1. ¹Department of Dermatology and Allergy, University of Bonn, Bonn, Germany
2. ²Department of Epidemiology, GSF-National Research Center for Environment and Health, Neuherberg, Germany
3. ³Institute for Medical Statistics and Epidemiology IMSE, Technical University Munich (TUM), Munich, Germany
4. ⁴Institute of Social Medicine, Medical University Schleswig-Holstein, Campus Lübeck, Germany
5. ⁵Division of Environmental Dermatology and Allergy, GSF-National Research Center for Environment and Health and ZAUM-Center for Allergy and Environment, Technical University Munich, Munich, Germany
6. ⁶Department of Dermatology and Allergy Biederstein, Technical University Munich (TUM), Munich, Germany

Correspondence: Dr Natalija Novak, Department of Dermatology and Allergy, University of Bonn, Sigmund-Freud-Str 25, Bonn 53105, Germany. E-mail: Natalija.Novak@ukb.uni-bonn.de

Received 10 July 2007; Revised 23 August 2007; Accepted 12 October 2007; Published online 29 November 2007.

Abstract

Allergic contact dermatitis is one of the most frequent dermatological problems affecting 7% of the general population. Impaired skin barrier function facilitates the penetration of contact allergens and irritants into the epidermal layer and is regarded as an important cofactor promoting the process of allergic contact sensitization. Filaggrin is crucial for the maintenance of the skin barrier function. Loss-of-function mutations within the filaggrin (FLG) gene are associated with skin barrier diseases such as ichthyosis vulgaris and atopic eczema (AE). To assess the impact of FLG on allergic contact sensitization and plausible intermediate traits, the two prevalent FLG mutations R501X and 2282del4 were typed in 1,502 individuals of the KORA C population-based cohort with extensive dermatologic phenotyping. Associations of FLG mutations with AE could be replicated. Strong associations were seen with dry skin, palmar hyperlinearity, and keratosis pilaris. In addition, an association with contact sensitization to nickel and contact sensitization to nickel combined with intolerance to fashion jewelry, but not with other contact allergens, was observed. From these data, we conclude that a genetically determined FLG deficiency manifests as dry skin and features of ichthyosis vulgaris. In addition, FLG deficiency may also represent a risk factor for contact sensitization to allergens.