Inflammatory skin condition characterised by dry, pruritic skin with a chronic relapsing course.
Can affect all age groups, but it is most commonly diagnosed before 5 years of age and affects 10% to 20% of children.
Patients often have a personal or family history of other atopic diseases such as asthma or allergic rhinitis.
Food allergens may occur at increased rates in this population.
Atopic dermatitis can be described as acute or chronic.
Acute atopic dermatitis is used to describe a flare-up of symptoms.
Chronic is used to describe the condition when the patient develops signs of chronic inflammation (e.g., lichenification).
The period of time before the condition is termed chronic is not clearly defined.
Age <5 years
45% of patients with atopic dermatitis are diagnosed by 6 months of age, and 70%-85 % of patients are diagnosed by the age of 5 years.
Characteristic greasy scale that is not pruritic.
Often affects cheeks on face, scalp, extremities and trunk.
Unlike atopic dermatitis, the nappy area is often affected.
Common in nappy area, face, and extensor surfaces in children resulting from exposure to irritating substances.
Typically less pruritic than atopic dermatitis.
Well-circumscribed erythematous lesions, often with spongiotic papules, vesicles, and crusting.
Lesions are usually pruritic.
Eruptions are due to contact with specific allergen, and removal of offending agent results in resolution of symptoms.
Severe pruritus, particularly at night.
In addition to papules or vesicles, burrows may be evident and will help to make the diagnosis.
The wrists, ankles, palms, soles, interdigital spaces, axilla, waist and groin are the most commonly affected sites.
Patients will often report similar symptoms in family members or other close contacts. 
Well-circumscribed, erythematous lesions with silver scale that show a predilection for extensor surfaces, particularly elbows and knees.
The nail pitting seen in psoriasis has smaller pits and is more common than that seen in patients with atopic dermatitis.
The initial stages of mycosis fungoides (cutaneous T cell lymphoma) may look similar to atopic dermatitis.
Erythematous plaques in random distribution are common and scale is often present.
As opposed to patients with atopic dermatitis, patients with mycosis fungoides tend to be older at the time of diagnosis, with an average age of 50 years.
Atopic dermatitis affects males and females equally.
The prevalence is 10% to 20% in US children, and 1% to 3% in adults. 
This is significantly higher than the prevalence reported several decades ago, and mirrors that seen in many industrialised nations. 
The prevalence in European and Japanese children has been estimated to be 15% and 24% respectively. 
In addition, atopic dermatitis occurs more commonly in urban areas and in smaller families, supporting the theory that environment plays a significant role in disease development.
Atopic dermatitis has a multifactorial aetiology, with a combination of genetic susceptibility and environmental factors contributing to disease development.
Defects in the skin's barrier function and immune dysregulation following allergen exposure are thought to be key components in the development of this disease.
This genetic predisposition is supported by the increased incidence in family members, and by studies showing concordance rates of 77% in monozygotic twins and 15% in dizygotic twins. 
The aetiopathogenesis of atopic dermatitis has been increasingly attributed to abnormal skin barrier function. 
Evidence to support that both inherited and acquired insults to the barrier worsen the overall disease state has become increasingly strong. 
Common loss of function variants of the epidermal barrier protein filaggrin are a major predisposing factor for atopic dermatitis.
The loss-of-function mutation in the structural protein filaggrin predisposes the affected individual to a less effective mechanical barrier against the environment. 
The stratum corneum of those individuals with loss-of-function mutations in the filaggrin gene have lower levels of natural moisturising factor in their stratum corneum. 
Additionally, the skin of those affected with atopic dermatitis is deficient in extra-cellular lipids including ceramides. 
Breaks in the epidermal barrier allow increased exposure and sensitisation to antigens.
Mutations in genes that are crucial to normal epidermal barrier function have been identified and are thought to predispose patients to the development of atopic dermatitis.
Links have also been identified between atopic dermatitis and areas of the genome that are known to encode cytokines and receptors involved in the Th2-mediated immune response that predominates in atopic dermatitis. 
The role of environmental factors in the development of this skin disorder is supported by the increased rate of disease seen in urban areas, smaller families and higher socio-economic classes.
Infants typically show involvement of the cheeks, forehead, scalp, and extensor surfaces.
Affected skin is often oedematous, with prominent weeping and crusting.
Impairment of the skin's barrier function leads to an increased sensitisation to cutaneous antigens and is a major factor in the pathophysiology. 
Recent studies have demonstrated that the development of atopic dermatitis shows genetic linkage to chromosome 1q21, which contains the genes of the epidermal differentiation complex (EDC).
These genes are integral to the formation of the epidermal layer, and several mutations have been identified that lead to the impaired barrier function seen in atopic dermatitis.
Filaggrin mutations that result in impairments in the barrier function of the epidermis result in increased exposure and sensitisation to cutaneous antigens.
In the acute phase of atopic dermatitis, the immune response following sensitisation is predominantly Th2 mediated, with over-expression of IL-4, IL-5, and IL-13.
Susceptibility has been linked to polymorphisms in the gene encoding a subunit of the IgE receptor as well as to a region on chromosome 5q31-33 that includes genes for cytokines expressed by Th2 cells. 
Persistent inflammation and scratching can eventually lead to chronic atopic dermatitis, with thick, lichenified skin.
Lesions demonstrate a different complement of immune cells and cytokines, with a predominant Th1 response, and increased levels of IL-12. 
Allergy testing may be beneficial in assisting the patient to avoid exacerbating allergens, but up to 60% of children with atopic dermatitis do not have demonstrable IgE-mediated sensitivity to allergens
Early atopic sensitisation has been associated with a poorer prognosis in patients with atopic dermatitis.
May be used to differentiate atopic dermatitis from allergic contact dermatitis and psoriasis
This is less frequently employed than a careful skin examination
Careful attention to the primary lesions, their distribution, the associated symptomatology and the duration and associations at the time of onset of the skin disease.
Treatment is carried out in a step-wise approach starting with emollients and then progressing to topical corticosteroids and calcineurin inhibitors
In this way symptom control is achieved in most patients, but a few with particularly treatment-resistant dermatitis will need other treatments such as coal tar, UV light therapy or systemic immunosuppressants.
The use of oral corticosteroids is not advocated in the treatment of atopic dermatitis.
Atopic dermatitis is a chronic disease with a varying course.
Approximately 60% of children will have symptom resolution as they enter puberty, but relapse may occur in 50%. 
Although it can be difficult to predict the course of this disease, certain factors place patients at risk for a more aggressive course.
A prospective study of 1314 German children evaluated the natural course of atopic dermatitis from birth to the age of 7 years.
It found that disease severity and early atopic sensitisation were associated with a poorer prognosis.
Atopic sensitisation was quantified by measuring specific IgE levels, and although there was a strong association between IgE level and disease severity, no prognostic cutoff values were established. 
Many patients with milder disease are able to be maintained on emollient treatment with intermittent use of other topical agents during flares.
Patients with more severe disease often require combination treatment that includes coal tar, UV light therapy and systemic immunosuppressants.