Irritant or allergic contact dermatitis usually presents as an eczematous process, clinically characterized by erythematoedematovesicous lesions with intense itching in the acute phase. Such manifestations become erythematous-scaly as the condition progresses to the subacute phase and papular-hyperkeratotic in the chronic phase. Not infrequently, however, contact dermatitis presents with noneczematous features. The reasons underlying this clinical polymorphism lie in the different noxae and contact modalities, as well as in the individual susceptibility and the various targeted cutaneous structures. The most represented forms of non-eczematous contact dermatitis include the erythema multiforme-like, the purpuric, the lichenoid, and the pigmented kinds. These clinical entities must obviously be discerned from the corresponding “pure” dermatitis, which are not associated with contact with exogenous agents. 1. Introduction Allergic contact dermatitis (ACD) is a common cutaneous eczematous disorder caused by contact (either direct or aeromediated) with a range of environmental substances. Pathogenetically, ACD results from an immune reaction involving both innate and adaptive immunologic mechanisms. In particular, hyperreactive response to small chemicals (haptens) penetrating the skin depends on a series of events, such as haptens capability to activate and mobilize cutaneous dendritic cells (cDC), generation of hapten-epitopes for T-cell recognition, and hapten-cDC complex ability to prime effector T cells with skin homing proprieties [1–3]. In sensitized individuals, skin or systemic challenge with the specific sensitizer determines rapid recruitment of effector T cells, along with natural killer lymphocytes, which mediate tissue damage through release of proinflammatory cytokines and through hapten-loaded keratinocytes killing. Clinics of ACD are generally polymorphic. Besides the classic eczematous form, in fact, different noneczematous clinical variants are possible [1, 4–6]. The causes for such variability in ACD clinical aspects are many (Table 1). According to our data (unpublished), considering >30.000 patch tested individuals for contact dermatitis, noneczematous forms are slightly more common (52%) than the classic eczematous one (48%). Various clinical patterns of noneczematous ACD have been described: some are linked to topical use of specific haptens and others more often dependent on allergens systemic administration (Table 2). The most represented forms are described as follows. Table 1: Factors determining the peculiar polymorphic clinical
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