The word atopy is derived from the Greek word “ατoπiα” and depicts a condition “out of place/placelessness,” or unusual. From a medical point of view atopy describes a polygenic inherited disposition to develop at least one of the following disorders: atopic dermatitis (AD), allergic rhinitis (AR), or allergic asthma (AA). Atopic disorders (AD, AR, AA) are marked by a manifestation of the interface of the organism to the environment (skin, mucosal skin, lungs) and have in common genetically based increased susceptibility to react to environmental factors. it appears that atopy is more prevalent in highly industrialized societies and higher socioeconomic classes.

AD is characterized by a genetically based hypersensitivity of the skin with predisposition to develop eczema in typical anatomic localizations according to stage. Current estimates show that 15% of schoolchildren and 2% of adults in industrialized countries suffer from AD, with a slight predominance of females. A myriad of possible intrinsic and extrinsic triggers include stress, aeroallergens, microbial products, and/or food allergens. The manifestation of the disease is typically most severe in childhood, with a chronic relapsing course and improvement in most cases occurring during adulthood. Important hallmarks comprise pruritus and xerosis cutis.

The pathogenesis and etiology of the disease are still not fully understood. Most likely the AD phenotype results from a complex interplay between genetic, immunologic, metabolic, and neuroendocrine alterations and their interaction with the environment.

The majority of patients are infants and children. Up to 90% of cases arise before the age of 5 years. At each stage AD may show acute, subacute, or chronic skin changes. However, certain presentations are more common in specific stages. AD of infants and children is predominately an acute, exudative inflammation, with secondary excoriations. In adulthood, chronic inflammation with hyperkeratotic skin-thickening, lichenification (accentuated skin markings), and scaling are more prominent. Postinflammatory pigment changes, either hyper- or hypopigmentation, can be observed. Pruritus is almost always present. The typical anatomic distribution of AD varies by stages, changing over lifetime. AD lesions of infants are predominantly located on the face and the extensor surface of the extremities, while the childhood pattern is typified by flexural
involvement. For the adult with atopic dermatitis, the earlier classic locations are often involved, such as flexural areas (Fig. 15-3). There also is more frequent facial (especially eyelid) and hand/foot eczema.

Diagnostic criteria for AD are based primarily on clinical presentation, patients/family history, and the exclusion of other disease entities. Hanifin and Rajka compiled, in the early 1980s, important diagnostic features, which attained international recognition. Since that time, the criteria have evolved into the current schema. A consensus conference, convened by the American Academy of Dermatology (AAD) suggested the clinical criteria for the diagnosis of AD given in Table 15-1.

Diagnosis is made using the above-mentioned criteria. In questionable cases, a supportive biopsy with histopathologic interpretation may help, especially when other differential diagnoses, such as cutaneous T-cell lymphoma must be excluded. Biopsy is not appropriate to classify the eczema according to a specific etiology because of many histologic similarities between eczema types. Analytical measurement of total IgE is used to distinguish between intrinsic and extrinsic forms of AD. Extrinsic AD, with elevated serum IgE, is characterized by a personal or family history of respiratory allergy and can be found in 70% of AD individuals. Patients without IgE reactivity or obvious allergic respiratory conditions have intrinsic AD.

The inherited hypersensitivity and the disposition of the skin to develop eczema is a lifelong condition. Thus, whether disease is active or not, avoidance of potential triggers and maintenance of physiologic skin barrier function with hydration (e.g., with urea 3% to 5% as an ingredient) and thick
emollients is essential. Generally, patients with AD should limit potentially skin-irritating activities such as wet work and contact to chemicals/detergents. Moreover the use of mild, perfume-free, nonalkali soaps is recommended. Although bathing dries the skin, patients often sense a general relief and reduction of pruritus while immersed. Hence recommendation for bathing patients includes the immediate reapplication of moisture. Use of a cream containing ceramides (either prescription or over-the-counter) is helpful for many patients.

Reduction of house dust mites with vacuum cleaning, removal of carpets and curtains, and the use of special bed covers seems to improve the skin condition as well. Cotton clothing is preferred to wool and synthetics. Avoidance of specific food products such as eggs, milk, or nuts in those patients who experience a flare when eating them can be helpful too.

In case of active flares, intensity and distribution of skin lesions, as well as specific symptoms, determine the therapeutic choices. The mainstay of treatment for pruritus is antihistamines whereas corticosteroids are used to gain control of skin inflammation. Advantages of topical corticosteroids include ease of application, possibility of combination with other therapies (e.g., phototherapy), and the opportunity of choices with regard to ingredient potency. Rapid flares are best treated with 5 days of a medium- to high-potency topical corticosteroid ointment. Application should be once to twice a day. Once disease control is achieved, the topical corticosteroid can be tapered to a less-potent class and eventually withdrawn. Adjustment of steroid class when used in the groin area and the face should be considered, as these areas are more vulnerable for cutaneous atrophy. Alternating therapy with topical immunomodulators (calcineurin inhibitors tacrolimus and pimecrolimus, FDA approved for patients > 2 years) or days of therapeutic pause decrease the risk of cutaneous atrophy. Especially for moderate to severe AD, phototherapy in combination with topical therapy can improve AD. Appropriate regimens comprise narrow-band UVB and PUVA (Psoralen + UVA). Disadvantages of phototherapy are the inconvenience of traveling to clinic for tri- or bi-weekly treatments, as well as the risk of photoaging and/or induction of cutaneous malignancies and sunburns.

If a patient is not already applying topical corticosteroid twice daily to all affected areas, a regimen of triamcinolone 0.1% cream dispensed in a 454-g jar often is helpful. This allows aggressive application topically as in many cases patients do not have enough to adequately treat affected areas (see Chapter 2). Using triamcinolone 0.1% in conjunction with open wet dressings (Table 15-2) is very helpful for patients able to apply them once or twice daily.

For severe, unresponsive AD, systemic use of corticosteroids may be employed judiciously. Chronic utilization of oral corticosteroids should be avoided because of possible systemic complications. Tapering should be done carefully, because abrupt cessation of therapy may be associated with a rebound flaring.

Another helpful systemic medication in severe AD is systemic cyclosporine in daily dosage of 2 to 5 mg/kg. It can improve the condition quickly, but its usefulness may be limited by side effects. Less often used systemic treatments include methotrexate and azathioprine.

Systemic antistaphylococcal therapy is helpful for all stages of infected AD. Antibiotics of choice are oral cephalosporin and dicloxacillin in doses of 250 mg four times daily for adults, or 125 mg twice a day (25 to 50 mg/kg/day divided into two doses) for young children. Future treatments may include the use of IgE-binding biologics for a subgroup of patients. A simple method to reduce bacterial colonization is bleach baths. These are simple and cost effective. In a standard 40-gallon bathtub, fill with comfortable temperature (not hot) water. Add ½ cup bleach (such as Clorox). Soak for ∼10 minutes. Gently
rinse the face with a washcloth, keeping eyes closed. Repeat this as maintenance 2 to 3 times weekly.

In most affected infants and children, the frequency of active inflammatory flares decreases with age until the teens. Around two thirds of childhood AD cases clear in early adolescence or become symptom free. Of note, patients with childhood AD are at risk for the later development of hand eczema, allergic rhinitis, and/or asthma. A minority of patients show a chronic relapsing course beyond puberty. Frequently these patients develop a moderate-severe AD accompanied by other atopic features such as allergic rhinitis and/or allergic asthma.

Even with diminution of active AD skin lesions, the inherited hypersensitivity and the disposition of the skin to develop eczema is a lifelong condition. This can be important when choosing a profession. Avoidance of potential triggers such as frequent contact to water, detergents, and chemicals is a lifelong necessity.