiencies may be helpful. This also helps identify peripheral eosinophilia, which may help to support the diagnosis.

A serum IgE level can be helpful to support the diagnosis.

Scraping to exclude tinea corporis is occasionally helpful.

Histologic Findings

Biopsy shows characteristic acute, subacute, or chronic spongiotic dermatitis, but findings are not specific.

 

Treatment

Medical Care

Patients with atopic dermatitis (AD) do not usually require emergency therapy, but they may visit the emergency department for treatment of acute flares caused by eczema herpeticum and bacterial infections.

Moisturization in atopic dermatitis

Depending on the climate, patients usually benefit from 5-minute, lukewarm baths followed by the application of a moisturizer such as white petrolatum. Frequent baths with the addition of emulsifying oils (1 capful added to lukewarm bath water) for 5-10 minutes hydrate the skin. The oil keeps the water on the skin and prevents evaporation to the outside environment. In infants, 3 times a day is not a great burden; in adults, once or twice a day is usually all that can be achieved. Leave the body wet after bathing.

Advise patients to apply an emollient such as petrolatum or Aquaphor all over the body while wet, to seal in moisture and allow water to be absorbed through the stratum corneum. The ointment spreads well on wet skin. The active ingredient should be applied before the emollient. Newer emollients such as Atopiclair and Mimyx have been advocated as having superior results, but they are expensive and need further evaluation.

Topical steroids in atopic dermatitis

Topical steroids are currently the mainstay of treatment. In association with moisturization, responses have been excellent.

Ointment bases are preferred, particularly in dry environments.

Initial therapy consists of hydrocortisone 1% powder in an ointment base applied 2 times daily to lesions on the face and in the folds.

A midstrength steroid ointment (triamcinolone or betamethasone valerate) is applied 2 times daily to lesions on the trunk until the eczematous lesions clear.

Steroids are discontinued when lesions disappear and are resumed when new patches arise.

Flares may be associated with seasonal changes, stress, activity, staphylococcal infection, or contact allergy.

Contact allergy is rare but accounts for increasing numbers of flares. These are seen mostly with hydrocortisone.

The results of a study from the Netherlands by Haeck et al. suggest that the use of topical corticosteroids for AD on the eyelids and periorbital region is safe with the respect to induction of glaucoma or cataracts.[46]

As a maintenance regimen, 1.25% hydrocortisone powder in Acid Mantle used diffusely as a steroid-based emollient is both effective and safe for longer periods (eg, months) to prevent acute flares in addition to using higher-class steroids to treat acute flares rapidly.

Immunomodulators in atopic dermatitis

Tacrolimus (topical FK506) is an immunomodulator that acts as a calcineurin inhibitor. Studies have shown excellent results compared with placebo and hydrocortisone 1%. Little absorption occurs. A stinging sensation may occur following application, but this can be minimized by applying the medication only when the skin is dry. The burning usually disappears within 2-3 days. Tacrolimus is available in 2 strengths, 0.1% for adults and 0.03% for children, although some authorities routinely use the 0.1% preparation in children. Tacrolimus is an ointment and is indicated for moderate-to-severe AD. It is indicated for children older than 2 years.

Pimecrolimus 1% is also an immunomodulator and calcineurin inhibitor. It is more effective than placebo. Pimecrolimus is produced in a cream base for use twice a day; it is indicated for mild AD in persons older than 2 years and is particularly useful on the face.

A 2006 black box warning has been issued in the United States based on research that has shown an increase in malignancy in association with the calcineurin inhibitors. While these claims are being investigated further, the medication should likely only be used as indicated (ie, for AD in persons older than 2 years and only when first-line therapy has failed).

These agents are much more expensive than corticosteroids and should only be used as second-line therapy.

Omalizumab is a monoclonal antibody that blocks IgE function. Case reports suggest that it may be an effective therapy for AD; however, a recent randomized, placebo-controlled trial did not demonstrate improvement in the clinical course.[47]

Targeted biologic therapeutics in atopic dermatitis

Anti-IL-4Ra therapy (dupilumab)

Dupilumab is a monoclonal antibody that inhibits interleukin (IL)–4 and IL-13 signaling by blocking the shared IL-4Ra and originally demonstrated efficacy in phase 2 clinical trials.[48, 49] It was approved by the US Food and Drug Administration (FDA) in 2017 for adults with moderate-to-severe atopic dermatitis not adequately controlled with topical prescription therapies or when those therapies are not advisable. In 2019, this indication was expanded to include adolescents aged 12 years or older. It is a subcutaneous injection administered every 2 weeks.

Approval of dupilumab was based on clinical trials investigating dupilumab as monotherapy (SOLO 1 and SOLO 2) and in concomitant administration with topical corticosteroids (CHRONOS). Results from the SOLO 1 (n=671) and SOLO 2 (n=708) trials showed 36-38% of patients who received dupilumab had scores of 0 or 1 (clear or almost clear) on the Investigator's Global Assessment scale compared with placebo (8-10%) (P< .001). Additionally, improvement from baseline to week 16 of at least 75% on the Eczema Area and Severity Index (EASI) was reported in significantly more patients who received each regimen of dupilumab than in patients who received placebo (P< .001).[50] Approval in adolescents was based on a phase 3 trial showing statistically significant improvement of EASI-75 in the dupilumab-treated group compared with placebo.[51]

Given its unprecedented efficacy, dupilumab is emerging as a first-line therapeutic for moderate-to-severe atopic dermatitis.

Anti-IL-33 therapy (ANB020)

IL-33 is an epithelial cell–derived cytokine that promotes downstream type 2 cytokine (eg, IL-4) responses by acting on multiple cell types, including Th2 cells, basophils, and ILC2s. A 2017 small phase 2a study using a therapeutic anti-IL-33 antibody (ANB020) demonstrated promising results in terms of EASI as early as at day 15.[52] However, larger randomized trials are required to fully determine the efficacy of this drug.

Janus kinase (JAK) inhibitors

Multiple proinflammatory cytokines, including type 2 cytokines, are dependent on the JAK-STAT signaling pathway to mediate their effects.[53] Thus, in addition to cytokine receptor blockade, phase 2 clinical trials have been performed for both oral and topical JAK inhibitors. The oral JAK1-selective inhibitor upadacitinib (ABT-494) demonstrated significant improvement in terms of EASI compared with placebo at 16 weeks and improvement of itch severity as early as 1 week in a 2017 phase 2b clinical trial.[54] In support of the direct antipruritus effect of JAK inhibitors, a 2017 study identified that neuronal JAK1 signaling critically regulates AD-associated itch in mice, independently of any effect on the immune system.[19] Thus, these studies may explain why JAK inhibitors are demonstrating such unique anti-itch properties in clinical trials. Similarly, the JAK1/2-selective inhibitor, baricitinib, also demonstrated improvement in both itch and disease severity in patients with moderate-to-severe AD.[55] Finally, a phase 2a clinical trial for a topical JAK1/2 inhibitor (tofacitinib) was also found to be effective and demonstrated improvement in disease severity at 4 weeks compared with placebo.[56] Thus, both oral and topical JAK inhibition represents a potential new treatment strategy for AD. The topical formulations likely offer more opportunities to target milder forms of AD in contrast to the oral form, which, owing to its potency, is being investigated for moderate-to-severe AD.

Topical phosphodiesterase-4 (PDE-4) inhibitors in atopic dermatitis

Crisaborole topical ointment 2% (Eucrisa) was approved by the FDA in December 2016 for mild-to-moderate atopic dermatitis in adults and children aged 2 years or older. The approval was based on two placebo-controlled trials (n=1522). Patients who received crisaborole achieved greater response with clear or almost clear skin after 28 days compared with vehicle-treated patients (P< .001).[57]

Other treatments, effective and ineffective, in atopic dermatitis

Probiotics have recommended as a therapeutic option for the treatment of AD. The rationale for their use is that bacterial products may induce an immune response of the Th 1 series instead of Th 2 and could therefore inhibit the development of allergic IgE antibody production. Some report limited benefit in preventive and therapeutic roles.[58] A meta-analysis of 25 randomized placebo-controlled controlled trials involving 4031 subjects found that prenatal and postnatal administration of probiotics reduced IgE levels in infants and that it may protect against sensitization to hereditary allergies but may not protect against asthma or wheezing.[59, 60] In January 2015, the World Allergy Organization recommend the use of probiotics by pregnant and lactating women and their breastfed infants to prevent the development of AD. The recommendation was based on a meta-analysis of 29 studies in which probiotic use by pregnant women reduced the incidence of eczema by 9% during a 1- to 5-year follow-up period and use by lactating women was associated with a 16% reduction in eczema during a 6-month follow-up period. Probiotic consumption by breastfeeding infants was associated with a 5% reduction in eczema during the 6-month to 6-year follow-up period.[61, 62]

UV-A, UV-B, a combination of both, psoralen plus UV-A (PUVA), or UV-B1 (narrow-band UV-B) therapy may be used. Long-term adverse effects of skin malignancies in fair-skinned individuals should be weighed against the benefits.

In patients with eczema herpeticum, acyclovir is effective.

In patients with severe disease, and particularly in adults, phototherapy, methotrexate (MTX),[63, 64] azathioprine, cyclosporine, and mycophenolate mofetil[4] have been used with success.

Both hydroxyzine and diphenhydramine hydrochloride provide a certain degree of relief from itching but are not effective without other treatments.

Oil of evening primrose was believed to be effective, but in a randomized controlled study, it showed no benefit in children and little improvement in adults.

Unsuccessful therapy with everolimus, a rapamycin-derived macrolide, has been reported in 2 patients with severe AD. Combination therapy with either prednisone or cyclosporine A was not effective.[5] However, reports of the ineffectiveness of everolimus have been questioned.[6]

Results with many other medications, such as thymopentin, gamma interferon, and Chinese herbs, have been disappointing. Many medications are not practical to use, and they can be expensive. Some Chinese herbal preparations contain prescription medications, including prednisone, and have been associated with cardiac and liver problems.

Antibiotics are used for the treatment of clinical infection caused by S aureus or flares of disease. They have no effect on stable disease in the absence of infection. Laboratory evidence of S aureus colonization is not evidence of clinical infection because staphylococcal organisms commonly colonize the skin of patients with AD.

A randomized, investigator-blinded, placebo-controlled trial including 31 patients showed that intranasal mupirocin ointment and diluted bleach (sodium hypochlorite) baths improved AD symptoms in patients with clinical signs of secondary bacterial infection.[7] Multiple studies have now confirmed that bleach baths are highly effective in treating AD by limiting disease severity.[65] The most likely mechanism is reduction of superinfection with bacteria such as S aureus, thereby mitigating proinflammatory stimuli.

Nonmedical efforts in atopic dermatitis

Clothing should be soft next to the skin. Cotton is comfortable and can be layered in the winter. Wool products should be avoided.

Cool temperatures, particularly at night, are helpful because sweating causes irritation and itch.

A humidifier (cool mist) prevents excess drying and should be used in both winter, when the heating dries the atmosphere, and in the summer, when air conditioning absorbs the moisture from the air.

Clothes should be washed in a mild detergent with no bleach or fabric softener.

Food avoidance is discussed in Diet, below, and in Causes.

Consultations

Consulting an allergist may be necessary, particularly if the patient develops asthma and/or hay fever or an acute reaction to a food.

Diet

Avoid foods that provoke acute allergic reactions (hives, anaphylaxis). Most frequently, allergic reactions occur to peanuts (peanut butter), eggs, seafood, milk, soy, and chocolate. Additionally, advise patients to apply a barrier of petroleum jelly around the mouth prior to eating to prevent irritation from tomatoes, oranges, and other irritating foods.

Activity

Advise patients to avoid activities that cause excessive sweating. Also, swimming in an outdoor pool (or wading pool for babies) in summer provides therapeutic benefit by exposing the person to the sun but avoiding the heat.

Complications

If topical corticosteroids are used inappropriately or if superpotent steroids are used in teenagers during rapid growth, striae may occur. Skin thinning can result if steroids are used inappropriately in older patients.

Whether verrucae vulgaris and mollusca contagiosa are more frequent is difficult to assess, but they are more widespread and difficult to eliminate.

Tachyphylaxis to topical steroids occurs if they are not used on a stop-start basis.

Patients may develop other related allergic disorders such as urticaria, food allergy, asthma and allergic rhinitis.

Superinfection with S aureus may require topical and/or systemic antibiotic treatment with antistaphylococcal agents.

Superinfection with herpes simplex virus, referred to as eczema herpeticum, can require admission to the hospital in children for systemic treatment with acyclovir and evaluation of other complications such as herpes keratitis.

Prevention

Moisturization is important on an ongoing basis and may prevent flares.

 

Guidelines

Guidelines Summary

Guidelines on diagnosis and assessment, topical therapy, phototherapy and systemic agents, and disease flares and adjunctive therapy are available from the American Academy of Dermatology at Atopic dermatitis clinical guideline.[66]

 

Medication

Medication Summary

The basis of treatment for atopic dermatitis (AD) is to provide moisturization for dryness, allay pruritus, and manage inflammation of the eczematous lesions.

Anti-inflammatory agents

Class Summary

Anti-inflammatory agents provide relief of inflammation of eczematous lesions. The ointment base provides moisturization. White petrolatum is useful to avoid potential sensitization to preservatives in water-based moisturizers.

Hydrocortisone ointment 1% (Cortaid)

Hydrocortisone ointment 1% is a mild topical corticosteroid mixed in petrolatum. It has mineralocorticoid and glucocorticoid effects and anti-inflammatory activity. Use 1% ointment 2-3 times daily.

Betamethasone topical (Beta-Val)

Betamethasone topical is a medium-strength topical corticosteroid for body areas. It decreases inflammation by suppressing the migration of polymorphonuclear leukocytes and reversing capillary permeability. It affects the production of lymphokines and has an inhibitory effect on Langerhans cells. Use 0.05-0.1% ointment in adults and 0.05% ointment in children.

Triamcinolone topical (Kenalog Orabase, Kenalog topical, Pediaderm TA)

Triamcinolone topical is a medium-strength topical corticosteroid for body areas. It decreases inflammation by suppressing the migration of polymorphonuclear leukocytes and reversing capillary permeability. It affects the production of lymphokines and has an inhibitory effect on Langerhans cells. Use 0.1% ointment in adults and 0.025% ointment in children.

Antihistamines

Class Summary

Antihistamines provide symptomatic relief of pruritus associated with acute urticaria in atopic dermatitis patients.

Hydroxyzine (Atarax)

Hydroxyzine is an antihistamine with antipruritic, anxiolytic, and mild sedative effects. It antagonizes H1 receptors in the periphery, and it may suppress histamine activity in the subcortical region of the CNS. Syrup is available as 10 mg/5 mL.

Diphenhydramine (Benadryl)

Diphenhydramine is an antihistamine used for pruritus and allergic reactions.

Immunomodulators

Class Summary

Immunomodulators are for treatment of patients with severe disease in whom conventional therapy is ineffective. In more severe cases and particularly in adults, consider using both MTX and cyclosporine. The latter is more efficacious, but lesions recur when it is stopped.

Cyclosporine (Neoral, Sandimmune)

Cyclosporine has been demonstrated to be helpful in a variety of skin disorders, especially psoriasis. It acts by inhibiting T-cell production of cytokines and ILs. Like tacrolimus and pimecrolimus (ascomycin), cyclosporine binds to macrophilin and then inhibits calcineurin, a calcium-dependent enzyme, which, in turn, inhibits phosphorylation of nuclear factor of activated T cells and inhibits transcription of cytokines, particularly IL-4. Discontinue treatment if no response occurs within 6 weeks.

Methotrexate (Folex PFS, Rheumatrex)

Methotrexate is an antimetabolite that inhibits dihydrofolate reductase, thereby hindering DNA synthesis and cell reproduction. Satisfactory response is seen 3-6 weeks following administration. Adjust the dose gradually to attain a satisfactory response.

Tacrolimus (Protopic) ointment 0.03% or 0.1%

Tacrolimus is an immunomodulator that suppresses humoral immunity (T-lymphocyte) activity. It is used for refractory disease.

Azathioprine (Azasan, Imuran)

Azathioprine is an imidazolyl derivative of mercaptopurine. It works by blocking the pathway for purine synthesis. The 6-thioguanine nucleotide metabolites mediate most of azathioprine’s immunosuppressive and toxic effects.

Mycophenolate (CellCept, MMF, Myfortic)

Mycophenolate mofetil is an inhibitor of inosine monophosphate dehydrogenase (IMPDH), which blocks de novo guanosine nucleotide synthesis. T and B cells are dependent on this pathway for proliferation.

Targeted Biologic Therapies (Interleukin Inhibitors)

Class Summary

Interleukin (IL)–4, IL-5, and IL-13 appear to play critical roles in the etiology of atopic dermatitis in response to activation by epidermal cell–derived cytokines.

Dupilumab (Dupixent)

Dupilumab is a monoclonal antibody that inhibits IL-4 and IL-13 signaling by blocking the shared IL-4Ra. It is indicated for patients aged 12 years or older with moderate-to-severe atopic dermatitis whose disease is not adequately controlled with topical prescription therapies or when those therapies are not advisable. It is administered as a subcutaneous injection every 2 weeks. It may be used with or without topical corticosteroids. It also be coadministered with topical calcineurin inhibitors, but these should be reserved for problem areas only (eg, face, neck, intertriginous and genital areas).

Topical Phosphodiesterase-4 (PDE-4) Inhibitors

Class Summary

A topical PDE-4 inhibitor is a nonsteroidal option for atopic dermatitis treatment.

Crisaborole topical (Eucrisa)

PDE-4 inhibitors allow for cyclic adenosine monophosphate (cAMP) to remain intact in order to decrease the proinflammatory response (eg, cytokine release) associated with atopic dermatitis. Crisaborole is indicated for mild-to-moderate atopic dermatitis in adults and children aged 2 years or older.

Antiviral agents

Class Summary

Antiviral agents are for the management of herpetic infections and to treat atopic dermatitis in patients who develop chickenpox.

Acyclovir (Zovirax)

Acyclovir inhibits the activity of both HSV-1 and HSV-2. It has affinity for viral thymidine kinase and, once phosphorylated, causes DNA-chain termination when acted on by DNA polymerase. Patients experience less pain and faster resolution of cutaneous lesions when used within 48 hours of rash onset. Acyclovir may prevent recurrent outbreaks. Early initiation of therapy is imperative. The zoster dose is 4 times higher than that for herpes simplex. The duration of therapy varies.

Antibiotics

Class Summary

Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context of the clinical setting. For the treatment of clinical infection by S aureus, cloxacillin or cephalexin is used. In streptococcal infections, cephalexin is preferred. If not effective, penicillin and clindamycin in combination are effective. Consider staphylococcal infection in every flare of atopic dermatitis.

Cephalexin (Keflex)

Cephalexin is a first-generation cephalosporin that arrests bacterial growth by inhibiting bacterial cell wall synthesis. It has bactericidal activity against rapidly growing organisms. Its primary activity is against skin flora; it is used for skin infections or prophylaxis in minor procedures.

Cephalexin suspension includes mauve granules (125 mg/5 mL) and peach granules (250 mg/5 mL).

Penicillin VK (Beepen-VK, Betapen-VK, Veetids)

Penicillin VK inhibits the biosynthesis of cell wall mucopeptide. It is bactericidal against sensitive organisms when adequate concentrations are reached, and it is most effective during the stage of active multiplication. Inadequate concentrations may produce only bacteriostatic effects.

Clindamycin (Cleocin)

Clindamycin is a lincosamide for the treatment of serious skin and soft tissue staphylococcal infections. It is also effective against aerobic and anaerobic streptococci (except enterococci). It inhibits bacterial growth, possibly by blocking the dissociation of peptidyl t-RNA from ribosomes, causing RNA-dependent protein synthesis to arrest.

Mupirocin (Bactroban, Bactroban Nasal, Centany)

Mupirocin is used as a topical treatment for bacterial skin infections such as furuncle, impetigo, and open wounds. It is also useful in the treatment of methicillin-resistant Staphylococcus aureus (MRSA) infection.

Trimethoprim/sulfamethoxazole (Bactrim, Bactrim DS, Cotrim)

Sulfamethoxazole disrupts bacterial folic acid synthesis and growth via inhibition of dihydrofolic acid formation; trimethoprim inhibits dihydrofolic acid reduction to tetrahydrofolate, resulting in the inhibition of enzymes of the folic acid pathway.

 

Questions & Answers

Overview

What is atopic dermatitis (eczema)?

What are the symptoms of atopic dermatitis (eczema)?

What are the primary physical findings of atopic dermatitis (eczema)?

Which constellation of symptoms and features are commonly seen in atopic dermatitis (eczema)?

What are the AAD diagnostic guidelines for atopic dermatitis (eczema)?

Which conditions should be considered in the differential diagnosis of atopic dermatitis (eczema)?

What should be considered prior to the workup for atopic dermatitis (eczema)?

Which topical medications are typically used in the treatment of atopic dermatitis (eczema)?

Which less common treatments have been tried for atopic dermatitis (eczema)?

What nonmedical measures may be helpful in the management of atopic dermatitis (eczema)?

How is atopic dermatitis (eczema) characterized?

What other atopic conditions are associated with atopic dermatitis (eczema)?

What is the pathophysiology of atopic dermatitis (eczema)?

What is the role of T and B cells in the pathophysiology of atopic dermatitis (eczema)?

What is epidermal barrier dysfunction hypothesis of the pathogenesis of atopic dermatitis (eczema)?

What is the role of genetics in the etiology of atopic dermatitis (eczema)?

What is the role of infection in the etiology of atopic dermatitis (eczema)?

What is the role of hygiene in the etiology of atopic dermatitis (eczema)?

What is the role of climate in the etiology of atopic dermatitis (eczema)?

What is the role of food antigens in the etiology of atopic dermatitis (eczema)?

What is the role of probiotics in the etiology of atopic dermatitis (eczema)?

What is the role of aeroallergens in the etiology of atopic dermatitis (eczema)?

What is the role of tobacco in the etiology of atopic dermatitis (eczema)?

What is the prevalence of atopic dermatitis (eczema) in the US?

What is the global prevalence of atopic dermatitis (eczema)?

What are the racial predilections of atopic dermatitis (eczema)?

How does the prevalence of atopic dermatitis (eczema) vary among men and women?

How does the prevalence of atopic dermatitis (eczema) vary by age?

What is the prognosis of atopic dermatitis (eczema)?

What is the financial and psychological burden of atopic dermatitis (eczema)?

Which complication of atopic dermatitis (eczema) is caused by herpes simplex infection?

What is the risk of Kaposi varicelliform eruption (eczema herpeticum) following chickenpox vaccination in patients with atopic dermatitis (eczema)?

Which bacterial infection is common in patients with atopic dermatitis (eczema)?

The risk for which allergic reactions is increased in patients with atopic dermatitis (eczema)?

Which allergies are common in patients with atopic dermatitis (eczema)?

What information about atopic dermatitis (eczema) should be given to patients?

Presentation

What is the most debilitating symptom of atopic dermatitis (eczema)?

What is the natural course of atopic dermatitis (eczema)?

Which history findings are common in patients with atopic dermatitis (eczema)?

Which historical features must be present for a diagnosis of atopic dermatitis (eczema)?

What should be the focus of the physical exam for atopic dermatitis (eczema)?

Which physical findings are characteristic of atopic dermatitis (eczema)?

Which features are diagnostic of atopic dermatitis (eczema)?

Which features support a diagnosis of atopic dermatitis (eczema)?

What are the nonspecific features of atopic dermatitis (eczema)?

Which physical findings are characteristic of atopic dermatitis (eczema) in infancy?

Which physical findings are characteristic of atopic dermatitis (eczema) in childhood?

Which physical findings are characteristic of atopic dermatitis (eczema) in adulthood?

What are the diagnostic criteria for atopic dermatitis (eczema)?

DDX

How is atopic dermatitis (eczema) distinguished from other causes of dermatitis?

How is scabies differentiated from atopic dermatitis (eczema)?

How is allergic contact dermatitis from nickel distinguished from atopic dermatitis (eczema)?

How is atopic dermatitis diagnosed in infants?

How does mycosis fungoides differentiated from atopic dermatitis (eczema) in children?

How is tinea corporis differentiated from atopic dermatitis (eczema)?

When is viral testing indicated in the workup of atopic dermatitis (eczema)?

What are the differential diagnoses for Atopic Dermatitis?

Workup

What is the role of lab studies in the evaluation of atopic dermatitis (eczema)?

Which histologic findings are specific for atopic dermatitis (eczema)?

Treatment

When is emergency therapy for atopic dermatitis (eczema) indicated?

What nonmedical therapies are used in the management of atopic dermatitis (eczema)?

What is the role of topical steroids in the treatment of atopic dermatitis (eczema)?

What is the role of immunomodulators in the treatment of atopic dermatitis (eczema)?

What is the role of dupilumab in the treatment of atopic dermatitis (eczema)?

What is the role of anti-IL-33 therapy (ANB020) in the treatment of atopic dermatitis (eczema)?

What is the role of janus kinase (JAK) inhibitors in the treatment of atopic dermatitis (eczema)?

What is the role of crisaborole topical ointment 2% (Eucrisa) for the treatment of atopic dermatitis (eczema)?

What is the role of probiotics in the treatment of atopic dermatitis (eczema)?

What is the role of phototherapy in the treatment of atopic dermatitis (eczema)?

What is the indication for acyclovir in the treatment of atopic dermatitis (eczema)?

Which treatments for atopic dermatitis (eczema) have been shown to be effective?

Which medications have not been shown to be effective in the treatment of atopic dermatitis (eczema)?

What is the efficacy of diluted bleach (sodium hypochlorite) baths for the treatment of atopic dermatitis (eczema)?

Which nonmedical measures are helpful in the treatment of atopic dermatitis (eczema)?

Which specialist consultations are useful in the treatment of atopic dermatitis (eczema)?

What are dietary restrictions for patients with atopic dermatitis (eczema)?

What activity restrictions are required for patients with atopic dermatitis (eczema)?

What are possible complications of atopic dermatitis (eczema)?

How is atopic dermatitis (eczema) prevented?

Guidelines

What guidelines have been published for diagnosis and management of atopic dermatitis (eczema)?

Medications

What is the focus of treatment for atopic dermatitis (eczema)?

Which medications in the drug class Anti-inflammatory agents are used in the treatment of Atopic Dermatitis?

Which medications in the drug class Antihistamines are used in the treatment of Atopic Dermatitis?

Which medications in the drug class Immunomodulators are used in the treatment of Atopic Dermatitis?

Which medications in the drug class Targeted Biologic Therapies (Interleukin Inhibitors) are used in the treatment of Atopic Dermatitis?

Which medications in the drug class Topical Phosphodiesterase-4 (PDE-4) Inhibitors are used in the treatment of Atopic Dermatitis?

Which medications in the drug class Antiviral agents are used in the treatment of Atopic Dermatitis?

Which medications in the drug class Antibiotics are used in the treatment of Atopic Dermatitis?