> Table of Contents > Dermatitis, Atopic
Dermatitis, Atopic
Dennis E. Hughes, DO, FACEP
image 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
EPIDEMIOLOGY
  • 45% of all cases begin in the first 6 months of life with 95% onset prior to age 5 years.
  • 70% of affected children will have a spontaneous remission before adolescence.
  • Incidence on the rise for the past 3 decades in industrialized countries; overall, affects ˜15% of children at some time (United States)
  • Also, may have late-onset dermatitis in adults or relapse of childhood condition—primarily hand eczema
  • Asians and blacks are affected more often than whites.
  • 60% if one parent is affected; rises to 80% if both parents are affected
ETIOLOGY
  • Two main hypothesis: immunologic with unbalanced immune response and/or skin barrier dysfunction (1)
  • 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 (on chromosome 1), which codes for a skin barrier protein (2)
  • 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)
  • Exposure to tobacco smoke
  • Family history of atopy
    • Asthma
    • Allergic rhinitis
COMMONLY ASSOCIATED CONDITIONS
  • Food sensitivity/allergy in many cases
  • Asthma
  • Allergic rhinitis
  • Hyper-IgE syndrome (Job syndrome)
    • AD
    • Elevated IgE
    • Recurrent pyodermas
    • Decreased chemotaxis of mononuclear cells
image DIAGNOSIS
PHYSICAL EXAM
Primarily skin manifestations
  • Distribution of lesions
    • Infants: trunk, face, and flexural surfaces; diaper-sparing
    • Children: antecubital and popliteal fossae
    • Adults: hands, feet, face, neck, upper chest, and genital areas
  • Morphology of lesions
    • Infants: erythema and papules; may develop oozing, crusting vesicles
    • Children and adults: Lichenification and scaling are typical with chronic eczema as a result of persistent scratching and rubbing (lichenification rare in infants).
  • Associated signs
    • Facial erythema, mild to moderate
    • Perioral pallor
    • Infraorbital fold (Dennie sign/Morgan line)-atopic pleat
    • Dry skin progressing to ichthyosis
    • Increased palmar linear markings
    • Pityriasis alba (hypopigmented asymptomatic areas on face and shoulders)
    • Keratosis pilaris
DIFFERENTIAL DIAGNOSIS
  • Photosensitivity rashes
  • Contact dermatitis (especially if only the face is involved)
  • Scabies
  • Seborrheic dermatitis (especially in infants)
  • Psoriasis or lichen simplex chronicus if only localized disease is present in adults
  • Rare conditions of infancy
    • Histiocytosis X
    • Wiskott-Aldrich syndrome
    • Ataxia-telangiectasia syndrome
  • Ichthyosis vulgaris
DIAGNOSTIC TESTS & INTERPRETATION
Initial Tests (lab, imaging)
  • No test is diagnostic.
  • Serum IgE levels are elevated in as many as 80% of affected individuals, but test is not routinely ordered.
  • Eosinophilia tends to correlate with disease severity.
  • Scoring atopic dermatitis (SCORAD) is scoring system for AD comprising scores for area, intensity, and subjective symptoms.
image TREATMENT
GENERAL MEASURES
  • Minimize flare-ups and control the duration and intensity of flare-up.
  • Avoid agents that may cause irritation (e.g., wool, perfumes).
  • Minimize sweating.
  • Lukewarm (not hot) bathing
  • Minimize use of soap (superfatted soaps best).
  • Sun exposure may be helpful.
  • Humidify the house.
  • Avoid excessive contact with water.
  • Avoid lotions that contain alcohol.
  • If very resistant to treatment, search for a coexisting contact dermatitis.
Pediatric Considerations
Chronic potent fluorinated corticosteroid use may cause striae, hypopigmentation, or atrophy, especially in children.
MEDICATION
First Line
  • Frequent systemic lubrication with thick emollient creams (e.g., Eucerin, Vaseline) over moist skin is the mainstay of treatment before any other intervention is considered (1)[A].
  • Infants and children: 0.5-1% topical hydrocortisone creams or ointments (use the “fingertip unit [FTU]” dosing) (1)[C]
  • P.283

  • Adults: higher potency topical corticosteroids in areas other than face and skin folds
  • Short-course, higher potency corticosteroids for flares; then return to the lowest potency (creams preferred) that will control dermatitis.
  • Antihistamines for pruritus (e.g., hydroxyzine 10 to 25 mg at bedtime and as needed)
Second Line
  • Topical immunomodulators (tacrolimus or pimecrolimus) for episodic use for children >2 years. There is a black box warning from the FDA regarding potential cancer risk.
  • Plastic occlusion in combination with topical medication to promote absorption
  • For severe AD, consider systemic steroids for 1 to 2 weeks (e.g., prednisone 2 mg/kg/day PO [max 80 mg/day] initially, tapered over 7 to 14 days).
  • Topical tricyclic doxepin, as a 5% cream, may decrease pruritus.
  • Modified Goeckerman regimen (tar and ultraviolet light)
  • Low-dose methotrexate was established as effective treatment in adults, and recent review suggests it is safe for children and adolescents (3)[B].
ISSUES FOR REFERRAL
  • Ophthalmology evaluation for persistent vernal conjunctivitis
  • If using topical steroids around eyes for extended periods, ophthalmology follow-up for cataract evaluation
ADDITIONAL THERAPIES
  • Methods to reduce house mite allergens (micropore filters on heating, ventilation, and air-conditioning systems; impermeable mattress covers)
  • Behavioral relaxation therapy to reduce scratching
  • Bleach baths may reduce staph colonization, but definitive evidence for benefit in the condition is lacking. Recommend 1/2 cup of standard 6% household bleach for a full tub of water and soak for 5 to 10 minutes, blotting skin dry upon leaving the bath.
COMPLEMENTARY & ALTERNATIVE MEDICINE
  • Evening primrose oil (includes high content of fatty acids)
    • May decrease prostaglandin synthesis
    • May promote conversion of linoleic acid to omega-6 fatty acid
  • Probiotics may reduce the severity of the condition, thus reducing medication use.
image ONGOING CARE
FOLLOW-UP RECOMMENDATIONS
Patient Monitoring
Evaluate to ensure that secondary bacterial or fungal infection does not develop as a result of disruption of the skin barrier. Most patients with AD are colonized by Staphylococcus. There is a little evidence for the routine use of antimicrobial interventions to reduce skin bacteria, but treatment of clinical infection with coverage for Staphylococcus is recommended.
DIET
  • Trials of elimination may find certain “triggers” in some patients.
  • Breastfeeding in conjunction with maternal hypoallergenic diets may decrease the severity in some infants.
PATIENT EDUCATION
  • http://www.aad.org/skin-conditions/dermatology-a-to-z/atopic-dermatitis
  • National Eczema Association: www.nationaleczema.org
PROGNOSIS
  • Chronic disease
  • Declines with increasing age
  • 90% of patients have spontaneous resolution by puberty.
  • Localized eczema (e.g., chronic hand or foot dermatitis, eyelid dermatitis, or lichen simplex chronicus) may continue in some adults.
REFERENCES
1. Thomsen SF. Atopic dermatitis: natural history, diagnosis, and treatment. ISRN Allergy. 2014;2014:354250.
2. Wollenberg A, Seba A, Antal AS. Immunological and molecular targets of atopic dermatitis treatment. Br J Dermatol. 2014;170(Suppl 1):7-11.
3. Deo M, Yung A, Hill S, et al. Methotrexate for treatment of atopic dermatitis in children and adolescents. Int J Dermatol. 2014;53(8):1037-1041.
Additional Reading
&NA;
  • Boguniewicz M, Leung DY. Recent insights into atopic dermatitis and implications for management of infectious complications. J Allergy Clin Immunol. 2010;125(1):4-13.
  • Catherine Mack Correa M, Nebus J. Management of patients with atopic dermatitis: the role of emollient therapy. Dermatol Res Pract. 2012;2012:836931.
  • Lifschitz C. The impact of atopic dermatitis on quality of life. Ann Nutr Metab. 2015;66(Suppl 1): 34-40.
See Also
&NA;
Algorithm: Rash, Focal
Codes
&NA;
ICD10
  • L20.9 Atopic dermatitis, unspecified
  • L20.89 Other atopic dermatitis
  • L20.83 Infantile (acute) (chronic) eczema
Clinical Pearls
&NA;
  • Institute early and proactive treatment to reduce inflammation. Use the lowest potency topical steroid that controls symptoms.
  • Monitor for secondary bacterial infection.
  • Frequent systemic lubrication with thick emollient creams (e.g., Eucerin, Vaseline) over moist skin is the mainstay of treatment before any other intervention is considered.