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Atopic eczema

Definition
  • 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.
Epidemiology
  • 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.
Aetiology
  • 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
Pathophysiology
  • 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]
Investigations
  • 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.
Management

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
Prognosis
  • 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.
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