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61497191.Pdf View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Repositório Institucional dos Hospitais da Universidade de Coimbra Metadata of the chapter that will be visualized online Chapter Title Phototoxic Dermatitis Copyright Year 2011 Copyright Holder Springer-Verlag Berlin Heidelberg Corresponding Author Family Name Gonçalo Particle Given Name Margarida Suffix Division/Department Clinic of Dermatology, Coimbra University Hospital Organization/University University of Coimbra Street Praceta Mota Pinto Postcode P-3000-175 City Coimbra Country Portugal Phone 351.239.400420 Fax 351.239.400490 Email [email protected] Abstract • Phototoxic dermatitis from exogenous chemicals can be polymorphic. • It is not always easy to distinguish phototoxicity from photoallergy. • Phytophotodermatitis from plants containing furocoumarins is one of the main causes of phototoxic contact dermatitis. • Topical and systemic drugs are a frequent cause of photosensitivity, often with phototoxic aspects. • The main clinical pattern of acute phototoxicity is an exaggerated sunburn. • Subacute phototoxicity from systemic drugs can present as pseudoporphyria, photoonycholysis, and dyschromia. • Exposure to phototoxic drugs can enhance skin carcinogenesis. Comp. by: GDurga Stage: Proof Chapter No.: 18 Title Name: TbOSD Page Number: 0 Date:1/11/11 Time:12:55:42 1 18 Phototoxic Dermatitis 2 Margarida Gonc¸alo Au1 3 Clinic of Dermatology, Coimbra University Hospital, University of Coimbra, Coimbra, Portugal 4 Core Messages photoallergy, both photoallergic contact dermatitis and 45 5 ● Phototoxic dermatitis from exogenous chemicals can systemic photoallergy, and autoimmunity with photosen- 46 6 be polymorphic. sitivity, as in drug-induced photosensitive lupus 47 7 ● It is not always easy to distinguish phototoxicity from erythematosus in Ro-positive patients taking terbinafine, 48 8 photoallergy. thiazide diuretics, calcium channels blockers, or taxanes 49 9 ● Phytophotodermatitis from plants containing (Farhi et al. 2006; Sontheimer et al. 2008; Cohen 2009). 50 10 furocoumarins is one of the main causes of phototoxic Phototoxic dermatitis, on the other hand, does not involve 51 11 contact dermatitis. specific immune hypersensitivity reactions. 52 12 ● Topical and systemic drugs are a frequent cause of Although these mechanisms are well characterized, their 53 13 photosensitivity, often with phototoxic aspects. participation in each case of photosensitivity can be more 54 14 ● The main clinical pattern of acute phototoxicity is an complex. For instance, in chronic actinic dermatitis, 55 15 exaggerated sunburn. the extreme photosensitivity to UV light may be initially 56 16 ● Subacute phototoxicity from systemic drugs can present triggered by a photosensitive reaction or by contact allergy 57 17 as pseudoporphyria, photoonycholysis, and dyschromia. to perfumes, sesquiterpene lactones, or colophony, but in its 58 18 ● Exposure to phototoxic drugs can enhance skin evolution, individuals become extremely photosensitive even 59 19 carcinogenesis. with no further exposure to an exogenous chromophore or 60 allergen: An autoantigen may have been formed during the 61 acute reaction (DNA or RNA modified by plant products) 62 1 Introduction and/or, in the absence of the expected UV-induced immu- 63 20 nosuppression, sensitization to a new epidermal autoantigen 64 21 Photosensitivity represents an abnormal inflammatory has occurred (Hawk 2004; Be´ani 2009). 65 22 skin reaction to the sun, presenting under a wide spectrum When considering only phototoxic and photoallergic 66 23 of clinical reaction patterns. It is usually due to the abnor- dermatitis there is also an overlap between these two 67 24 mal presence, in the skin, of an endogenous or exogenous reaction patterns. Except for a few chemicals, as piroxicam 68 25 substance that is selectively activated by solar radiation – and olaquindox, which do not have an intrinsic photo- 69 Au2 26 a chromophore. Apart from exogenous photoactive toxic potential and induce only photoallergic reactions 70 27 chemicals, there are several causes for photosensitivity: (Figueiredo 1994), most substances can induce both 71 28 congenital or acquired errors may hinder DNA repair photoallergic and phototoxic reaction. For instance, 72 29 after ultraviolet (UV) aggression (xeroderma potent phototoxic agents like psoralens can induce 73 30 pigmentosum, Bloom’s syndrome) and reduce the natural photoallergy in some individuals. There is also some over- 74 31 UV protection (albinism and vitiligo) or the antioxidative lap between phototoxicity and photoallergy in the clinical 75 32 response to UV light (pellagra due to reduced levels of characteristics of the reaction and their time course. 76 33 niacin in diet or from alcohol consumption); accumula- Most phototoxic reactions are well recognized, are not 77 34 tion of endogenous photoactive chemicals, like in por- severe, and do not call medical attention. Others may be 78 35 phyria; idiopathic photodermatosis, inflammatory or severe and are often misdiagnosed, as their relation to sun 79 36 immune-mediated reactions whose antigen has not been exposure is not so obvious, namely, the recently described 80 37 well characterized, like solar urticaria, polymorphos light UV-induced skin cancers in patients on voriconazole 81 38 eruption, ‘‘lucite estvial benigne,’’ actinic prurigo, and (McCarthy et al. 2007; Cowen et al. 2010). 82 39 chronic actinic dermatitis (Hawk 1999). Photosensitivity from exogenous agents is now con- 83 40 Considering only photosensitivity from exogenous sidered rare (Darvay et al. 2001; Bryden et al. 2006), but it 84 41 agents, both chemicals applied topically or those that may be underreported or underdiagnosed (Zeeli et al. 85 42 reach the skin by the systemic route, there is still a wide 2006). Many photosensitizers have been recognized and 86 43 spectrum of skin reactions. Some involve predominantly removed from the market (salicylanilides, PABA) or sun 87 44 a specific T-cell-dependent response, including avoidance is recommended when they are used 88 T. Rustemeyer, H.I. Maibach, P. Elsner & S.M. John (eds.), Textbook of Kanerva’s Occupational Skin Diseases, DOI 10.1007/978-3-642-02035-3_18, # Springer-Verlag Berlin Heidelberg 2011 Comp. by: GDurga Stage: Proof Chapter No.: 18 Title Name: TbOSD Page Number: 0 Date:1/11/11 Time:12:55:42 2 18 Phototoxic Dermatitis 89 (lomefloxacin). Also, there is an increasing concern on Several phototoxic substances, like psoralens, chlor- 136 90 premarketing studies on the photosensitizing potential promazine, and fluorquinolones, apart from the capacity 137 91 of chemicals for human use. Nevertheless, photosensitiv- to generate free radicals and cell death responsible for 138 92 ity is still a field on intense research. New photosensitizers acute phototoxicity, also enhance chromosomal damage 139 93 are discovered, either causing skin disease (Chang et al. in the presence of UVR, both in vitro and in vivo (Seto 140 94 2009) or for therapeutic purposes. Also, new mechanisms et al. 2010). Therefore, they are photogenotoxic and 141 95 underlying the photosensitizing potential of chemicals photomutagenic, which is usually associated with 142 96 and new aspects of clinical presentation of photosensitiv- photoimmunosupression, and have consequent implica- 143 97 ity are recognized, which may be important to understand tions in animal photocarcinogenesis (Klecak et al. 1997; 144 98 diseases that course with photosensitivity, as HIV infec- Marrot et al. 2003; Lhiaubet-Vallet et al. 2009; Mu¨ller et al. 145 99 tion (Be´ani 2009). 1998). Epidemiological studies and recent reports also 146 show enhancement of photocarcinogenesis in humans 147 exposed to photoactive chemicals (Cowen et al. 2010; 148 100 2 General Mechanisms of Placzek et al. 1999; Miller et al. 2010). 149 101 Phototoxicity from Exogenous From the solar spectrum that reaches the earth, UV 150 Chemicals radiation, and particularly UVA (320–400 nm), is respon- 151 102 sible for most cases of photosensitivity. Even though 152 103 Normal skin is prepared to live with sunlight and takes some chromophores absorb in the UVB (290–320 nm) 153 104 benefit from it. Skin chromophores are activated upon sun and UVB is more energetic, UVA penetrates the skin more 154 105 exposure and undergo chemical reactions which are deeply and, particularly for systemic chromophores, this is 155 106 important for survival under the sun and necessary for certainly the most important spectrum for inducing 156 107 human life: 7-dehydrocholesterol is activated by UVB to photodermatosis (Hawk 1999). Only exceptional cases 157 108 form pro-vitamin D3 and Vitamin D. have a well-documented exogenous photosensitivity 158 109 Photosensitivity develops when an abnormal chromo- exclusively from UVB (Fujimoto et al. 2009). 159 110 phore is present in the skin or when a normal chromo- 111 phore in present in exaggerated amounts. When excited by 112 a photon these molecules receiving the energy suffer 2.1 Phototoxicity Versus Phototoallergy 160 113 changes within the molecule itself, often also within 114 neighboring molecules, in a cascade of events that result In theory, it is easy to differentiate photoallergy from 161 115 in skin damage and inflammation. The energy received by phototoxicity, but there are many overlapping aspects, as 162 116 the molecule excites the electrons in the outer orbits; the presented below. 163 117 molecule becomes reactive and can undergo several types Classically,
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