Background: Atopic dermatitis of the head and neck (HNAD) has been recognized as a separate entity. Malassezia furfur, a lipophilic yeast, is considered to be a pathogenic allergen in this form of atopic dermatitis. Objective: The purpose of this study was to determine the level of IgE anti-M.-furfur antibodies and their relation to the severity of the disease. Methods: IgE anti-M.-furfur antibodies were assayed in 106 patients with HNAD. Controls included 25 patients with non-HNAD, 20 with nonatopic dermatitis and 16 with seborrheic dermatitis (including 4 with AIDS). Results: There was a highly significant correlation between the level of anti-M.-furfur IgE and clinical severity. Furthermore, there was a significant but smaller correlation between total IgE and clinical severity. In patients with HNAD, total IgE was higher amongst men. Conclusion: IgE anti-M.-furfur antibodies are a good and specific marker for HNAD. IgE M. furfur levels are strongly correlated with the severity of the disease.

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An occupational physician reported to the French Health Products Safety Agency (Afssaps) a case of adverse effect of acute pancreatitis (AP) in a teaching nurse, after multiple demonstrations with ethanol-based hand sanitizers (EBHSs) used in a classroom with defective mechanical ventilation. It was suggested by the occupational physician that the exposure to ethanol may have produced a significant blood ethanol concentration and subsequently the AP. In order to verify if the confinement situation due to defective mechanical ventilation could increase the systemic exposure to ethanol via inhalation route, a physiologically based pharmacokinetic (PBPK) modeling was used to predict ethanol blood levels. Under the worst case scenario, the simulation by PBPK modeling showed that the maximum blood ethanol concentration which can be predicted of 5.9 mg/l is of the same order of magnitude to endogenous ethanol concentration (mean = 1.1 mg/L; median = 0.4 mg/L; range = 0–35 mg/L) in nondrinker humans (Al-Awadhi et al., 2004). The present study does not support the likelihood that EBHS leads to an increase in systemic ethanol concentration high enough to provoke an acute pancreatitis.

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