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A. Epidemiology navigator

  1. Also called eczema, atopic eczema, or IgE dermatitis
  2. Poorly defined erythema with edema, vesicles, weeping acutely
  3. May lead to skin thickening (lichenification) in chronic stage
  4. Onset primarily in infants and children
    1. Overall, lifetime prevalence 15-30% of children in developed countries
    2. Overall 2-10% of adults are affected in developed countries
    3. Thus, >70% of children have resolution of symptoms by adolescence / adulthood
    4. Onset before first year of life in 60% and before 5 years in 90% of patients
    5. Far less common adult onset (prevalence <3%)
    6. Apparent increase in incidence over past decades in developed countries
  5. Slight male predominance
  6. Symptoms typically abate with increasing age
  7. Majority have a personal or family history which includes
    1. Hay fever
    2. Asthma
    3. Allergic rhinitis
    4. Atopic dermatitis
    5. Association with food allergies
  8. Common superinfections with bacteria, especially S. aureus [4]

B. Pathogenesis [5] navigator

  1. Genetic contribution with environmental sensitizations
    1. High concordance rate of 77% in monozygotic twins
    2. Low concordance rate of 15% in dizygotic twins
  2. Antigen interacts with specific IgE
    1. Early onset atopic dermatitis usually emerges in absence of IgE
    2. IgE production is uncommon in early onset, especially in girls
  3. Epidermal Langerhans cells may present antigen
    1. Dermatophagoides pteronyssinus antigens may be involved
    2. Abnormal blood monocytes may also play a role in the disease
  4. Activated CD4+ T helper cells
    1. T helper lymphocyte type 2 (Th2) biased cells
    2. Produce IL4, 5, 10, and 13
    3. Th2 specific for Dermatophagoides pteronyssinus in lesional skin
    4. Raised concentrations of Th2 cell specific CD30 also found
    5. Reduced levels of interferon gamma are found in patients with allergic dermatitis
    6. Increased levels of C-C chemokines including RANTES, MCP-4, eotaxin
  5. Th2 Cells Produce "Allergic" Cytokines
    1. Sensitized basophils and mast cells release vasoactive substances
    2. Eosinophils are also stimulated
    3. Type I (IgE mediated) Hypersensitivity reaction results
    4. May have some linkage to high-affinity IgE receptor
  6. Th2 Cytokines Reduce Antimicrobial Defense Mechanisms [4]
    1. Innate immune system of skin contains antimicrobial peptides
    2. These include cathelicidins (such as LL-37) and ß-defensins (such as HBD-2)
    3. Th2 cytokines reduce expression of these antimicrobial proteins
    4. Levels of cathelicidins and ß-defensins are substantially reduced in affected skin
    5. Levels of these antimicrobial peptides are normal in psoriasis, a Th1 skin disease
  7. Role of Staphylococcus [1]
    1. Th2 cytokines suppress innate immune system of skin and lead to S. aureus colonization
    2. Thus, >90% of patients with atopic dermatitis have S. aureus skin colonization
    3. Scratching increases binding of S. aureus to skin, increasing ceramidase deposition
    4. S. aureus enteroxins, superantigens, increase inflammation (polyclonal T cell activation)
  8. Food allergies implicated in some cases primarily in infants [3]

C. Symptoms navigator

  1. Pruritus, may be intense
  2. Infants
    1. Erythematous vesicular and exudative lesions
    2. Located on facial and extensor surfaces
    3. In black children, follicuarl papular lesions are prominant and striking
    4. In black children, hypo- and hyperpigmentation
    5. Facial involvement is common
    6. Wrists, hands, ankles, feet, fingers, and toes are often involved
  3. Older Children and Adults
    1. Dry, lichenified (thickened), erythematous lesions due to chronic nature of disease
    2. Located on the flexural surfaces, front and sides of the neck, eyelids
    3. Also on forehead, face, wrists, and dorsa of the feet and hands
  4. Associated with other symptoms of atopy
    1. White dermatographism
    2. Allergic rhinitis
    3. Conjunctival irritation
  5. Exacerbating Factors
    1. Allergens: contact, food, inhalants
    2. Skin dehydration: frequent bathing
    3. Emotional stress
    4. Hormonal: pregnancy, menstruation
    5. Infections: S. aureus, group A streptococcus, fungus or HSV skin infections
    6. Seasons: winter in temperate climates

D. Skin Lesionsnavigator

  1. Acute
    1. Poorly defined erythematous patches, papules or plaques
    2. Scale may be present
    3. Edema occurs with widespread skin involvement
    4. Excoriations result from scratching
    5. Skin barrier breakdown can lead to major complications
  2. Chronic
    1. Seen first in puberty
    2. Lichenification (thickening) results from repeated rubbing or scratching
    3. Painful fissures seen on palms, fingers or soles
    4. Periorbital pigmentation from compulsive eye rubbing
  3. Complications
    1. Repeated cutaneous infections
    2. Anterior or subscapular cataracts
    3. Predilection to ichthyosis vulgaris and keratosis pilaris

E. Diagnostic Guidelines [2]navigator

  1. Pruritus Plus 3 or more of the following:
    1. Typical morphology and distribution
    2. flexural lichenification or linearity in adults
      1. facial and extensor involvement in infants and children
      2. involvement of skin creases (fronts of elbows, backs of knees, ankles, neck, eyes)
    3. Chronic or chronically-relapsing flexural dermatitis
    4. Personal or family history of atopy
    5. Onset in a child <2 years of age (criterion not used if child is <4 years of age)
    6. History of generally dry skin in past year
    7. History of asthma or hay fever
  2. Minor Criteria
    1. Immediate skin test reactivity
    2. Raised serum IgE
    3. Cheilitis, xeorosis, ichthyosis, palmer hyperlinearity, keratosis pilaris
    4. Early age of onset
    5. Nipple eczema
    6. Recurrent conjunctivitis
    7. Food intolerance
    8. Multiple other criteria

F. Laboratory Studiesnavigator

  1. Raised serum IgE - may be markedly ellevated
    1. Antibodies against aeroallergens
    2. Antibodies against food allergens
  2. HSV isolation from crusted lesions (eczema herpeticum)
  3. Radioallergosorbent testing (RAST)
  4. Immediate skin testing reactivity
  5. Staphylococci
    1. Staphylococci commonly superinfect skin lesions
    2. Nasal culture for S. aureus colonization of nares (90% of severe cases)
    3. Levels of ß-defensins and cathelicidins are reduced [4]

G. Differential Diagnosis (Table 2, Ref [1])navigator

  1. Seborrheic dermatitis of infancy
  2. Seborrheic dermatitis in adult
  3. Discoid (nummular) Eczema
  4. Irritant contact dermatitis
  5. Allergic contact dermatitis
  6. Frictional lichenoid dermatitis
  7. Other Exogenous Skin Conditions
    1. Scabies
    2. Onchocerciasis
    3. Insect Bites

H. Treatment [2] navigator

  1. Minimize Itching
    1. Healthy skin mainenance to sustain barrier function is critical
    2. Hydration with skin emollients (hydrated petrolatum)
    3. Emolients do not improve atopic dermatitis directly, but improve symptoms, appearance
    4. Oral antihistamines for relief from pruritus
    5. Topical glucocorticoids (see below)
  2. Reduce Allergen Exposure
    1. Reduce exposures, particularly to house dust mites
    2. Care must be taken to identify allergic triggers
  3. Glucocorticoids [2,10,12]
    1. Topical glucocorticoids for acute exacerbations
    2. Effective acutely but long term, causes skin thinning and hypopigmentation
    3. Pulse of systemic glucocorticoids for severe disease
    4. Glucocorticoids are ranked from Class I (superpotent) to Class VII (least potent)
    5. Are applied 1-2 times per day to affected areas; once daily as effective as twice daily
    6. Note that ointments are more potent than creams
    7. Skin atrophy occurs rapidly with superpotent agents and must be monitored
    8. Only mild (lower potency) topical agents are used on face and in genital area
    9. High potency topical glucocorticoids should not be used for >2-3 weeks
    10. These high potency agents, often fluorinated, cause skin atrophy and systemic absoprtion
    11. Reduced efficacy usually associated with disease severity, not glucocorticoid resistance
  4. Class I Topical Glucocorticoids: Superpotent
    1. Clobetasol (Temovate®) 0.05% foam
    2. betamethasone 0.05% ointment (Diprolene®)
    3. Halobetasol 0.05% cream
  5. Class II: Potent
    1. Mometasone ointment 0.1% (Elocon®)
    2. betamethasone 0.05% cream (Valisone®)
    3. Halcinonide 0.05% (Halog®)
  6. Class III: Upper Mid-Strength
    1. Triamcinolone ointment 0.1% (Kenalog®)
    2. betamethasone foam 0.12% (Valisone®)
    3. Fluticasone ointment 0.005%
  7. Class IV: Mid-Strength
    1. Triamcinolone cream 0.1%
    2. Mometasone cream 0.1%
    3. Hydrocortisone ointment 0.2%
  8. Class V: Lower Mid-Strength
    1. Triamcinolone lotion 0.1%
    2. Prenicarbate cream 0.1%
    3. Fluocinolone cream 0.025% (Synalar®)
  9. Class VI: Mild
    1. Alclometasone ointment/cream
    2. Fluocinolone cream 0.01%
    3. Desonide cream 0.05%
    4. Triamcinolone (Aristocort A®)
    5. Flumethasone (Locorten®)
  10. Class VII: Least Potent
    1. Hydrocortisone
    2. Methylprednisolone
    3. Prenisolone
  11. Tacrolimus (Protopic®) [6]
    1. Topical tacrolimus formuation useful for moderate to severe eczema
    2. Strengths of 0.03% and 1.0% available for bid application
    3. Responses usually seen within 7 days
    4. Well tolerated; does not cause skin thinning or hypopigmentation
    5. Main side effects are mild burning sensation, erythema, pruritus on applied area
    6. Some concern about skin tumors (sunscreens should be used) and systemic absorption
  12. Pamicrolimus (Elidel®) [7]
    1. Topical pimecrolimus 1.0% cream for bid application
    2. Approved for use in patients 2 years or older for mild to moderate disease
    3. Allows glucocorticoid-free control of atopic dermatitis
    4. May cause less systemic immunosuppression than tacrolimus or glucococorticoids
    5. Does not cause skin atrophy
    6. Concerns about skin tumors as for tacrolimus (sunscreens
  13. Topical Doxepin
    1. Some relief from itching within 48 hours
    2. Mainly due to its antihistamine activity
    3. Drowsiness due to systemic absorption may be a problem
  14. Antibiotics
    1. Eliminate S. aureus carriage and/or to treat superinfection
    2. Combined with topical glucocorticoids lead to improved healing of lesions [4]
  15. Ultraviolet Radiation [8]
    1. Ultraviolet (UV) radiation ± psoralen phototherapy effective in some cases
    2. Narrow band UVB is an effective adjuvant and generally well tolerated
    3. Broad band UVA is not effective
  16. Severe or Resistant Disease [2]
    1. Oral azathioprine, dosed to white blood cell thiopurine methyltransferase activity, is safe and beneficial in moderate to severe atopic dermatitis [11]
    2. Systemic methotrexate may be useful in resistant disease
    3. Mycophenolate has a better tolerability profile than many other immunosuppressives
    4. Low dose cyclosporin
    5. Interferon gamma also has efficacy, though with flu-like syndromes
  17. Perinatal administration of probiotic Lactobacillus rhamnosus strain GG appears to reduce risk of developing atopic eczema by >40% [9]

References navigator

  1. Bieber T. 2008. NEJM. 358(14):1483 abstract
  2. Leung DYM and Bieber T. 2003. Lancet. 361(9352):151 abstract
  3. Williams HC. 2005. NEJM. 352(22):2314 abstract
  4. Ong PY, Ohtake T, Brandt C, et al. 2002. NEJM. 347(15):1151 abstract
  5. Leung DYM, Diaz LA, DeLeo V, Soter NA. 1997. JAMA. 278(22):1914 abstract
  6. Topical Tacrolimus. 2001. Med Let. 43(1102):33 abstract
  7. Topical Pimecrolimus. 2002. Med Let. 44(1131):48 abstract
  8. Reynolds NJ, Franklin V, Gray JC, et al. 2001. Lancet. 357(9273):2013
  9. Kalliomaki M, Salminen S, Poussa T, et al. 2003. Lancet. 361(9372):1869 abstract
  10. Linden KG and Weinstein GD. 1999. Am J Med. 107(6):595 abstract
  11. Meggitt SJ, Gray JC, Reynolds NJ. 2006. Lancet. 367(9513):839 abstract
  12. Clobetasol Spray. 2006. Med Let. 48(1231):27 abstract