AUTHOR AND EDITOR INFORMATION

Section 1 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
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INTRODUCTION

Section 2 of 11  

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• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
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Background

Atopic dermatitis (AD) is a pruritic disease of unknown origin that usually starts in early infancy and is typified by pruritus, eczematous lesions, xerosis (dry skin), and lichenification on the skin (thickening of the skin and increase in skin markings). AD is associated with other atopic diseases (eg, asthma, allergic rhinitis, urticaria, acute allergic reactions to foods, increased immunoglobulin E [IgE] production) in many patients. It is a disease of great morbidity, and the incidence appears to be increasing.

Pathophysiology

The pathophysiology of AD is poorly understood. Several cell types seem to be involved, including T lymphocytes, eosinophils, Langerhans cells, and keratinocytes. Other factors, including cytokines and IgE, are also implicated.

Laboratory findings suggest a number of different pathogenetic mechanisms. One invokes an immune defect involving an abnormality of T_H2 cells that interacts with Langerhans cells and results in increased production of interleukin (IL)–4, IL-5, IL-6, IL-10, and IL-13. This leads to increased IgE and decreased gamma interferon levels. The imbalance of T_H2 cells occurs in the acute process, with a swing toward T_H1 cells in the chronic stages of the disease. Another theory involves defective barrier function in the stratum corneum leading to the entry of antigens, which results in the production of various inflammatory cytokines.

Xerosis is known to be an associated sign in most AD patients. The xerosis is thought to involve defective lipid (particularly ceramide) production. A third mechanism involves environmental antigens from food (the gut), dust mites (the lungs), and other factors and portals of entry that react with antibodies to produce increased levels of IgE and, possibly, increased histamine reactions from mast dells. Superimposed with these mechanisms is a genetic predisposition to react to various environmental allergens.

Frequency

United States

The prevalence rate is 10-12% in children and 0.9% in adults.

International

The prevalence rate is as high as 18% and is rising, especially 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.

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 seen with some frequency in patients with AD. It usually occurs with a primary herpes simplex infection, but it also may be seen recurrently. Vesicular lesions can begin at any location, but they are particularly common in areas of eczema. The virus spreads rapidly to involve all eczematous areas and healthy skin. Lesions may become secondarily infected. Although vaccination with the vaccinia vaccine for the prevention of small pox is now no longer mandatory, patients with AD can contract eczema vaccinatum either from the vaccination of themselves or their 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.
• With regard to bacterial infection (eg, with Staphylococcus aureus or Streptococcus pyogenes), note that the skin of most patients with AD is colonized by S aureus. Clinical infection may occur and is worsened by scratching and occlusion from medications. 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, soya, fish, and seafood.
• Latex allergy is more common in patients with AD than in the general population.
• Of patients with AD, 30% develop asthma and 35% have nasal allergies.

Race

AD may be more common among whites, but it affects persons of all races.

Sex

The male-to-female ratio 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.

• Disease is most prevalent 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 diminishes to 0.9%. Rarely, onset may be delayed until adulthood, when the disease is more difficult to control.

CLINICAL

Section 3 of 11  

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• Clinical
• Differentials
• Workup
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• Medication
• Follow-up
• Miscellaneous
• Multimedia
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History

Incessant pruritus is the only symptom. 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 approximately age 3 months; children then scratch themselves uncontrollably.

Physical

Primary findings include xerosis, lichenification, and eczematous lesions. The eczematous changes are seen in different locations, and the morphology changes with age.

• Infancy
• • AD may be noticed soon after birth. Xerosis also occurs in the neonatal period. Xerosis involves the whole body but usually spares the diaper area.
  • The earliest lesions are often evident in the creases (ie, antecubital and popliteal fossae), where the lesions consist of erythema with exudation. Over the following few weeks, lesions localize to the cheeks and forehead and extensors of the lower legs, but they may occur in any location on the body, often sparing the diaper area. Lesions are xerotic, erythematous, and scaly (eczematous) ill-defined patches and plaques.
  • The scalp is frequently involved with a pruritic scaly dermatitis.
  • Lichenification is seldom seen in infancy.
• 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 and bony protuberances.
  • Lesions are eczematous and exudative. Pallor of the face is common; erythema and scaling occur around the eyes. Dennie-Morgan folds (increased folds below the eye) are often seen. Flexural creases, particularly the antecubital and popliteal fossae, and buttock-thigh creases are often affected.
  • Excoriations and crusting are common.
• Adulthood
• • Lesions become more diffuse with an underlying background of erythema. The face is commonly involved and has a dry, scaling appearance.
  • Xerosis is prominent.
  • Lichenification is present.
  • A brown macular ring around the neck is typical but not always present.
• Hanifin diagnostic criteria: In 1980, Hanifin and Rajka¹ developed criteria for the diagnosis of AD. They developed main criteria and numerous minor criteria. Many articles have questioned the validity of the minor criteria, and the original criteria have been modified on numerous occasions. Following are the criteria for 2001.
• • Essential features: These features must be present and, if complete, are sufficient for diagnosis.
  • • Pruritus
    • Eczematous changes
    • • Typical and age-specific changes: Patterns include facial, neck, and extensor involvement in infants and children, current or prior flexural lesions in adults or persons of any age, and sparing of the groin and axillary regions.
      • Chronic and relapsing course
  • Important features (seen in most cases): These features are seen in most cases and add support to the diagnosis
  • • Early age of onset
    • Atopy (IgE reactivity)
    • Xerosis
  • Associated features (clinical associations): These changes help in suggesting the diagnosis of AD but are too nonspecific to be used for defining or detecting AD for research and epidemiologic studies.
  • • Keratosis pilaris/ichthyosis/palmar hyperlinearity
    • Atypical vascular responses
    • Perifollicular changes
    • Ocular/periorbital changes
    • Perioral/periauricular lesions
  • Exclusions: Note that a firm diagnosis of AD depends on excluding conditions such as scabies, allergic contact dermatitis, seborrheic dermatitis (SD), cutaneous lymphoma, ichthyosis, psoriasis, and other primary disease entities.
• Williams diagnostic criteria: According to the criteria of Williams et al, proposed diagnostic guidelines include the following:
• • Patients must have an itchy skin condition (or parental report of scratching or rubbing in children).
  • Patients also must have 3 or more of the following:
  • • History of involvement of the skin creases, such as folds of the elbows, behind the knees, fronts of the ankles, or neck
    • Personal history of asthma or hay fever or a history of atopic disease in a first-degree relative in patients younger than 4 years
    • History of generally dry skin in the last year
    • Visible flexural dermatitis or dermatitis involving the cheeks or forehead and outer limbs in children younger than 4 years
    • Onset younger than age 2 years (not used if child is <4 y)

Causes

• A genetic abnormality is possibly related to bands 11q13 or 5q31.² These findings have yet to be corroborated; a family history of AD is common.
• The skin of patients with AD is colonized by S aureus. Lesions flare following infection by S aureus, but they may occur with any type of skin or systemic infection. S aureus has been proposed as a cause of AD by acting as a superantigen.
• 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. All these external factors may act as antigens, ultimately setting up an inflammatory cascade.
• The role of food antigens in the pathogenesis of AD is controversial, both in the prevention of AD and by their effect with withdrawal of certain foods in persons with established AD. Most reported research has methodologic flaws. One article showed improvement at 1 year with continued breastfeeding. At 4 years, no difference was noted in the incidence of AD between the group that had not been exclusively breastfed and the group that had.
• A role for aeroallergens and house dust mites has been proposed, but this awaits further corroboration.

DIFFERENTIALS

Section 4 of 11  

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• Clinical
• Differentials
• Workup
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• Follow-up
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• Multimedia
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Other Problems to be Considered

Immunodeficiency
Mycosis fungoides

AD occasionally is indistinguishable from other causes of dermatitis. In infancy, the most common difficulty is distinguishing it from SD. This entity is not seen with the same frequency as a decade ago. Both AD and SD are associated with cradle cap (a scale 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, where marked erythema and a greasy scale can be seen over the eyebrows and the sides of the nose. In AD, xerosis of the skin and severe pruritus are seen, 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 may be 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 common in infancy. Facial involvement is rare, and xerosis does not occur.

Other causes of dermatitis, particularly contact dermatitis from nickel in infants, are sometimes difficult to distinguish from AD. A central area of dermatitis (from nickel snaps in undershirts or 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.

Children 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.

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 2 conditions.

WORKUP

Section 5 of 11  

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• Follow-up
• Miscellaneous
• Multimedia
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Lab Studies

• Laboratory testing is seldom necessary.
• Allergy and radioallergosorbent testing is of little value.
• A platelet count for thrombocytopenia helps exclude Wiskott-Aldrich syndrome, and testing to rule out other immunodeficiencies may be helpful.
• Scraping to exclude tinea corporis is occasionally helpful.

Histologic Findings

Biopsy shows an acute, subacute, or chronic dermatitis, but no specific findings are demonstrated.

TREATMENT

Section 6 of 11  

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Medical Care

Patients with 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
• • Depending on the climate, patients may benefit from short, cool showers or baths followed by the application of a moisturizer such as white petrolatum. Another regimen includes "soaking and greasing." Frequent baths with oil (1 capful of emulsifying oil added to lukewarm bath water) for 5-10 minutes comprise this regimen. 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. Oil and water are kept in solution by an emulsifier in the oil, thus preventing evaporation of water to the outside environment.
  • Advise patients to apply an emollient such as petrolatum 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.
• Topical steroids
  • Topical steroids are currently the mainstay of treatment. In association with moisturization, responses to this regimen are excellent.
  • Ointment bases are preferred, particularly in dry environments.
  • Patients with AD may develop a contact allergy to topical medications and moisturizers. The allergy may be to a preservative or the active ingredient. Allergy to hydrocortisone is recognized with increasing frequency. Preservatives are less commonly present in ointments.
  • Initial therapy consists of hydrocortisone 1% powder in an ointment base applied 3 times daily to lesions on the face and in the folds.
  • A midstrength steroid ointment (desonide for milder areas or higher-strength steroids such as triamcinolone or betamethasone valerate for more severe areas) is applied 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.
• Immunomodulators
  • Tacrolimus (topical FK506) is an immunomodulator and 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 very 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. The latter 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.
  • A recent black box warning has been issued in the United States based on research that has shown an increase in malignancy in associated 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 y and only when first-line therapy had failed).
• Other treatments, effective and ineffective
  • Probiotics have recently been explored 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 T_H1 series instead of T_H2 and could therefore inhibit the development of allergic IgE antibody production. This research, although garnering fairly convincing support, has yet to be proven.
  • 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), azathioprine, and cyclosporine 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.
  • Ketotifen (a calcium channel blocker) may be effective.
  • 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.
  • 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.
  • 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 is not evidence of clinical infection because staphylococcal organisms commonly colonize the skin of patients with AD.
• Nonmedical efforts
  • Clothing should be soft next to the skin. Cotton 100% is comfortable and can be layered in the winter.
  • Cool temperatures, particularly at night, are better 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 the air conditioning absorbs the moisture from the air.
  • Clothes should be washed in a mild detergent with no bleach or fabric softener.

Consultations

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

Diet

• Avoid foods that provoke acute allergic reactions (hives, anaphylaxis). Most frequently, allergic reactions occur to peanuts (peanut butter), eggs, fish and seafood, milk, soya, and chocolate.
• 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.
• 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.

MEDICATION

Section 7 of 11  

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• References

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

Drug Category: Anti-inflammatory agents

Provide relief of inflammation of eczematous lesions. Ointment base provides moisturization. White petrolatum is useful to avoid potential sensitization to preservatives in water-based moisturizers.

Drug Category: Antihistamines

Provide symptomatic relief of pruritus.

Drug Category: Immunomodulators

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.

Drug Category: Antiviral agents

For management of herpetic infections and to treat AD in patients who develop chickenpox.

Drug Category: Antibiotics

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 AD.

FOLLOW-UP

Section 8 of 11  

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• Follow-up
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Further Outpatient Care

• Monitor patients frequently.
• Reinforce therapeutic regimens with patients.

In/Out Patient Meds

• Medications are used as described in Medication.

Deterrence/Prevention

• Moisturization is important on an ongoing basis and seems to prevent flares.

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 certainly, they can be more widespread and difficult to eliminate.
• Tachyphylaxis to topical steroids occurs if they are not used on a stop-start basis.

Prognosis

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

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.
• Show videos to patients that show how to apply medication and that discuss the role of moisturization.
• For excellent patient education resources, visit eMedicine's Skin, Hair, and Nails Center. Also, see eMedicine's patient education article Eczema.

MISCELLANEOUS

Section 9 of 11  

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• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Medical/Legal Pitfalls

• Failure to explain the adverse effects of topical steroids to patients may result in medicolegal problems.

Special Concerns

• Other children in the family may develop AD.
• Patients may develop acute food allergies (eg, to peanuts and/or eggs). EpiPen should be available.
• Patients may develop a generalized reaction to herpes simplex virus (eczema herpeticum).
• One third of patients develop asthma, and one third develop allergic rhinitis.

MULTIMEDIA

Section 10 of 11  

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• Follow-up
• Miscellaneous
• Multimedia
• References

Media file 1:  Typical atopic dermatitis on the face of an infant.
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Media file 2:  Flexural involvement in childhood atopic dermatitis.
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Media file 3:  Dirty neck sign in chronic atopic dermatitis.
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Media file 4:  Irritation around mouth of an infant with atopic dermatitis.
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REFERENCES

Section 11 of 11

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17. Nilsson EJ, Henning CG, Magnusson J. Topical corticosteroids and Staphylococcus aureus in atopic dermatitis. J Am Acad Dermatol. Jul 1992;27(1):29-34. [Medline].
18. Novak N, Bieber T, Leung DY. Immune mechanisms leading to atopic dermatitis. J Allergy Clin Immunol. Dec 2003;112(6 Suppl):S128-39. [Medline].
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Article Last Updated: Apr 7, 2006