Description

• A chronic, relapsing, pruritic eczematous condition affecting characteristic sites
• Although called atopic, the majority of children with the typical clinical presentation will not have a measurable IgE-mediated sensitivity to allergens.
• System(s) affected: Skin/Exocrine

Epidemiology

Environmentally triggered in susceptible individuals

• 45% of all cases begin in the first 6 months of life.
• 70% of affected children will have a spontaneous remission before adolescence.
• Incidence on the rise for the past 3 decades; overall, affects ~15% of children at some time.

• Also may have late-onset dermatitis in adults
• Asians and blacks affected more often than whites
• 60% if 1 parent affected; rises to 80% if both parents affected

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)
• Exposure to tobacco smoke
• Family history of atopy:
  • Asthma
  • Allergic rhinitis

• Arises from gene–gene and gene–environment interactions
• Both epidermal and immune coding likely involved

Pathophysiology

• Alteration in stratum corneum results in transepidermal water loss and defect in barrier function.
• Epidermal adhesion is reduced either as a result of: (a) Genetic mutation resulting in altered epidermal proteins or (b) 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 (1)

Commonly Associated Conditions

• Food sensitivity/allergy in many cases
• Asthma
• Allergic rhinitis
• Hyper-IgE syndrome (Job syndrome):
  • Atopic dermatitis
  • Elevated IgE
  • Recurrent pyodermas
  • Decreased chemotaxis of mononuclear cells