Epidemiology

 AD onset is most common between 3 and 6 months of age, with approximately 60% of patients developing
the eruption in the first year of life and 90% by 5 years of age.
 Periods of remission appear as the person grows older
 Spontaneous resolution of AD has been reported to occur after age 5 years in 40%-60% of patients affected
during infancy, if the disease is mild.
 AD disappears in 20% of children followed from infancy until adolescence, but become less severe in 65%
 More than half of adolescence treated for mild dermatitis may experience a relapse of disease as adults.
 Approximately 70% of AD patients have a positive family history of atopic diseases. (JAAD)
 The odds of developing AD are 2- to 3-fold higher in children with 1 atopic parent, and this increases to 3- to
5-fold if both parents are atopic
o A maternal history of AD is possibly more predictive (JAAD)
 35% of infants with AD develop asthma later in life (Fitzpatrick)

Management

A. Immediate

 Systemic corticosteroids are indicated only for severe acute exacerbations.

 Oral prednisone dosages should be high enough to suppress the dermatitis quickly, usually starting with 1
mg/kg daily for adults.
 Immunomodulators (calcineurin inhibitors)
o Tacrolimus
o Pimecrolimus
 Pimecrolimus cream and tacrolimus ointment may cause skin burning and pruritus, especially when applied
to acutely inflamed skin. Initial treatment of patients with AD using topical corticosteroids should be
considered to minimize TCI application site reactions. Patients with AD should be counseled about the
possibility of these reactions.

B. Short term

 Steroids are discontinued when lesions disappear and are resumed when new patches arise.
o Owing to the chronic nature of atopic dermatitis and the side effects of long-term systemic
corticosteroids, ongoing use of these agents is not recommended for maintenance therapy
 A midstrength steroid ointment (triamcinolone or betamethasone valerate) is applied 2 times daily to lesions
on the trunk until the eczematous lesions clear.
 Bedtime doses of hydroxyzine, diphenhydramine, or doxepin may be helpful via their sedative properties to
mitigate perceived pruritus.

C. Long term
NON-PHARMACOLOGIC

 Limit exposure to environmental and chemical factors known to cause exacerbations

o low humidity
 Gentle skin care
 Apply moisturizer  reduce inflammation and severity, to combat xerosis and transepidermal water loss
o Emollients (eg, glycol and glyceryl stearate, soy sterols) lubricate and soften the skin
o Occlusive agents (eg, petrolatum, dimethicone, mineral oil) form a layer to retard evaporation of
water
o Humectants (eg, glycerol, lactic acid, urea) attract and hold water
 Should not bathe more than a once daily
 Soap should be confined to the armpits, groin, scalp, and feet (or use of nonsoap cleansers)
 Washcloths and brushes should not be used
 After rinsing, the skin should be patted dry (not rubbed) and then immediately—within minutes—covered
with a thin film of an emollient or a corticosteroid as needed
 Vanicream can be used if contact dermatitis resulting from additives in medication is suspected
 Atopic patients may be irritated by rough fabrics, including wools and acrylics
 Cottons are preferable, but synthetic blends also are tolerated
 Other triggers of eczema in some patients include sweating, ointments, and heat.
 Maintenance treatment—Once symptoms have improved, constant application of effective moisturizers is
recommended to prevent flares. In patients with moderate disease, use of topical anti-inflammatories only
on weekends or three times weekly can prevent flares.

 Phototherapy is a second-line treatment, after failure of first-line treatment (emollients, topical steroids, and
topical calcineurin inhibitors).
 Phototherapy can be used as maintenance therapy in patients with chronic disease.