Atopic Dermatitis (Eczema)

Atopic dermatitis, also known as eczema, is a chronic, relapsing, pruritic, inflammatory skin disease that occurs more frequently in children, although adults can also be affected. The condition is often associated with elevated serum levels of IgE and a personal or family history of atopy. Skin dryness, erythema, oozing, crusting, and lichenification are present. Pruritus is a cardinal symptom. Diagnosis is established clinically. The mainstays of management are avoidance of triggers, emollients, and topical corticosteroids.

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Atopic dermatitis (also known as eczema) is a disorder of altered skin barrier integrity and immune dysregulation that presents as a chronic relapsing inflammatory skin disease.


  • Prevalence:
    • School-aged children: approximately 17%
    • Adults: 2%–10%
  • Atopic triad (present in 30%–50% of patients):
    • Atopic dermatitis
    • Allergic rhinitis
    • Asthma
  • 30% of patients develop asthma.
  • Vast majority of cases in children; linked with family history of atopy
  • Most cases occur prior to age 5.
  • Slight female preponderance
  • Previous history of atopy is an important risk factor.
  • Incidence higher in:
    • Urban areas
    • Developed countries


  • Multifactorial and not completely understood
  • Genetics:
    • Family history of atopy
    • Filaggrin gene mutations (loss-of-function mutation):
      • Strongest known genetic risk factor
      • Keratinocyte barrier dysfunction
      • Increased susceptibility to potential antigens
  • Immune defects: Th2 disease (T helper cells)
  • Prenatal factors: elevated cord blood IgE
  • Infection:
    • Staphylococcus aureus colonization:
      • Often causes flares
      • Acts as a superantigen
    • HSV
  • Hygiene hypothesis: Early childhood exposure to microbes and allergens prevents atopy.

Pathophysiology and Clinical Presentation


  • Pathogenesis is poorly defined.
  • Characterized by spongiosis (epidermal edema)
  • Edema leads to breaking of intercellular attachments → vesicle formation
  • Lymphocytic dermal infiltrates are present.
  • Acanthosis and hyperkeratosis may be present.
  •  2 interrelated pathways have been implicated:
    •  Primary epithelial barrier disruption (outside-in hypothesis):
      • Disruption of tight junctions and increased permeability of stratum corneum
      • Increased transepidermal water loss
      • Can be associated with defects in structural proteins (filaggrin is the major one implicated)
      • Barrier disruption can also be caused by microbial colonization and release of inflammatory cytokines.
    • Immune-response defect (inside-out hypothesis):
      • Secondary immunologic dysregulation
      • Defect in toll-like receptors has been implicated in the loss of epidermal innate immunity (colonization with S. aureus leads to severe inflammation).
      • IgE–mediated allergic sensitization → increased susceptibility to irritants/allergens secondary to structural epidermal defects
Histological findings atopic dermatitis

Atopic dermatitis:
Histological image of the epidermal layer with a mild lymphohistiocytic and granulocytic infiltrate, predominantly eosinophilic

Image: “Atopic dermatitis, short stature, skeletal malformations, hyperimmunoglobulin E syndrome, hypereosinophilia and recurrent infections” by Leonardi S, Filippelli M, Costanzo V, Rotolo N, La Rosa M. License: CC BY 2.0

Clinical presentation

  • Chronic course with periods of remission and exacerbation
  • Intense pruritus: cardinal symptom
  • Cutaneous hyperreactivity to environmental stimuli
  • Age:
    • Infants and younger children:
      • Papulovesicular lesions
      • Intense pruritis
      • Erythema
      • Edema
      • Excoriations: result of itching
      • Location: face, scalp, extensor surfaces, with sparing of the diaper area
    • Older children and young adults:
      • Chronic lesions with lichenification
      • Flexor surfaces of elbows, knees and sides of the neck, wrists, and ankles
      • Improves with age with remission seen by 13 years of age in approximately 50% of cases
  • Severity:
    • Mild:
      • Areas of dry skin
      • Pruritus: infrequent
      • Minimal impact on activities, sleep, and psychosocial well-being
    • Moderate:
      • Areas of dry skin
      • Pruritus: frequent
      • Redness
      • Localized skin thickening with or without excoriation
      • Moderate impact on activities and psychosocial well-being
      • Sleep frequently disturbed
    • Severe:
      • Widespread dry skin
      • Pruritus: incessant
      • Redness
      • Extensive skin thickening, bleeding, oozing, cracking, and pigmentation alteration
      • Severe impact on activities, psychosocial functioning, and sleep



  • Pruritus
  • 3 or more of the following (in addition to pruritus):
    • Skin creases involved:
      • Antecubital fossae
      • Popliteal fossae
      • Neck
      • Periorbital areas
      • Ankles anteriorly
    • Asthma or hay fever history (or 1st-degree relative if child < 4 years of age)
    • Dry skin in the past year
    • Symptoms beginning prior to age 2 (not used if child is < 4 years old)
    • Dermatitis of flexural surfaces (if child < 4 years old, cheeks, forehead, or outer aspects of extremities)
  • Chronic or relapsing history
  • Environmental stimuli (certain foods, allergens, medications)

Physical exam (skin)

  • Young children/infants:
    • Face
    • Scalp
    • Neck
    • Extensor surfaces
    • Papulovesicular lesions
    • Erythema
    • Edema
    • Excoriations
  • Older children and adults:
    • Lichenification
    • Flexor surfaces:
      • Elbows
      • Knees
      • Sides of neck, wrists, ankles
  • Dry skin

Laboratory studies

  • Only to rule out other skin conditions
  • Serum IgE: elevated in 80% of patients
  • Skin biopsy
  • Potassium hydroxide preparation of skin scrapings to rule out Tinea corporis
  • Patch testing to rule out contact dermatitis
  • Genetic testing


Supportive/prophylactic measures

Patient education:

  • Children
  • Parents

Elimination of exacerbating factors:

  • Avoid triggers:
    • Heat
    • Low humidity
    • Excessive bathing (without moisturization)
    • Stress and anxiety
    • Exposure to solvents and detergents
    • Xerosis (dry skin)
    • Overheating of skin
    • Harsh detergents
  • Treat associated skin infections:
    • S. aureus
    • Herpes simplex

Skin hydration (mainstay of treatment to reduce itching and episodes of inflammation):

  • Emollients:
    • Apply at least twice a day
    • Immediately after bathing or handwashing
  • Moisturizers containing:
    • Glycyrrhetinic acid
    • Urea
    • Glycerol


Topical treatments:

  • Corticosteroids: Prolonged use may cause skin atrophy or other adverse effects.
  • Calcineurin inhibitors: 2nd-line treatment
  • Phosphodiesterase 4 (PDE4) inhibitors (crisaborole)

Oral antihistamines:

  • H1 agents
  • Beneficial when sleep disturbed by pruritus
  • Diphenhydramine
  • Hydroxyzine
  • Cyproheptadine

Oral immunosuppressants:

  • Cyclosporin
  • Recurrence common upon discontinuation of treatment

Human monoclonal antibody:

  • Dupilumab
  • Inhibits IL-4 and IL-13


  • Used in patients with diffuse pruritus not controlled with topical therapy alone
  • Reduced production of histamine from mast cells and basophils
  • Narrowband ultraviolet B (NBUVB)
  • Ultraviolet A1 (UVA1)

Differential Diagnosis

  • Contact dermatitis: an erythematous, papular dermatitis, often with areas of vesiculation. Occurs due to direct skin exposure to an offending irritant with a direct cytotoxic effect. Diagnosis is made by history and physical exam findings. Treatment is with avoidance of offending irritants and adoption of protective measures as well as emollients and moisturizers. Topical steroids are the 1st-line intervention.
  • Seborrheic dermatitis: a chronic, relapsing, and usually mild form of dermatitis with a biphasic incidence in infants and adults. The condition is characterized by well-demarcated, erythematous plaques with greasy-appearing, yellow-like scales in sebaceous gland rich areas. The cause is unknown, but sebaceous glands appear to be necessary for the development of the disorder. The diagnosis is made clinically. Treatment is with topical antifungal, anti-inflammatory, and over-the-counter agents.
  • Diaper dermatitis: a form of irritant dermatitis most common in infants and children. Excessive moisture, friction, increased pH, and high enzymatic activity contribute to local disruption of the skin barrier. The condition is limited to the groin area and often spares folds where urine/feces do not contact the skin. The diagnosis is made clinically. Treatment involves general skin care measures (frequent diaper changes, exposure to air, and cleaning), topical steroids, and antifungals (in severe cases of superinfection by Candida).
  • Mycosis fungoides: a type of cutaneous T cell lymphoma. The disease presents in the skin but also can involve the lymph nodes, blook, and viscera. Mycosis fungoides often involves sites beneath undergarments and is uncommon in children. The disease presents with persistent progressive skin lesions of varying shapes and sizes and can be localized or widespread plaques or tumors, or generalized erythroderma. Pruritus is common. Diagnosis is clinical along with skin biopsy with routine histology. Treatment involves topical agents, including steroids, chemotherapy, retinoids, imiquimod, local radiation, and phototherapy. 
  • Psoriasis: a common chronic inflammatory skin disorder characterized by erythematous papules and plaques with a silver scale. Psoriasis is a complex immune-mediated disease whereby T lymphocytes, cytokines, dendritic cells, and tumor necrosis factor play a predominant role. Previously, it was viewed as a disease of hyperproliferation. Diagnosis is made by physical exam. Management is with topical corticosteroids, phototherapy, retinoids, methotrexate, cyclosporin, or biologic immune modifying agents.
  • Scabies: a cutaneous infestation caused by the mite Sarcoptes scabiei. Scabies is an intensely pruritic eruption with small erythematous papules on the fingers, wrists, axillae, areolae, waist, genitalia, and buttocks areas. Diagnosis is by history and physical exam along with detection of mites, eggs, or fecal pellets under microscopic evaluation. Treatment is aimed at both the patient and close contacts. Topical permethrin and oral ivermectin are the mainstays of therapy.


  1. Weston, W., Howe, W. (2021). Atopic dermatitis (eczema): Pathogenesis, clinical manifestations, and diagnosis. In Corona, R. (Ed.). UpToDate. Retrieved March 15, 2021, from
  2. Weston, W., Howe, W. (2021). Treatment of atopic dermatitis (eczema). In Corona, R. (Ed.). UpToDate. Retrieved March 15, 2021, from
  3. Spergel, J., Lio, P. (2021). Management of severe atopic dermatitis (eczema) in children. In Corona, R. (Ed.). UpToDate. Retrieved March 15, 2021, from
  4. Kim, B. (2020). Atopic Dermatitis. In James, W. (Ed). Medscape. Retrieved March 15, 2021, from
  5. Eichenfield, L.F., et al. (2014). Guidelines of care for the management of atopic dermatitis: section 2. Management and treatment of atopic dermatitis with topical therapies. J Am Acad Dermatol. 71(1), 116–132.
  6. Weidinger, S., Novak, N. (2016). Atopic dermatitis. Lancet. 387(10023), 1109–1122.

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