Chapter 145. Atopic Dermatitis

A 1-year-old Asian American girl is brought to her family physician for a new rash on her face and legs (Figures 145-1 and 145-2). The child is scratching both areas but is otherwise healthy. There is a family history of asthma, allergic rhinitis, and atopic dermatitis (AD) on the father's side. The child responded well to low-dose topical corticosteroids and emollients.

AD is a chronic and relapsing inflammatory skin disorder characterized by itching and inflamed skin that is triggered by the interplay of genetic, immunologic, and environmental factors.

Eczema, atopic eczema.

• AD is the most frequent inflammatory skin disorder in the United States and the most common skin condition in children.1
• Worldwide prevalence in children is 15% to 20% and is increasing in industrialized nations.2
• Sixty percent of cases begin during the first year of life and 90% by 5 years of age.1 One third will persist into adulthood.2
• Sixty percent of adults with AD have children with AD (Figure 145-3).1

• Strong familial tendency, especially if atopy is inherited from the maternal side.
• Associated with elevated T-helper (Th) 2 cytokine response, elevated serum immunoglobulin (Ig) E, hyperstimulatory Langerhans cells, defective cell-mediated immunity, and loss of function mutation in filaggrin, an epidermal barrier protein.
• Exotoxins of Staphylococcus aureus act as superantigens and stimulate activation of T-cells and macrophages, worsening AD without actually showing signs of superinfection.
• Patients may have a primary T-cell defect. This may be why they can get more severe skin infections caused by herpes simplex virus (eczema herpeticum as seen in Figure 145-4) or bacteria (widespread impetigo). They are also at risk of a bad reaction to the smallpox vaccine with dissemination of the attenuated virus beyond the vaccination site. Eczema vaccinatum is a potentially deadly complication of smallpox vaccination (Figure 145-5).

• History—Pruritus is the hallmark symptom of AD. It is referred to as “the itch that rashes” as patients will often feel the need to scratch before a primary lesion appears. If it does not itch, it is not AD. Persons with AD often have a personal or family history of other allergic conditions, namely asthma and allergic rhinitis.
• The atopic triad is AD, allergic rhinitis, and asthma. Atopic persons have an exaggerated inflammatory response to factors that irritate the skin.
• Physical examination—Primary lesions include vesicles, scale, papules, and plaques.
• Secondary (or sequential) lesions include linear excoriations from scratching or rubbing which may result in lichenification (thickened skin with accentuation of skin lines), fissuring, and prurigo nodularis. Crust may indicate that a secondary infection has occurred. Postinflammatory hyperpigmentation and follicular hyperaccentuation (more prominent hyperkeratotic follicles) (Figure 145-6) may also be identified.

Typical Distribution

• AD often starts on the face in infancy and childhood (Figures 145-1 and 145-7) and then appears in the flexural folds, especially the antecubital and popliteal fossa (Figures 145-8, 145-9, 145-10).
• Involvement of the neck, wrists, and ankles also may occur (Figures 145-11 and 145-12).
• AD in adults can occur on the hands, around the mouth, or eyelids as well as all the other areas (Figures 145-13 and 145-14).
• In one series, the prevalence of hand involvement in patients with active AD was 58.9%. There was a significant trend toward an increasing prevalence of hand involvement with increasing age.3

Other Features or Conditions Associated with Atopic Dermatitis

• Keratosis pilaris (Figure 145-15).
• Ichthyosis (Figure 145-16).
• Pityriasis alba (Figures 145-17 and 145-18).
• Palmar or plantar hyperlinearity.
• Dennie-Morgan lines (infraorbital fold) (Figure 145-14).
• Hand or foot dermatitis (see Chapter 147, Hand Eczema).
• Cheilitis (see Chapter 32, Angular Cheilitis).
• Susceptibility to cutaneous infections (Figures 145-4 and 145-5).
• Xerosis (dry skin) (Figure 145-19).
• Eye findings—Recurrent conjunctivitis, keratoconus (Figure 145-20), cataracts, orbital darkening.
• A horizontal nasal crease may be seen over the bridge of the nose in a patient with allergic rhinitis prone to performing the allergic salute. In some patients this crease may become hyperpigmented (Figure 145-21).

Laboratory Studies

Labs are rarely needed if the history and physical examination support the diagnosis. Occasionally, a KOH preparation may be needed to rule out tinea or a skin scraping to rule out scabies. Of course, both of these conditions can occur on top of AD. RAST (radioallergosorbent test) testing for food allergies and serum IgE levels are not of proven benefit.

• Dyshidrotic eczema—Dry inflamed scaling skin on the hands and feet with tapioca-like vesicles, especially seen between the fingers (see Chapter 147, Hand Eczema).
• Seborrheic dermatitis—Greasy, scaly lesions on scalp, face, and chest (see Chapter 151, Seborrheic Dermatitis).
• Psoriasis—Thickened plaques on extensor surfaces, scalp, and buttocks; pitted nails (see Chapter 152, Psoriasis).
• Lichen simplex chronicus (sometimes called neurodermatitis)—Usually, a single patch in an area accessible to scratching such as the ankle, wrist, and neck (see Chapter 149, Self-Inflicted Dermatoses).
• Contact dermatitis—Positive exposure history, rash in area of exposure; absence of family history. Patch testing may be helpful in distinguishing from AD (see Chapter 146, Contact Dermatitis).
• Scabies—Papules, burrows, finger web involvement, positive skin scraping (see Chapter 143, Scabies).
• Dermatophyte infection—On the hands or feet can look just like hand or foot dermatitis; a positive KOH preparation for hyphae can help make the diagnosis (see Chapter 140, Tinea Pedis).

• There is some evidence suggesting that controlling house dust mites reduces severity of symptoms in patients with the atopic triad. Bedding covers were found to be the most effective method to control dust mites and AD symptoms in this subgroup of AD patients. Unfortunately, dust mite interventions are not proven to be effective for patients with AD that do not have the full atopic triad.1 SOR B
• Dietary restriction is controversial but may be useful for infants with proven egg allergies. SOR B There is insufficient evidence that dietary manipulation in children or adults reduces symptom severity and may cause iatrogenic malnourishment.
• Patient education, avoidance of possible triggers (enzyme-rich detergents, wool clothing), and dry skin care should be optimized.
• Dilute bleach baths (0.5 cup of 6% bleach in tub of bath water) lower the S. aureus burden on the skin, decreasing severity of AD.4 SOR B
• There is some evidence suggesting probiotic treatment of pregnant mother and prolonged nursing of child may delay onset of AD.1 SOR B

Topical Therapies

• Topical steroids and emollients have been proven to work for AD and are the mainstay of treatment.1 SOR A
• Vehicle selection and steroid strength area based on age, body location, and lesion morphology. The ointments are best for dry and cracked skin and are more potent. Creams are easier to apply and are better tolerated by some patients.
• Use stronger steroids for thicker skin, severe outbreaks, or lesions that have not responded to weaker steroids. Avoid strong steroids on face, genitals, and armpits and in infants and small children.
• To avoid adverse effects, the highest potency steroids (e.g., clobetasol) should not be used for longer than 2 weeks continuously. However, they can be used intermittently for recurring AD in a pulse-therapy mode (e.g., apply every weekend, with no application on weekdays).
• Topical calcineurin inhibitors (immunomodulators, such as pimecrolimus and tacrolimus) reduce the rash severity and symptoms in children and adults.1 SOR A These work by suppressing antigen-specific T-cell activation and inhibiting inflammatory cytokine release. These are steroid-sparing medications that are helpful for eyelid eczema and in other areas when steroids may thin the skin (Figure 145-22). These agents are now only approved for persons older than 2 years of age and the FDA states that they should not be used as first-line agents because of a possible risk of causing cancer. The American Academy of Dermatology (AAD) has released a statement that the “data does not prove that the proper topical use of pimecrolimus and tacrolimus is dangerous.”
• Short-term adjunctive use of topical doxepin may aid in the reduction of pruritus.1 SOR A
• Topical and systemic antibiotics are used for AD that has become secondarily infected with bacteria. The most common infecting organism is S. aureus. Weeping fluid and crusting during an exacerbation should prompt consideration of antibiotic use1 (Figures 145-7, 145-8, and 145-23). SOR A

Oral/Systemic Therapies

• For extensive flares, consider oral prednisone or an IM shot of triamcinolone (40 mg in 1 mL of 40 mg/mL suspension for adults).1 SOR C
• The value of antihistamines in AD is controversial. If antihistamines are to be used, the sedating agents are most effective and can be given at night.1 SOR B
• Cyclosporine for severe refractory AD can be used in long-term maintenance therapy to treat and avoid relapse.1 SOR A Cyclosporine is approved for 1 year of lifetime therapy for skin diseases in the United States and 2 years in Europe (Figure 145-24).
• UV phototherapy may also be used in severe refractory AD with some success.1 SOR A
• Azathioprine, methotrexate, and mycophenolate mofetil are of possible benefit, but there is less evidence for their effectiveness.1 SOR C

Patients need to know that scratching their AD makes is worse. Behavior modification is especially challenging in young children and may involve cutting fingernails short and occluding hands/body at night with cotton gloves or clothing. Because of its chronicity and cyclic nature, AD patients may have poor adherence. In one recent study, overall adherence was 32%. A written action plan may be employed to improve adherence (Table 145-1).

Regular follow-up should be given to patients with chronic and difficult-to-control AD. Establishing a good regimen is crucial to good control and then visits may be adjusted to longer intervals between visits.