Dermatitis, Atopic

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Basics

Description

  • A chronic, relapsing, inflammatory, intensely pruritic skin diease
  • Early-onset cases have coexisting allergen sensitization more often than late onset.
  • Clinical phenotypical presentation is highly variable, suggesting multifactorial pathophysiology.
  • May have significant effect on quality of life for patient and family—recurrent symptoms affect lifestyle and mental health.

Epidemiology

  • 45% of all cases begin in the first 6 months of life with 80–95% onset prior to age 5 years.
  • 50–66% of affected children will have a spontaneous remission before adolescence.
  • Also, may have late-onset dermatitis in adults or relapse of childhood condition—primarily hand eczema
  • Darker pigmented individuals are affected more often than whites.
  • 60% incidence if one parent previously affected; rises to 80% if both parents previously affected. Monozygotic twins have 80% concordinance for the disorder.

Incidence
Varies worldwide, but all countries’ populations are affected. The only consistent signal favored lower incidence in rural versus urban locations (exceptions are Canada, Mexico) (1).

Prevalence
Approaching 20% prevalence in children and 10% in young adults; still present in later adulthood 2%

Etiology and Pathophysiology

  • Current understanding is atopic dermatitis is a systemic T-helper cell driven disorder.
  • Alteration in stratum corneum results in transepidermal water loss and defect in barrier function.
  • Epidermal adhesion is reduced either as a result of (i) genetic mutation resulting in altered epidermal proteins or (ii) defect in immune regulation causing an altered inflammatory response.
  • Interleukin-31 (IL-31) upregulation is thought to be a major factor in pruritus mediated by cytokines and neuropeptides rather than histamine excess.

Genetics

  • Recent discovery of association between atopic dermatitis (AD) and mutation in the filaggrin gene (FLG), which codes for a skin barrier protein
  • Both epidermal and immune coding likely involved

Risk Factors

  • “Itch–scratch cycle” (stimulates histamine release)
  • Skin infections
  • Emotional stress
  • Irritating clothes and chemicals
  • Excessively hot or cold climate
  • Food allergy in children (in some cases). Studies of breastfeeding conveying decreased risk versus increased risk are mixed in conclusion (2).
  • Exposure to tobacco smoke
  • Some evidence suggests that repeated exposure to “hard” water may exacerbate condition.
  • Family history of atopy
    • Asthma
    • Allergic rhinitis

Commonly Associated Conditions

  • Food sensitivity/allergy in many cases; strong association with asthma and allergic rhinitis
  • Association with both cutaneous and extra-cutaneous infections: URI, OM, UTI, cellulitis, erysipelas, zoster, endocarditis, MRSA, MSSA, pharyngitis, and rarely sepsis
  • Hyper-IgE syndrome (Job syndrome)
    • AD
    • Elevated IgE
    • Recurrent pyodermas
    • Decreased chemotaxis of mononuclear cells

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Basics

Description

  • A chronic, relapsing, inflammatory, intensely pruritic skin diease
  • Early-onset cases have coexisting allergen sensitization more often than late onset.
  • Clinical phenotypical presentation is highly variable, suggesting multifactorial pathophysiology.
  • May have significant effect on quality of life for patient and family—recurrent symptoms affect lifestyle and mental health.

Epidemiology

  • 45% of all cases begin in the first 6 months of life with 80–95% onset prior to age 5 years.
  • 50–66% of affected children will have a spontaneous remission before adolescence.
  • Also, may have late-onset dermatitis in adults or relapse of childhood condition—primarily hand eczema
  • Darker pigmented individuals are affected more often than whites.
  • 60% incidence if one parent previously affected; rises to 80% if both parents previously affected. Monozygotic twins have 80% concordinance for the disorder.

Incidence
Varies worldwide, but all countries’ populations are affected. The only consistent signal favored lower incidence in rural versus urban locations (exceptions are Canada, Mexico) (1).

Prevalence
Approaching 20% prevalence in children and 10% in young adults; still present in later adulthood 2%

Etiology and Pathophysiology

  • Current understanding is atopic dermatitis is a systemic T-helper cell driven disorder.
  • Alteration in stratum corneum results in transepidermal water loss and defect in barrier function.
  • Epidermal adhesion is reduced either as a result of (i) genetic mutation resulting in altered epidermal proteins or (ii) defect in immune regulation causing an altered inflammatory response.
  • Interleukin-31 (IL-31) upregulation is thought to be a major factor in pruritus mediated by cytokines and neuropeptides rather than histamine excess.

Genetics

  • Recent discovery of association between atopic dermatitis (AD) and mutation in the filaggrin gene (FLG), which codes for a skin barrier protein
  • Both epidermal and immune coding likely involved

Risk Factors

  • “Itch–scratch cycle” (stimulates histamine release)
  • Skin infections
  • Emotional stress
  • Irritating clothes and chemicals
  • Excessively hot or cold climate
  • Food allergy in children (in some cases). Studies of breastfeeding conveying decreased risk versus increased risk are mixed in conclusion (2).
  • Exposure to tobacco smoke
  • Some evidence suggests that repeated exposure to “hard” water may exacerbate condition.
  • Family history of atopy
    • Asthma
    • Allergic rhinitis

Commonly Associated Conditions

  • Food sensitivity/allergy in many cases; strong association with asthma and allergic rhinitis
  • Association with both cutaneous and extra-cutaneous infections: URI, OM, UTI, cellulitis, erysipelas, zoster, endocarditis, MRSA, MSSA, pharyngitis, and rarely sepsis
  • Hyper-IgE syndrome (Job syndrome)
    • AD
    • Elevated IgE
    • Recurrent pyodermas
    • Decreased chemotaxis of mononuclear cells

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