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INTRODUCTION

Eczema spans a large area in dermatology, including atopic dermatitis, contact dermatitis, and various eczematous disorders. It represents a category of diseases in which the skin is inflamed, usually due to a topical allergy or irritant, and in which host factors such as an atopic tendency may also play a part. The skin surface barrier is disrupted and water is lost. The underlying skin dries out, and more irritants or allergens are able to make their way into the skin. Pruritus is typical. Scratching further disrupts the water barrier and protective function of the skin, worsening the condition. Note that the terms eczema and dermatitis in common usage are synonymous and do not imply internal or external causation.

  The clinical appearance of eczematous skin should be differentiated from that of papulosquamous conditions such as psoriasis. Both conditions are red and scaly, but the edges of eczema are less well defined, and the entire area is not significantly raised compared with papulosquamous conditions. Scales are generally larger in papulosquamous conditions compared with the scaling in eczemas.

    Allergic contact dermatitis is an entire area unto itself. Not only is it an important area clinically, but it is a model for the skin’s participation in the immune system. Indeed, the skin plays an active role in the body’s immune system, with Langerhans cells playing a key role in antigen processing and presentation to T cells.

    One should suspect a cutaneous allergy when the eruption is acutely eczematous or bullous and the lesions are linear, streaky, or in unusual shapes. An eczematous condition on certain parts of the body should raise at least the consideration of allergy (e.g. the earlobe in a woman, the hands, or the periorbital area). If not obvious by history, patch testing can be invaluable in determining the exact offending agent. It should be noted that different types of eczema may coexist, for example a patient with atopic eczema may also have an irritant dermatitis (e.g. from exposure to detergents) or an allergic contact dermatitis. Although the risk of allergic contact dermatitis may be reduced in atopic eczema due to altered T-lymphocyte responses (discussed later), patients with atopic eczema may be more exposed than the general population to some topical agents that can cause allergy (e.g. preservatives or even corticosteroids in treatment creams).

    Finally, it appears that atopic dermatitis is often either caused or aggravated by a type of cutaneous allergy. After epidermal penetration, aeroallergens bind to allergen-specific IgE on Langerhans cells and are subsequently presented to

Figure. 6.1 Infantile atopic dermatitis (AD) on the cheeks. The patient with AD often has a personal or family history of asthma or hay fever. The infant often presents with bilaterally symmetric, red, scaly, chapped, dry, glazed cheeks. An irritant dermatitis from saliva may be contributory.

 

Figure. 6.2  Fingertip eczema. Eczema of the fingertips in a child can be very difficult to treat. Any sucking or biting must be stopped.

Figure. 6.3  Follicular eczema in a dark-skinned patient. Such patients with atopic dermatitis often show follicular accentuation. At times, only the follicles are involved, as shown here.

Figure. 6.4  (a,b) Diffuse atopic dermatitis (AD). The red, scaly rash of AD may spread to cover much or all of the body. The child scratches incessantly and sleep may be significantly disrupted, both for the child and for the parents. In children, the rather follicular pattern shown may signify secondary infection.

T lymphocytes. Interleukins (IL-4 and IL-5) seem to be important in the migration and maintenance of eosinophils in the area (which do not appear in standard allergic contact dermatitis). It appears that the eosinophils release their granular contents in the epidermis and damage it, resulting in altered barrier function. This allows for the vicious cycle of increased epidermal permeability to aeroallergens, more epidermal damage, etc.

White/Cox: Diseases of the Skin, 2ed.(c) 2006, Elsevier Inc. All rights reserved.