Photoallergy

Abstract

There are two mechanisms underlying photosensitivity to exogenous agents: phototoxicity and photoallergy. While the phototoxic reaction is mediated mainly by free radicals, the photoallergic reaction is induced and elicited by immunological consequences. Photosensitive chemicals have a haptenic moiety, and two hypotheses have been put forward to explain the formation of photoallergens: prohaptens and photohaptens. Photohaptens need to coexist with a protein and, upon UV irradiation, a covalent bond is formed. The vast majority of clinically photoallergic chemicals are photohaptens rather than prohaptens. In a clinical photopatch test, a causative chemical is applied to the skin and UVA is irradiated to the site. This method tests the photohaptenic property. Clinically, photocontact dermatitis and drug photosensitivity are the two major disorders caused by topical and systemic exogenous photosensitizers, respectively. In photocontact dermatitis, halogenated salicylanilide and the related compounds musk ambrette, 6-methylcoumarin and benzophenone-3 (oxybenzone), were causative and, recently, topical NSAIDs have been another leading cause. In drug photosensitivity there have been many photosensitive drugs, including quinolones, piroxicam, afloqualone, griseofluvin, tegafur and tilisolol. The underlying mechanisms involve topically applied or orally administered chemicals diffusing from the skin surface or blood to the epidermis, and epidermal cells are photoderivatized with a given chemical upon UVA irradiation. Antigen-presenting dendritic cells are photomodified with the chemical upon exposure of the skin to UVA and become photohapten-bearing, T-cell stimulatory cells.