Background: Genetically determined defects in epidermal skin barrier function may contribute to the development of irritant and/or allergic contact dermatitis in chronic hand eczema (CHE).

Objectives: To assess whether a deletion in the late cornified envelope genes LCE3B and LCE3C may constitute a genetic predisposition for the development of CHE or any of its subtypes.

Patients and Methods: A total of 153 German patients with clearly defi ned CHE subtypes and 268 healthy individuals were screened for the deletion LCE3C_LCE3B-del by allele-specific polymerase chain reaction.

Results: Classification of the patients by etiologic subtypes revealed an association between the LCE3C_LCE3B-del allele and CHE due to allergic contact dermatitis. In this subtype, 19/37 patients (51.4%) were homozygous deletion carriers, 11/37 (29.7%) were heterozygous carriers, and just 7/37 (18.9%) were wild-type individuals. Compared to the other CHE subgroups and the healthy control group (homozygous, 88/268 [32.83%]; heterozygous, 133/268 [49.63%]; and wild-type, 47/268 [17.54%]), the prevalence of LCE3C_LCE3B-del in these patients reached statistical significance (P=.03977), as did homozygous deletion carrier status (P=.01044 for other subtypes and P=.02695 for controls).

Conclusions: A deletion of LCE genes may promote the development of allergic contact dermatitis, which is a form of CHE involving delayed-type hypersensitivity.

Key words: Chronic hand eczema. Susceptibility. Late cornified envelope. Allergic contact dermatitis. Epidermal skin barrier function