A subgroup of patients with atopic dermatitis are known to have normal serum total immunoglobulin E levels, undetectable specific immunoglobulin E, and negative skin prick tests towards allergens. This form of the disease has been termed nonallergic atopic dermatitis. In this study, we found that, among 1151 chronic atopic dermatitis patients, about 10% had normal serum immunoglobulin E levels with no evidence for immunoglobulin E sensitization. We investigated immunologic mechanisms of patients with "allergic" and "nonallergic" atopic dermatitis using peripheral blood and skin biopsy samples. Our data suggest that T cells are likely involved in the pathogenesis of both forms of atopic dermatitis. Skin T cells equally responded to superantigen, staphylococcal enterotoxin B, and produced interleukin-2, interleukin-5, interleukin-13, and interferon-gamma in both forms of the disease. Interleukin-4, however, was not detectable in the skin biopsies of both atopic dermatitis types and was secreted in very low amounts by T cells cultured from the skin biopsies. Moreover, skin T cells from nonallergic atopic dermatitis patients expressed lower interleukin-5 and interleukin-13 levels compared with allergic atopic dermatitis patients. Accordingly, T cells isolated from skin biopsies of atopic dermatitis, but not from the nonallergic atopic dermatitis, induced high immunoglobulin E production in cocultures with normal B cells that was mediated by interleukin-13. In addition, B cell activation with high CD23 expression was observed in the peripheral blood of atopic dermatitis, but not nonallergic atopic dermatitis patients. These data suggest, although high numbers of T cells are present in lesional skin of both types, a lack of interleukin-13-induced B cell activation and consequent immunoglobulin E production in nonallergic atopic dermatitis.

Botulinum toxin type A injections are an effective and well-tolerated treatment for hyperhidrosis. This paper proposes a positioning of this treatment along with current established treatments, and highlights the role of botulinum toxin type A as a valuable therapy for the treatment of hyperhidrosis.

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The pathogenesis of palmoplantar hyperhidrosis (HH) remains unknown. A causative therapy is therefore not possible yet. Step by step treatment for palmoplantar HH is advised. This includes: topical aluminium salts, tap water iontophoresis (TWI), botulinum toxin (BTX) injections and endoscopic thoracoscopic sympathectomy (ETS). The mechanism of action of TWI has been previously studied but is still not completely understood. A widely accepted hypothesis is that the anodal current causes accumulation of H(+) within the sweat duct. It is presumed that this causes an unknown lesion in the acrosyringium that inhibits sweating. TWI is non-invasive, safe, well tolerated, efficient and cheap. The patient can perform the therapy at home without medical assistance. TWI remains the best treatment for palmoplantar HH that has defied aluminium salts. This article provides a review of the literature concerning TWI, including its historical development, its mechanism of action and its indication and also describes the method of administration of this helpful treatment.

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