Atopic Dermatitis and Contact Dermatitis

Atopic dermatitis (eczema) is the most common chronic inflammatory skin disease in children and adults. The etiology of this disease is multifactorial and not fully understood, with likely contribution from genetic, epigenetic, and environmental factors. Current hypotheses implicate the breadth of the immune system (i.e., type 2 helper T cell and immunoglobulin E), epidermal structural defects (i.e., loss-of-function mutation of the filaggrin gene), environmental exposures, and the skin microbiome.

Atopic Dermatitis

Diagnosis

The following table describes the basic criteria for the diagnosis of atopic dermatitis:

(Source: Atopic Dermatitis. N Engl J Med 2005.)

Risk Factors

Risk factors that are consistently and strongly linked to a diagnosis of atopic dermatitis include:

• personal history of allergic rhinitis or asthma

• family history of atopy (i.e., asthma, eczema, and allergic rhinitis)

• loss-of-function mutation of the filaggrin gene (not routinely tested clinically)

Clinical Manifestations

Cutaneous findings of atopic dermatitis are highly variable and depend on the age of the patient, baseline skin color, the morphologic variant of atopic dermatitis, and therapeutic attempts. Key findings include symmetry, pruritus, and evidence of excoriation.

(Source: Atopic Dermatitis. N Engl J Med 2021.)

(Source: Atopic Dermatitis. N Engl J Med 2005.)

(Source: Atopic Dermatitis. N Engl J Med 2008.)

(Source: Atopic Dermatitis. N Engl J Med 2008.)

(Source: Hand Eczema. N Engl J Med 2012.)

Always consider the following alternative diagnoses for atypical presentations:

• allergic or irritant contact dermatitis

• scabies

• dermatitis herpetiformis

• seborrheic dermatitis

• cutaneous T-cell lymphoma

• transient acantholytic dermatosis

Management

The AAD Atopic Dermatitis Clinical Guideline provides a description of various therapy options (topical medicine, light therapy, and systemic therapy) and basic skin care and lifestyle changes.

Initial management:

• Apply ultra-potent topical glucocorticoid (e.g., clobetasol 0.05% cream) twice daily for 2 weeks, followed by maintenance therapy with mid-potency topical glucocorticoid (e.g., triamcinolone 0.1% cream) every other day, limited to fewer than 14 days per month.

• Use less-potent topical glucocorticoids for genitalia and face due to thinner stratum corneum.

• Topical tacrolimus and pimecrolimus are alternatives to topical glucocorticoids and ideal for the face and genitalia. Potency is similar to mid-potent topical glucocorticoids.

• Systemic therapy with immunosuppressive drugs (methotrexate, cyclosporine, azathioprine, and mycophenolate).

• Light therapy, using narrow-band ultraviolet B, can be used as an adjunct to both systemic and topical therapies.

• Avoid systemic glucocorticoids due to severe rebound effect during taper.

• Several other medications approved by the U.S. Food and Drug Administration are available:

  • crisaborole (a nonglucocorticoid topical therapy)

  • dupilumab (a monoclonal antibody targeting interleukin-4 receptor alpha)

  • tralokinumab (a monoclonal antibody targeting interleukin-13)

  • abrocitinib and upadacitinib (oral Janus kinase [JAK] inhibitors)

  • ruxolitinib (a topical JAK inhibitor)

Management of pediatric atopic dermatitis: Pediatric dermatologists often recommend the “eczema boot camp,” first described by Maguiness and Lio. This approach defines a 2-week plan of intensive topical therapy in addition to dilute bleach baths and wet wraps followed by maintenance and preventative therapies (see Atopic Dermatitis in the Pediatric Dermatology rotation guide).

Contact Dermatitis

Contact dermatitis is an inflammatory skin condition that occurs after contact with a foreign substance. It is a major cause of occupational skin diseases. The two types of contact dermatitis are:

• irritant contact dermatitis (a nonimmune-mediated reaction)

• allergic contact dermatitis (a type-IV delayed hypersensitivity reaction)

Although any area of the skin can be affected, common sites are the hands, face, and neck. Lesions are usually located at the site of contact and have a well-defined border; they are characterized by erythema (figure 1) and scaling (figure 2) and are pruritic. Bullae (figure 4) may also develop.

(Source: Coral Dermatitis. N Engl J Med 2015.)

(Source: The Mango-Poison Ivy Connection. N Engl J Med 1998.)

Diagnosis

• Diagnosis of contact dermatitis is made through history, physical examination, and symptom resolution after avoidance of a suspected substance.

• Common substances include nickel, poison ivy, and fragrances.

• If allergic contact dermatitis is suspected, the patient should be referred to a dermatologist for patch testing.

• A list of allergens in a patch test for contact dermatitis can be found here (table 3) and the process for patch testing can be found here (box 1).

Management

• The main priority of management of contact dermatitis is identification and avoidance of causative substances.

• Regular use of emollients is effective for managing acute symptoms and maintaining the barrier function of skin.

• Topical glucocorticoids are effective in treating allergic contact dermatitis, but data are limited to support its use for irritant contact dermatitis. If the lesions are widespread and cover large areas of the body, systemic glucocorticoid therapy can be used.

• Lesions should be monitored closely for bacterial superinfections.