High-concentration topical capsaicin may abolish the clinical manifestations of allergic contact dermatitis by effects on induction and elicitation.

Allergic contact dermatitis (ACD) is a common skin condition caused by a type-IV hypersensitivity reaction. Even though ACD is considered as a T-cell mediated disease, indications exists that peptidergic nerve fibers at the site of allergen exposure and associated with the draining lymph node play a prominent role in both induction and elicitation of ACD. This neuro-immune cross talk seems rely on neuropeptides such as Substance P secreted by nerve fiber terminals. It is hypothesized that local complete or partial cutaneous denervation/defunctionalization of peptidergic fibers in humans could be a feasible approach towards treating allergic contact dermatitis. Recently, human experimental protocols for prominent, temporary defunctionalization of peptidergic fibers have been published relying on prolonged application of 8% topical capsaicin patches. Combined with human experimental ACD models the importance of peptidergic nerve fibers in the induction and elicitation phases of ACD could be accurately established. Understanding the role of cutaneous peptidergic fibers in the pathogenesis and potentially of ACD and how contact sensitization can be modulated by topical defunctionalization of these fibers could lead to new approaches to treatment for ACD. In patients with localized ACD occurring to an allergen that is difficult or unfeasible to evade this would have particular relevance.