Abstract

AbstractDrugs are one of the representative exogenous agents that cause photosensitive dermatitis. Both phototoxic and photoallergic mechanisms exist in photosensitivity to exogenous agents. While the phototoxic reaction is mediated mainly by reactive oxygen species, the photoallergic reaction is induced and elicited by immunological consequences. Two hypotheses have been put forward to explain the formation of photoallergen: prohapten and photohapten. The vast majority of clinically photoallergic drugs are photohapten rather than prohapten. Clinically, photocontact dermatitis and drug photosensitivity are the two major disorders caused by topical and systemic exogenous photosensitizers, respectively. The main cause of photocontact dermatitis is nonsteroidal anti‐inflammatory drugs. In drug photosensitivity, various causative agents have been reported and are recently represented by hydrochlorothiazide, quinolones, piroxicam, and flutamide. Orally administered drugs diffuse from the blood to the epidermis, and keratinocytes are photoderivatized with a given drug upon ultraviolet (UV) A irradiation, leading to photoantigen formation and cytokine production. In parallel, dendritic cells become photohapten‐bearing, T‐cell–sensitizing cells. Considering the mechanisms of photoallergy to chemicals, several in vitro assessments have been proposed to detect the photoallergenicity. Finally, a recent observation with newly marketed drugs has demonstrated that drugs may function as immunomodulators and induce photosensitivity as typically seen in anti‐CCR4 antibody.

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