No abstract

3851 consecutive patients patch tested between January 1985 and March 1990 have been analysed for rubber allergies. The incidence of rubber allergy was 3.8% (n = 145). In 80/145 patients (55%), the source of rubber sensitization was occupational, 67 of whom (84%) had acquired allergy from wearing rubber gloves at work. Most of them (36%) were employed in the health services. The most commonly positive rubber-mix in this group was thiuram-mix (72%) followed by carba-mix (25%). 13/80 patients (16%) had occupational rubber allergy from industrial rubber products other than gloves. Patch tests revealed thiuram-mix (62%) as the most commonly positive rubber-mix but, in contrast to the group with glove-induced rubber allergy, black-rubber-mix came second (38%). In 47/145 patients (32%), the source of rubber sensitization was non-occupational; in 18/145 (13%) the origin remained unknown.

To prevent contact with specific rubber accelerators, sensitized patients have to know in which glove brands these accelerators are present. Additionally, quantitative measurements of the bioavailable amounts of accelerators are needed to assist consumers in selecting gloves with the lowest possible amount of residual rubber accelerators. The aim of the study was to develop an analytical method by which residuals of rubber accelerators in single-use medical gloves could be determined qualitatively and quantitatively. 19 different glove brands were analysed for content of accelerators, and the results were compared to manufacturers' ingredient claims of the identical gloves. ZDEC, ZDBC, ZMBT and ZPC were the most frequently detected chemicals. In 9 of 15 gloves discrepancies were found, usually minor, between content of accelerators declared by manufacturers to be present and accelerators detected by analysis. Both phosphate buffer and acetone were tested as extraction media. No accelerators were detectable with the described chemical analysis in phosphate extracts, whereas acetone was demonstrated to be a technically suitable medium for extraction. However, more kinetic studies of the extraction procedure and studies of skin penetration are needed to document that the extraction procedure simulates the clinical situation.

Increased serum IgE and enhanced susceptibility to viral infections, decreased levels of interferons, lymphocytic skin infiltrates and IgE-bearing epidermal Langerhans cells are striking features in patients with atopic eczema (AE). Since the hyper-IgE syndrome is known to improve under α-interferon (α-IFN) therapy, we treated 7 patients with severe AE and high serum IgE exclusively with 3 × 10⁶ units IFNα2b thrice weekly for 3 months. Before treatment the skin infiltrates mainly consisted of CD3+/CD4+/TcRα/β+ lymphocytes, whereas the CD3+/CD8+ phenotype was limited to about 10% of cells. After 6 weeks of therapy, epidermal inflammation with CD4+ and CD8+ cells was reduced but dense infiltrates remained in papillary perivascular areas. Expression of TcRγ/δ, HLA-DR and CD25 showed no significant changes. Initially high serum IgE and soluble CD23 as well as cell-bound IgE dropped under therapy, whereas a short-term elevation in serum IL-2 receptor was observed. On peripheral blood lymphocytes slightly reduced expression of HLA-DR, LFA-1, CD23 and ICAM-1 was seen after 100 days. LFA-3 expression became reduced in 4 patients, the CD4/CD8 ratio decreased in all cases. After an initial therapeutic response of all patients, significant longer-lasting improvement of the skin lesions could only be observed in 2 of 7 patients. The data of our long-term study suggest that systemic IFNα2b treatment leads to a remarkable reduction in epidermal inflammation but does not significantly influence cutaneous cell subsets. Immunomodulatory effects became obvious by reduced peripheral cell subsets expressing TcRα/β, MHC class II and adhesion molecules.