Dermatitis, Atopic

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Basics

Description

  • A chronic, relapsing, pruritic eczematous condition affecting characteristic sites
  • 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 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 lighter skinned individuals.
  • 60% if one parent is affected; rises to 80% if both parents are affected

Incidence
On the rise over the past 3 decades in industrialized countries.

Prevalence
Approximately 13% of children and 7–10% of adults in the US (1)

Etiology and Pathophysiology

  • Two main hypothesis: immunologic with unbalanced immune response and/or skin barrier dysfunction
  • 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)[C].
  • 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 (1)
  • Hyper-IgE syndrome (Job syndrome)
    • AD
    • Elevated IgE
    • Recurrent pyodermas
    • Decreased chemotaxis of mononuclear cells

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Basics

Description

  • A chronic, relapsing, pruritic eczematous condition affecting characteristic sites
  • 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 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 lighter skinned individuals.
  • 60% if one parent is affected; rises to 80% if both parents are affected

Incidence
On the rise over the past 3 decades in industrialized countries.

Prevalence
Approximately 13% of children and 7–10% of adults in the US (1)

Etiology and Pathophysiology

  • Two main hypothesis: immunologic with unbalanced immune response and/or skin barrier dysfunction
  • 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)[C].
  • 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 (1)
  • Hyper-IgE syndrome (Job syndrome)
    • AD
    • Elevated IgE
    • Recurrent pyodermas
    • Decreased chemotaxis of mononuclear cells

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