DEFINITION

Atopic dermatitis (Fig. 1) and hereditary eczema are interchangeable terms for an inflammatory condition of the skin characterized by erythema, pruritus, scaling, lichenification, and papulovesicles. Atopic dermatitis is a distinct condition in persons who are genetically predisposed to developing immunoglobulin (Ig) E-mediated hypersensitivity reactions. It is characterized by the itch-scratch cycle: Affected persons have the sensation of itch, followed by scratching and the subsequent creation of a rash. The classic triad of atopy includes eczema, asthma, and allergies. A wide range of environmental factors, such as contact allergens, stress, food, skin flora, and humidity, play roles in the development and severity of atopic dermatitis.

Figure 1 Perioral and periorbital dermatitis with hyperlinearity on the lower eyelid (Dennie-Morgan lines).

PREVALENCE

Atopic dermatitis is a common condition affecting approximately 17% of the population,¹ with a slight female preponderance (1.3 : 1 in children). The incidence has increased twofold to threefold since the 1970s. The basis of this increase in not well understood; however, environmental factors appear to play an important role in disease prevalence.

Some factors associated with an increased risk of atopic dermatitis include small family size, higher socioeconomic and educational levels regardless of ethnicity, movement from rural to urban environment, and increased use of antibiotics (the Western lifestyle). This has led to the hygiene hypothesis, which postulates that infections in early childhood (from less-hygienic practices and older siblings) might prevent atopic dermatitis. This hypothesis is supported by evidence that infections induce type-1 helper T cells (Th1), whereas there is a predominance of type-2 helper T cells (Th2) in atopic dermatitis. Th1 responses antagonize the development of Th2 cells, thereby potentially decreasing the incidence of atopic dermatitis.²

PATHOPHYSIOLOGY

Atopic dermatitis is a type I IgE-mediated hypersensitivity reaction, but the exact etiology is unknown. The pathogenesis is multifactorial and involves a complex immunologic cascade, including disruption of the epidermal barrier, IgE dysregulation, defects in the cutaneous cell-mediated immune response, and genetic factors.

The major elements in immune dysregulation are Langerhans’ cells, inflammatory dendritic epidermal cells, monocytes, macrophages, lymphocytes, mast cells, and keratinocytes, all of which interact through an intricate cascade of cytokines leading to a predominance of Th2 cells over (Th1 cells).³ The Th2 cytokines, interleukin (IL)-4, IL-5, IL-10, and IL-13, are increased in the skin, and there is a corresponding decrease in Th1 cytokines, mainly interferon-γ and IL-2.

Patients with atopic dermatitis often have dry, sensitive skin due to changes in the epidermis, which serves as a barrier to the environment by maintaining the water balance of the skin. Essential fatty acids (EFAs), such as linoleic and linolenic acid, are important components of the epidermal barrier. In atopic dermatitis, Δ6-desaturase activity is deficient, which leads to decreased linoleic and linolenic acid metabolites. Loss of EFAs results in increased transepidermal water loss and subsequent xerosis (dryness). The EFAs form the substrate of the inflammatory mediators (prostaglandins and leukotrienes), resulting in a secondary deficiency of prostaglandin E₁ (PGE₁).

Defects in the epidermal barrier also lead to increased susceptibility to atopens (atopic allergens such as house dust mites, grass, or pollen). When such allergens contact atopic skin, they stimulate Th2 lymphocytes to produce cytokines such as IL-4, IL-5, and IL-13, which in turn promote an increase in IgE synthesis.⁴ Atopic dermatitis patients often have high levels of IgE antibodies to house dust mites and other allergens. Elimination of these allergens from the environment, an extremely difficult undertaking, can lead to improvement of atopic dermatitis.

Defective cell-mediated immunity leads to increased susceptibility to many bacterial, viral, and fungal infections of the skin. Children with atopic dermatitis are particularly susceptible to severe, widespread herpes simplex virus infection (eczema herpeticum), a systemic and potentially fatal infection affecting primarily areas of active eczema. Widespread infections with human papillomavirus (warts) and molluscum contagiosum are also common in children with atopic dermatitis.

Many factors exacerbate or trigger atopic dermatitis, including colonization with Staphylococcus aureus, stress, anxiety, systemic illness, and xerosis. The most common trigger is S. aureus colonization. More than 90% of patients with atopic dermatitis have S. aureus colonization of lesional skin, and more than 75% have colonization of uninvolved skin.⁵ Staphylococci exacerbate atopic dermatitis by two mechanisms: acting as superantigens by stimulating an augmented T cell response, thereby leading to exacerbation of skin disease, and promoting increased production of IgE. IgE has anti–S. aureus properties and helps to control colonization and infection in normal persons. In atopic dermatitis patients, the elevated IgE levels contribute to immune dysregulation. Treatment with topical or oral antistaphylococcal antibiotics (or both) decreases the colonization of the skin and often leads to improvement of the dermatitis.

Family studies support a genetic basis for atopic dermatitis. When both parents are atopic, their offspring have a 70% risk for atopic dermatitis,⁶ with a higher risk of inheritance if the mother is atopic. The mode of inheritance appears to be complex and likely involves several genes. To date, no specific single gene has been identified as a unique marker for atopic dermatitis or atopy.⁷

SIGNS AND SYMPTOMS

Atopic dermatitis is a chronic disease with periods of remissions and exacerbations. Three age-related stages exist: the infantile stage (up to 2 years old), the childhood stage (from 2 to 12 years), and the adult stage (puberty onward). The manifestations vary with age, even in the same patient. All stages are characterized by xerosis, fissures, pruritus, and lichenification. The main differentiating factor is the area of involvement.

The infantile stage is characterized by very pruritic, red, eczematous plaques on the cheeks and extensor extremities. Secondary impetiginization, with honey-colored crust, is common in infants. Scalp involvement can resemble seborrheic dermatitis. The diaper area is spared.

The childhood stage is primarily a papular dermatitis affecting the flexural areas, especially the antecubital and popliteal fossae, wrists, ankles, and neck. Thickened, lichenified plaques with excoriation (Figs. 2 to 4) are common. In darker-pigmented children, follicular papules may be the only manifestation. Hypopigmentation and hyperpigmentation can occur, which can cause great anxiety in parents. Pityriasis alba, characterized by hypopigmented, scaly patches on the face, is commonly seen. Keratosis pilaris, or spiny hair follicles, commonly affect the posterior aspects of the upper arms and the anterior thighs.

Figure 2 Linear superficial erosions of the neck and upper chest consistent with excoriations.

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