RESUMO
BACKGROUND: In addition to recreational tanning bed use, UV radiation exposures are sometimes sought to self-treat skin conditions. The ability of tanning bed radiation exposure to trigger toxic epidermal necrolysis has not been reported. OBSERVATIONS: A young woman attempted to treat a self-limiting drug hypersensitivity reaction via tanning bed radiation exposure, which resulted in a systemic toxic epidermal necrolysis-like reaction. Studies with cultured keratinocytes and an epithelial cell line reveal that UV-A radiation can synergize with other stimuli such as phorbol esters or interleukin 1 to produce large amounts of tumor necrosis factor, providing a potential mechanism for this exaggerated reaction. CONCLUSION: In addition to inducing photodamage and skin cancer, tanning bed radiation exposure can trigger a toxic epidermal necrolysis-like reaction, possibly via the exaggerated production of keratinocyte cytokines such as tumor necrosis factor.
Assuntos
Ibuprofeno/efeitos adversos , Síndrome de Stevens-Johnson/patologia , Banho de Sol , Raios Ultravioleta/efeitos adversos , Linhagem Celular , Progressão da Doença , Eritema/diagnóstico , Eritema/etiologia , Feminino , Humanos , Imunoglobulinas Intravenosas/uso terapêutico , Queratinócitos/metabolismo , Queratinócitos/efeitos da radiação , Síndrome de Stevens-Johnson/diagnóstico , Síndrome de Stevens-Johnson/tratamento farmacológico , Resultado do Tratamento , Fatores de Necrose Tumoral/biossíntese , Adulto JovemRESUMO
Ultraviolet B radiation (UVB) is a potent stimulator of epidermal cytokine production. In addition to cytokines, such as tumor necrosis factor-alpha (TNF-alpha), UVB generates bioactive lipids including platelet-activating factor (PAF). Our previous in vitro studies in keratinocytes or epithelial cell lines have demonstrated that UVB-mediated production of PAF agonists is due primarily to the pro-oxidative effects of this stimulant, resulting in the nonenzymatic production of modified phosphocholines (oxidized glycerophosphocholines). The current studies use human skin to assess whether UVB irradiation generates PAF-receptor agonists, and the role of oxidative stress in their production. These studies demonstrate that UVB irradiation of human skin results in PAF agonists, which are blocked by the antioxidant vitamin C and the epidermal growth factor receptor inhibitor PD168393. Inasmuch as UVB-generated PAF agonists have been implicated in animal model systems as being involved in photobiologic processes including systemic immunosuppression and cytokine (TNF-alpha) production, these studies indicate that this novel activity could be involved in human disease.
