The etiology of atopic eczema is unknown. Patients have increased levels of serum IgE and some have precipitating antibodies to environmental allergens, including foods and inhaled materials. Many patients will have a positive response to intracutaneous challenge with pollen, house dust mite, cat fur, and fish antigens. However, the significance of these positive reactions is unclear. Patients with atopic eczema have reduced numbers of circulating T-suppressor cells which are responsible for modulating immunoglobulin-producing B lymphocytes. Low levels of the unsaturated fatty acids y-linoleic and dihomo-y-linolenic acid have been reported (8).
In most patients there is a family history of eczema or of other atopic diseases, such as asthma or allergic rhinitis. Atopic eczema usually presents during infancy and, often, may resolve during childhood, whereas in others it may persist into adult life. Atopic eczema usually affects the face, wrists, and the flexural aspects of the elbows and knees (Fig. 2). There may be some involvement of the trunk, and the rash may become generalized. The eczema may be complicated by bacterial infection, and there is evidence to suggest that many exacerbations of atopic eczema may be due to occult infection with Staphylococcus aureus. Eczematous skin is also more prone to infections with wart viruses, molluscum contagiosum, and herpesviruses. Patients with atopic dermatitis may develop a widespread and potentially fatal rash, eczema herpeticum, following the development of herpes simplex or following contact with individuals affected with herpes simplex.
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