Atopic dermatitis

Grading & Level of Importance: B


W. Burgdorf, Munich; A. Salam, J. McGrath, London
Revised by M. Maurelli, P. Gisondi, G. Girolomoni, Verona




Atopic eczema, endogenous eczema, neurodermatitis.


Highly prevalent in infants and children (10-20%) and adults (2-4%). 


Dermatitis in patients with atopic diathesis with a chronic-recurrent course, characterized by classical findings of dry skin, pruritus and textural change.

Aetiology & Pathogenesis

  1. Genetically determined or acquired epidermal barrier defects (in some parts of the population mutation in profilaggrin gene and other structural epidermal proteins, alterations in the desquamation process), xerosis
  2. Genetically determined immune reaction pattern (excessive IgE production possible, disturbance in helper T-cell balance with Th2 favoured over Th1).
  3. Common triggers: environmental factors (humidity, water hardness, pollution), house dust mites, psychological stimuli.

Signs & Symptoms

Eczema appearance with erythema and vesiculation in the acute phase and erythema, scaling and lichenification in the chronic phases. Another clinical feature is prurigo. Pruritus always present; it can be devastating and interfere with sleeping and work productivity.

Additional signs:
Dry skin (xerosis).
An atopy score (SCORAD, EASI, POEM) can be used to quantify diagnosis.


  • Localisation may be age dependent
  • Face and neck
  • Flexures (antecubital, popliteal, flexor aspect of wrist)
  • Hands
  • All parts of the body can be affected, even extending to erythroderma.


Intrinsic and extrinsic atopic dermatitis. Extrinsic: also defined allergic type, characterized by high total serum IgE levels and the presence of IgE to allergens; associated with asthma and/or rhino-conjunctivitis. Intrinsic: non-allergic, normal total serum IgE levels and the absence of specific IgE. 

Laboratory & other workups

Total serum IgE >100 kU/l, sometimes blood eosinophilia, often multiple positive skin prick tests, consider patch testing against airborne allergens after tape stripping of stratum corneum (atopypatch test).


Acute: spongiosis, perivascular lymphohistiocytic infiltrates in upper dermis. Chronic: parakeratosis, acanthosis, perivascular lymphohistiocytic infiltrates in upper dermis.


Chronic-relapsing course. Cradle cap after 3 months of age, weeping dermatitis in childhood, dry, itchy skin in adolescents and adults.


Tendency to superinfection by bacteria (Staph. aureus: impetiginization) and viruses (eczema herpeticum/molluscum contagiosum).


Typical personal and family history, characteristic clinical picture, relevant laboratory tests, often coexisting atopic disorders (allergic rhinitis, conjunctivitis, asthma or type 1 food allergies).

Differential diagnosis

Seborrhoeic dermatitis, psoriasis, allergic contact dermatitis, tinea, scabies, early patch stage mycosis fungoides.

Prevention & Therapy

1. General measures:

  • Counselling regarding skin care, avoidance of aggravating factors. Patient handouts and educational material or links are valuable.
  • Moisturising, often with emollients containing urea.
  • Gentle cleansing (use of soap substitutes).


2. Mild forms:

  • Topical corticosteroids, perhaps combination products also containing antimicrobial agents (short-term to avoid bacterial resistance).
  • Topical immune modulators (tacrolimus, pimecrolimus, crisaborole).


3. Severe forms:

  • Ciclosporin or other immunosuppressants (methotrexate, azathioprine, mycophenolate mofetil).
  • Short-term systemic corticosteroids.
  • Biological therapy: Dupilumab, a human monoclonal antibody directed against IL-4/IL-13 receptor-α.
  • Several new treatments under development.
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