Autosensitization dermatitis refers to a phenomenon in which an acute dermatitis develops at cutaneous sites distant from an inflammatory focus, and where the secondary acute dermatitis is not explained by the inciting cause of the primary inflammation. The classic presentation of autosensitization is that seen in patients with venous stasis disease,1 where as many as 37% of patients have been reported to develop at least one episode of autosensitization,2 and those with dermatophyte infections, where 4–5% reported having had dermatophytid reactions.3

The term autosensitization dermatitis was coined in 1921 by Whitfield to describe reaction patterns ranging from a generalized, erythematous, morbilliform, and urticarial eruption after blunt trauma to a generalized, petechial, papulovesicular dermatitis after the acute irritation of chronic stasis dermatitis.4 Subsequently, the vesicular id reactions associated with infections caused by tuberculosis,5 histoplasmosis,6 dermatophytes,7 and bacteria8 were included under this rubric.9–11 Noneczematous reaction patterns, including erythema multiforme12 and neutrophilic lobular panniculitis,13 have also been ascribed to autosensitization associated with various infections. Other precipitating factors for autosensitization have included the application of irritant or sensitizing chemicals,14 ionizing radiation,15,16 and retained suture material.17

Although the disease was originally thought to be due to autosensitization to epidermal antigens,11 this concept has not been experimentally verified. In murine studies designed to determine whether keratinocyte-derived proteins can serve as antigenic carriers for hapten, Fehr et al18 derived major histocompatibility complex-restricted, T-cell receptor α/β, CD4+ T-cell clones that proliferated in response to keratinocyte extracts unconjugated to hapten. In these studies, such autoreactive T-cell clones could not be derived after treatment with irritants. Nonetheless, the authors speculated that T cells autoreactive to keratinocyte antigens may be generated during the course of contact hypersensitivity and lead to the development of an id reaction.

In the most extensive study to date,1 only 4 of 81 patients with autosensitization dermatitis had serum antibodies cytotoxic to autologous or homologous skin. However, the role of such autoantibodies in mediating the disorder, even in these four patients, must be interpreted cautiously, given the high frequency of epidermal autoantibodies in the normal adult population.19

In an experiment in which guinea pigs were injected with autologous skin, Wilhelmj et al20 reported dermatitis in 2 of 11 guinea pigs, but it was not clear whether these reactions were immunologic and, if so, what the causal allergen(s) was. Other investigators using similar techniques have been unable to induce cutaneous disease in animals by means of epidermal extracts.21 In contrast, 19 of 24 patients with active autosensitization who were intradermally challenged with water-soluble extracts of autologous epidermal scale developed a reaction.22

The term autosensitization is probably a misnomer. The disease is more likely due to a hyperirritability of the skin induced by either immunologic or nonimmunologic stimuli. Factors such as irritation, sensitization, infection, and wounding, which are known to precipitate autosensitization, have been reported to release a variety of epidermal cytokines.23,24 Once hematogenously disseminated in sufficient amounts, these cytokines could heighten the sensitivity of skin to a variety of nonspecific, but otherwise innocuous, stimuli, producing a pattern of “spillover” reactions25 that have been classically termed autosensitization. Such a hypothesis would account for (a) the results in humans of delayed-type hypersensitivity testing with autologous epidermal scale,22 (b) the histopathologic findings noted in the disease (see section “Clinical Findings”), and (c) the activated T lymphocytes occasionally observed in the blood of patients with autosensitization.26 The characteristic distribution of the disease might perhaps be explained if the skin overlying the arms and legs was found to contain increased numbers of, or more avid receptors for, various cytokines than the skin of the face or hands. Such a geographic variation in the distribution of bullous pemphigoid antigen has been observed and hypothesized to account for the clinical patterns of this autoimmune disease.27 Application of modern biotechnological tools should provide insight into the mysteries of autosensitization.