A Comprehensive Management Guide for Atopic Dermatitis

Jennifer D. Peterson, MD; Lawrence S. Chan, MD

Disclosures

Dermatology Nursing. 2006;18(6):531-542. 

In This Article

Identifying Triggers

When taking a history from a patient with atopic dermatitis, it is crucial to ask about possible triggers of his or her disease. Common triggers in AD include aeroallergens, climate, emotional stress, hormones, food, irritants, and microbes (see Table 3 ), but not every patient will react to every trigger that is listed (Bardana, 2004; Darsow et al., 2005; Leung & Bieber, 2003; Werfel & Kapp, 1999).

As mentioned earlier, patients with intrinsic AD are not exacerbated by aeroallergens and foods, but patients with extrinsic AD can produce antigen-specific IgE to various foods and aeroallergens. This production of IgE not only plays a role in triggering atopic dermatitis, but also the primary development and pathogenesis of AD. In atopic dermatitis, the most frequent aeroallergens are animal danders, cockroach, dust mites, human dander, molds, and pollens (Schmid-Grendelmeier et al., 2001). Cow milk, eggs, fish, peanuts, soy, tree nuts, and wheat are the most common foods allergies that can serve as triggers in atopic dermatitis (Rudikoff & Lebwohl, 1998). Between 20% to 40% of young children and infants with AD have clinically relevant food allergies that worsen his or her disease (Leung & Bieber, 2003; Rudikoff & Lebwohl, 1998). However, aeroallergens are more critical in exacerbating the disease process in adults and older children. If patients are suspected of having allergies to foods or aeroallergens, skin prick tests or RadioAllergoSorbent Tests (RASTs) can be done (Leung et al., 2004). A RAST measures antigen-specific IgE in a patient's blood. A negative test rules out a certain food or aeroallergen playing a role in the disease process. A positive skin test, especially in regards to foods, does not always correlate well with a patient's symptoms (Leung et al., 2004). It has been suggested that if a patient has three or more positive skin prick tests to foods, that they undergo a double-blind, placebo-controlled food challenge to verify the results (Burks et al., 1998). The double-blind, placebo-controlled food challenge is considered the gold standard at diagnosing food allergies, but should be avoided in patients with life-threatening symptoms or a history of anaphylaxis. It allows for identification of food allergies so that they can be avoided in the future and proves what foods do not play a role in the patient disease process (Niggemann, 2004). Studies show that symptoms often improve after the contributory food has been eliminated from the diet. Extensive elimination diets are not helpful in managing patients with AD and may lead to nutritional deficiencies; therefore, they are not encouraged (Leung & Bieber, 2003). Physicians should consider performing atopy patch tests (APTs) if the results of a skin prick test or RAST is positive for an aeroallergen (Darsow et al., 2005).

Certain climates may serve as triggers for patients with AD. The Winter is often troublesome as the associated decreased humidity allows the skin to dry out easier through increased transepidermal water loss (Abramovits et al., 2003). Sweating as a result of heat or exercise may act as an irritant in some patients causing burning in their eczematous lesions (Leung et al., 2004).

Emotional stress has been well documented to trigger and maintain lesions (Werfel & Kapp, 1999). Atopic dermatitis has a significant affect on quality of life secondary to stigmatization of the condition, psychological stress, lack of sleep secondary to pruritus and pain, and effects on social and financial well-being (The Lewin Group, Inc., 2005). Emotional stress can increase pruritus, scratching, and trigger the immune system (Leung et al., 2004). Children may experience a negative affect on their academic and social development as a result of AD-related stresses (The Lewin Group, Inc., 2005). Referral to a psychiatrist or therapist is beneficial for patients in which emotional stress plays a strong role in aggravating their disease. Relaxation therapies, behavioral modification strategies, and biofeedback have all been used to reduce exacerbations in AD precipitated by scratching (Leung et al., 2004).

In women, hormones may act as a trigger for AD. Patients have had exacerbations during menstruation, the first and second trimesters of pregnancy, the peripartum period, and menopause. Further studies are needed to investigate how these hormonal changes induce flares (Bardana, 2004; Werfel & Kapp, 1999).

The skin of patients with atopic dermatitis is very sensitive and vulnerable to irritants. Irritants play a provocative role in AD, but are not involved in the primary pathogenesis of the disease (Bardana, 2004). Hot water, soaps, cigarette smoke exposure, enzyme rich laundry detergents, household disinfectants (bleach and ammonia), solvents (alcohol, gasoline, and kerosene), clothing made with synthetic fibers (rayon and polyester) or wool, and juice from fresh fruits (tomatoes, citrus, and strawberries) are the most common irritants in AD (Abramovits et al., 2003; Bardana, 2004; Leung et al., 2004; Wuthrich, 1999).

A variety of microorganisms including bacteria, viruses, fungi, and yeast aggravate atopic dermatitis. Staphylococcus aureus is well known to play a role in the pathogenesis, maintenance, and exacerbation of atopic dermatitis. S. aureus can secrete toxins that act as superantigens to stimulate the proliferation of T cells and other cells of the immune system and thus worsen atopic dermatitis (Abramovits, 2005; Bardana, 2004). Over 90% of AD skin lesions are colonized with S. aureus as opposed to only a 5% rate of colonization in normal skin of healthy controls (Abramovits, 2005). IgE-specific antibodies against S. aureus superantigens have been found in the serum of patients with AD (Bardana, 2004). Most experts recommend using antibiotics against S. aureus if there is an active infection or the individual is heavily colonized with S. aureus. However, antibiotics are not recommended to treat common colonization due to the concern over antibiotic resistance (Darsow et al., 2005; Leung et al., 2004). If the patient has developed a secondary infection with S. aureus his/her skin lesions undergo impetiginization and the lesions become weeping and crusted (classically the honey-colored crust). Superficial pustules and periauricular fissures may also be present (Lubbe, 2003). b-hemolytic streptococcus infections occur at an increased rate in AD and may also play a role as a trigger in atopic dermatitis (Darsow et al., 2005; Lubbe, 2003). Children with AD who develop streptococcal infections present with beefy-colored erythema, crusts, pustules, fever, and adenopathy. It is recommended that these cases also be treated with antibiotics (Lubbe, 2003).

Atopic dermatitis carries a higher incidence of recurrent cutaneous viral infections as a consequence to local impaired T-cell function (Abramovits, 2005). These viral infections have the potential to disseminate because of the epidermal barrier damage in AD and become life-threatening in patients with atopic dermatitis (Leung et al., 2004; Lubbe, 2003). Eczema herpeticum is a disseminated form of herpes simplex which can occur in patients with AD and must be treated with antiviral medications (Leung et al., 2004). In young adults with AD, eczema herpeticum may be a recurrent infection (Lubbe, 2003). Widespread punched out erosions, vesicles, infected skin lesions that do not respond to antibiotics, fever, and lymphadenopathy are typical findings seen in eczema herpeticum (Darsow et al., 2005; Leung et al., 2004). Another cutaneous viral infection, molluscum contagiosum, has the potential to become extensively distributed in patients with AD and is known as eczema molluscatum. Eczema molluscatum is characterized by tens to hundreds of small, umbilicated, skin-colored papules (Leung et al., 2004). These lesions can be spread by auto-inoculation from scratching. A variety of treatment options are available for eczema molluscatum including destruction via cryotherapy, carbon dioxide vaporization, electrodessication and curettage, or topical treatment with imiquimod 5% cream (Aldara®) (a medication that enhances the immune response by increasing the release of cytokines) (Darsow et al., 2005). Eczema vaccinatum, a widespread skin infection in patients with atopic dermatitis, follows smallpox vaccination, has a clinical presentation similar to eczema herpeticum, and is extremely life threatening (Leung et al., 2004).

Finally, dermatophytes and yeasts can complicate and exacerbate a course of AD. The dermatophytes most commonly involved are Malassezia furfur (which affects the scalp and seborrheic areas), Trichophyton, and Epidermophyton, while the yeasts involved include Candida and Pityrosporum ovale (the yeast form of Malassezia furfur). Patients have clinical improvement of their atopic dermatitis following antifungal therapy aimed against their concomitant dermatophyte or yeast infection (Lubbe, 2003).

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