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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). Atopic dermatitis is a type I IgE-mediated hypersensitivity reaction, but the exact etiology is unknown. 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. Defects in the epidermal barrier also lead to increased susceptibility to atopens (atopic allergens such as house dust mites, grass, or pollen). Defective cell-mediated immunity leads to increased susceptibility to many bacterial, viral, and fungal infections of the skin. Many factors exacerbate or trigger atopic dermatitis, including colonization with Staphylococcus aureus, stress, anxiety, systemic illness, and xerosis.
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. The infantile stage is characterized by very pruritic, red, eczematous plaques on the cheeks and extensor extremities. The childhood stage is primarily a papular dermatitis affecting the flexural areas, especially the antecubital and popliteal fossae, wrists, ankles, and neck. Atopic dermatitis can resemble other types of dermatitis (seborrheic dermatitis, allergic contact dermatitis, irritant contact dermatitis) and dermatophytosis.
Most patients with atopic dermatitis require hydration though the liberal use of bland emollients, which serve to hydrate the stratum corneum and maintain the lipid barrier.
Topical calcineurin inhibitors (tacrolimus, pimecrolimus) are effective alternatives to the chronic use of topical corticosteroids.
The pruritus associated with atopic dermatitis can be severe and often interferes with school, work, and sleep.
Nonsedating antihistamines such as fexofenadine, cetirizine, loratidine, and desloratidine can help offset daytime itching without somnolence.
These should be used very cautiously and with close monitoring and should be reserved for the most severe cases. Allergic contact dermatitis from topical medications, cosmetics, or metals should be considered in patients with recalcitrant disease. Atopic dermatitis is a chronic disease with intermittent flares and spontaneous remissions.
With good skin care, moisturization, and the use of topical corticosteroids or topical calcineurin inhibitors, most patients with atopic dermatitis do well. First-line treatment consists of applying bland emollients, limiting soap, and decreasing bath temperature. Percutaneous sensitization through barrier-disrupted skin elicits a TH2-dominant cytokine response. Report of the Topical Calcineurin Inhibitor Task Force of the American College of Allergy, Asthma and Immunology and the American Academy of Allergy, Asthma and Immunology. An evidence-based review of the efficacy of antihistamines in relieving pruritus in atopic dermatitis. 1) and hereditary eczema are interchangeable terms for an inflammatory condition of the skin characterized by erythema, pruritus, scaling, lichenification, and papulovesicles.
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.


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. Essential fatty acids (EFAs), such as linoleic and linolenic acid, are important components of the epidermal barrier. 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. 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.
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). Affected patients may have had only a few outbreaks since infancy, or they may have had a chronic, relapsing course.
The goals of therapy should be to reduce the number and severity of flares and to increase the number of disease-free periods. Sufficient emollients applied liberally several times a day may be enough to significantly reduce the disease activity of atopic dermatitis. Patients can use a low-potency topical steroid (hydrocortisone or desonide) for day-to-day control of mild disease and a medium-potency steroid (triamcinolone acetonide, fluticasone, or fluocinolone) for more severe flares. Topical calcineurin inhibitors bind calcineurin and block the activation of T cells by cytokines, thus halting the inflammatory cascade that leads to atopic dermatitis.
Despite a lack of objective data to support their use, antihistamines are commonly used to break the itch-scratch-itch cycle. Sedating antihistamines such as diphenhydramine or hydroxyzine are often helpful for nighttime pruritus.
Evaluation by an environmental dermatologist and an allergist, including patch, pinprick, and serum radioallergosorbent testing (RAST), may be warranted. Atopic dermatitis is a distinct condition in persons who are genetically predisposed to developing immunoglobulin (Ig) E-mediated hypersensitivity reactions. The basis of this increase in not well understood; however, environmental factors appear to play an important role in disease prevalence. 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.
In atopic dermatitis, Δ-desaturase activity is deficient,6 which leads to decreased linoleic and linolenic acid metabolites. Elimination of these allergens from the environment, an extremely difficult undertaking, can lead to improvement of atopic dermatitis. Widespread infections with human papillomavirus (warts) and molluscum contagiosum are also common in children with atopic dermatitis.
To date, no specific single gene has been identified as a unique marker for atopic dermatitis or atopy. The hand dermatitis is common and may be the only manifestation of adult atopic dermatitis, which can lead to significant disability. Helpful diagnostic tests include a serum IgE level, serum protein electrophoresis, fungal scraping for potassium hydroxide preparation and culture, and skin biopsy.
The mainstay of treatment for atopic dermatitis is hydrating the skin with the regular use of emollients and suppressing cutaneous inflammation with topical corticosteroids. Parents of infants and toddlers should apply a bland emollient to the entire body with each diaper change.


Low-potency topical steroids are suitable for infants and for intertriginous and sensitive areas (face, genitals); more potent steroids should be avoided on these sites. Topical calcineurin inhibitors are especially suitable for more delicate areas such as the face and genitals because they do not carry the risks of atrophy, telangectasias, and striae associated with the chronic use of steroids. Topical medications that are known sensitizers, such as lidocaine, doxepin cream, and diphenhydramine cream, as well as topical antibiotics such as neomycin, should be strictly avoided. More than 75% of children with atopic dermatitis also have asthma or allergic rhinitis.
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. Th1 responses antagonize the development of Th2 cells, thereby potentially decreasing the incidence of atopic dermatitis.
Loss of EFAs results in increased transepidermal water loss and subsequent xerosis (dryness).
Like affected children, adults also commonly have lichenification of the flexures and facial dermatitis. Reports have surfaced suggesting a possible risk of lymphoma associated with high-dose oral pimecrolimus in animal studies,9 prompting the FDA to put out a black box warning advising against the use of topical calcineurin inhibitors in children younger than 2 years.
For open wounds, a topical antibiotic such as mupirocin can help to prevent secondary impetiginization (Figs.
Allergic contact dermatitis to topical steroids should be considered in any patient who fails to improve or worsens with the use of topical steroids. The EFAs form the substrate of the inflammatory mediators (prostaglandins and leukotrienes), resulting in a secondary deficiency of prostaglandin E1 (PGE1). Treatment with topical or oral antistaphylococcal antibiotics (or both) decreases the colonization of the skin and often leads to improvement of the dermatitis.
Hypopigmentation and hyperpigmentation can occur, which can cause great anxiety in parents.
For severe disease, especially during acute flares, systemic corticosteroids may be necessary. However, there are no data to support an increased risk of lymphoma with topical treatment in humans.9 Topical calcineurin inhibitors should be used for a limited time and only on affected skin.
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.
Pityriasis alba, characterized by hypopigmented, scaly patches on the face, is commonly seen. Soap, which dries and irritates the skin, should be avoided, but gentle lipid-free cleansers are beneficial.
Keratosis pilaris, or spiny hair follicles, commonly affect the posterior aspects of the upper arms and the anterior thighs.
In severe, recalcitrant cases, phototherapy or systemic immunosuppressive medications may be necessary.



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