There is now considerable evidence that colonization or infection with Staphylococcus aureus is an exacerbating factor in atopic dermatitis (AD) (1). Numerous studies have shown that the superantigens produced by staphylococci and streptococci are implicated in the pathogenesis of various inflammatory skin diseases. The skin lesions of patients with AD predominantly contain infiltrating T cells and monocyte/macrophages which can be activated by superantigenic toxins from these microbes. This review focuses on two specific aspects of the involvement of S. aureus in AD. These are mechanisms by which superantigens can induce skin inflammation and impair the response of the inflammatory process to corticosteroids, and the inability of the innate immune system in atopic skin to counteract staphylococcal skin colonization and infection.
Atopic dermatitis (AD) is a chronic inflammatory skin disease which develops on a complex genetic background, the so-called atopic diathesis. AD is in most, but not all, patients characterized by the presence of elevated total serum IgE levels. However, a subgroup of atopic patients exhibits normal IgE levels and mechanisms contributing to the so-called 'Intrinsic' or 'non-allergic' form have been the matter of intensive research work in the last years. These forms have been particularly studied in the context of AD, which has also led to a new nomenclature. Moreover, we now have increasing evidence for the putative role of autoimmune phenomena in the complex pathophysiology of AD. Mainly adult patients exhibit specific IgE directed against self proteins of epidermal origin. Therefore, AD may be considered as a continuous disease in which, however, depending on the age, different mutually not exclusive pathomechanisms may be of relevance.
Chronic hand eczema is frequent among atopic dermatitis (AD) patients. Due to the multifactorial causes of hand eczema, careful clinical and allergological examination is important for classification of the individual case, and hence for advice, treatment and preventive measures to be recommended. The importance of patient information and preventive strategies cannot be overemphasized.
One of the recent developments is to treat the disease very early in its development, exactly as is being done in asthma. The aim is to evaluate whether it is possible to modify the disease with long-term management. Can flare-ups be prevented? Is it possible to prevent the ‘atopic march’? The typical progress of a patient with atopic dermatitis (AD) was documented by Kissling & Wuthrich (1). They documented the development of eczema in 106 patients from the infantile phase, through childhood and adolescence into adulthood. The majority of patients experienced recurrent cycles of flare-ups, each of which was controlled by steroids. This recurrent cycle of events is distressing to parents who are also concerned about the ‘atopic march’ (2). Atopic eczema is in most cases the first manifestation of atopic disposition; eczema in childhood, compounded by food allergy, leading to asthma and long-term rhinitis. The general approach to treating AD is to treat relapses/flare-ups and when controlled to withdraw active treatment and use emollients (until the next flare-up). A recent trial has investigated whether continued application of a steroid can prevent or delay the cycle of relapses and treatment. Berth-Jones et al. (3) conducted a randomized vehicle (emollient) controlled trial in patients aged 12–65 with moderate to severe disease, to determine whether fluticasone propionate (at two strengths of 0.05% and 0.005%) can prevent relapses. There was a 1-month stabilization phase, followed by maintenance treatment of both ‘healed’ skin and new areas. The primary end point of the study was the time to relapse. A significant (pv0.001) prolongation of remission with application of fluticasone propionate 0.05% was seen. Significant benefit was also seen with fluticasone propionate 0.005%, but the benefit and statistical significance was reduced (p50.01). NEW THERAPEUTIC STATEGIES AND TARGETS
Medicament allergy is a not uncommon problem both with antibiotics and topical corticosteroids. Patients with atopic eczema have a significant degree of reactivity to these agents similar to non-atopics.
