Atopic eczema


    • 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.

Risk Factors

    • 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.

    • FHx

      • Concordance rates of 77% in monozygotic twins and 15% in dizygotic twins. [8]

      • Studies have estimated prevalence in siblings at 22%-24%. [15]

    • Allergic rhinitis

      • Occurs in 50%-80% of children with atopic dermatitis. [1] [3]

      • Allergen sensitisation and immune dysregulation are thought to be important components in atopic disease.

    • Asthma

      • Occurs in 40%-50% of children with atopic dermatitis. [1] [3]

Differential diagnosis

  • Seborrhoeic dermatitis

      • 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.

  • Irritant contact dermatitis

      • Common in nappy area, face, and extensor surfaces in children resulting from exposure to irritating substances.

      • Typically less pruritic than atopic dermatitis.

  • Allergic contact 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.

  • Scabies

      • 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. [3]

  • Psoriasis

      • 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.

    • Mycosis fungoides

      • 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 usually presents in childhood, with 45% of patients diagnosed by 6 months of age, and 70% to 85% by 5 years of age. [1] [2] [3]

    • Remission is noted by the age of 15 in 60% to 70% of cases, although relapse may occur later in life. [1] [2] [4]

    • Atopic dermatitis affects males and females equally.

    • The prevalence is 10% to 20% in US children, and 1% to 3% in adults. [5]

      • This is significantly higher than the prevalence reported several decades ago, and mirrors that seen in many industrialised nations. [3]

    • The prevalence in European and Japanese children has been estimated to be 15% and 24% respectively. [1]

    • 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.

    • It has been linked to mutations in genes that are crucial for normal epidermal differentiation as well as to genes involved in immune-system regulation. [6] [7]

      • 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. [8]

    • The aetiopathogenesis of atopic dermatitis has been increasingly attributed to abnormal skin barrier function. [9]

      • Evidence to support that both inherited and acquired insults to the barrier worsen the overall disease state has become increasingly strong. [10]

      • 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. [11]

      • 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. [12]

      • Additionally, the skin of those affected with atopic dermatitis is deficient in extra-cellular lipids including ceramides. [13]

    • 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. [8]

    • 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.

      • In a recent study, the prevalence of atopic dermatitis in Jamaican children living in London was twice as high as that of Jamaican children living in Jamaica. [2]

      • In addition, it has been noted over the last several decades that the prevalence of atopic dermatitis has increased significantly. [3]

Clinical features

    • Pruritis

    • Xerosis

    • Sites:

      • Infants typically show involvement of the cheeks, forehead, scalp, and extensor surfaces.

        • Affected skin is often oedematous, with prominent weeping and crusting.

      • Children typically have involvement of flexures, particularly the wrists, ankles, antecubital and popliteal fossae. [2] [6]

      • In addition to the areas affected by acute disease, chronic atopic dermatitis often affects the neck, upper back, and arms, as well as the hands and feet. [1] [3] [5] [23]

    • Erythema

    • Scaling

    • Vesicles

    • Papules

    • Keratosis pilaris

    • Excoriations

    • Lichenification

    • Hypopigmentation


    • Impairment of the skin's barrier function leads to an increased sensitisation to cutaneous antigens and is a major factor in the pathophysiology. [5]

    • 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.

    • Mutations in the filaggrin gene, which encodes a protein necessary for terminal differentiation of epidermis, have been shown to predispose patients. [6] [7] [7]

      • 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.

      • These interleukins lead to an increased production of IgE and peripheral eosinophilia. [1] [3] [14]

    • 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. [8]

    • 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. [3]


    • Allergy testing

      • 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

    • IgE levels

      • Early atopic sensitisation has been associated with a poorer prognosis in patients with atopic dermatitis.

    • Skin biopsy

      • 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.


a) conservative

b) medical

    • 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.

c) surgical

    • n/a


    • 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%. [2]

    • 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. [67]

    • 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.